Orals - short

What cells forms a Tubercule (granuloma)?

"G FML" Macrophages, lymphocytes, fibroblasts, giant cells- all these encapsulated

What is a stressed pulp?

(Abou-Rass) - Describes pulps that are neither healthy or diseased - Asymptomatic, previous hx of dental work or trauma - Pulp chamber recession, calcification, narrow canals, deep restorations - Weak response to pulp testing - Less than 2mm RDT (remaining dentin thickness) in pulp chamber - less chance of recovery, not enough blood supply - Before these teeth get more work, consider endo

Cause and diagnosis of perforations?

(Alhadainy) - Cause of perforations: Iatrogenic, internal or external resorption, caries - Danger zone in the coronal third of small curved canals like Mandibular molar mesials - Diagnosis - direct observation of bleeding, indirect bleeding by paper point, radiographically, apex locator o A file or reamer is placed in to an opening and the instrument appears loose rather than snug inside a canal. - Mid root perfs: attempt to prepare a canal with pulp stone, correcting a ledge or bypass an instrument - Apical perf: instrumentation beyond the apical foramen - Prognosis: Time, Location, size. The earlier you seal it, the better it is. Perforation close to gingival sulcus have poor prognosis. Away from sulcus have better prognosis.

What are some prognostic factors for root perforations?

(Fuss) ● Time - better to repair perforation immediately after it happens ● Size of perforation smaller perforations in big teeth have better prognosis ● Location Coronal, crestal, or apical worse prognosis when crestal: furcation or pulpal floor ○ The level of bone and epithlieum determine the prognosis of a perf ○ Crestal root level perfs have the worst prognosis.

What are different types of wounds in endodontic surgery?

(Harrison) - Incisional wound o Compared intrasulcular flap with submarginal flap that there was little difference in healing between the two flaps o Incisional wound healed quickly - epithelial seal and barrier formed in 2-3 days and by 14 days there was completed fibrous connective tissue - Dissectional wound - reflecting the flap o Rapid healing but slower than incisional wound o Periosteum is destroyed during flap reflection o Cells of the cambium layer are destroyed, and collagen undergoes depolymerization o New periosteum formation - Excisional wound o You can't reapproximate tissues so instead of a fibrin clot, a coagulum forms o Coagulum is replaced by granulation tissue o There was woven bone by 14 days and at 28 days, the woven bone was more mature and there was periosteum repairing the cortical plate - Repair vs Regeneration o Regeneration is where wounded tissues are restored to a normal anatomical pattern and function - happens during primary intention healing o Repair is when normal anatomy and function are not restored - ex. Scar tissue formation in secondary intention healing - Stages of wound healing for incisional wounds: 1. Clotting and inflammation, 2. Epithelial healing, 3. Connective tissue healing, 4. Maturation and remodeling o Injury, exposure of subendothelial surface causes start of clotting, platelet adhesion and formation of fibrin clot. o Then epithelium starts to proliferate and go toward each other and stop when they touch. Then you have thickening of the epithelial layer and you get the bridge formation from Day 2-3. (okay to remove sutures) o Granulation tissue starts to replace the fibrin clot as soon as the sealing happens. Starts by day 4. Very vascular, more collagen o By end of 2 weeks, connective tissue has replaced the granulation tissue o Then remodeling and maturation

What are considerations for hard tissue management?

(Hoskinson) - You don't want to damage bone by overheating - Threshold temp. for irreversible bone damage is 44-47 deg C for 1 min - The greater the speed of handpiece, the less heat generated - Use irrigation to cool while cutting bone - Use surgical handpiece to avoid emphysema from air - Burs - carbides are better than diamonds

What is the mechanism of local anesthesia in surgery?

(Kim) - Local anesthetic has two purposes: anesthesia AND hemostasis - Use 1:50k epinephrine - Epinephrine binds to both alpha receptors and beta receptors; There are primarily alpha receptors in the oral tissues that cause vasoconstriction; the beta 1 receptors are in the heart and increase heart rate and beta 2 receptors are in blood vessels that supply skeletal muscle and cause vasodilation. in oral mucosa, epinephrine primarily causes vasoconstriction - In the oral mucosa, 95% are alpha receptors, and 5% are beta receptors - Maximum dosage of epi for a normal human is 0.2 mg 5.5 carpules of 1:50 k - Maximum dosage of epi for a patient with cardiac conditions is 0.04 mg 2 carpules of 1:100k

How do you achieve good hemostasis during surgery?

(Kim) - Presurgical 1:50k epinephrine infiltration o Contricts blood vessels in the oral mucosa alpha receptors - Surgical epi pellets if small osteotomy, use ferric sulfate; If large osteotomy, use calcium sulfate o Ferric sulfate - chemical reaction that causes agglutination by acidic pH- forms a plug that occludes capillaries - Post-surgical moist gauze to compress the tissue and proper suturing

Why is the microscope essential for microsurgery?

(Kim) - You can see anatomical details such as lateral canals, isthmus, fractures - Precise removal of diseased tissue - You can see distinction between bone and root tip - Smaller osteotomy can be made - Better ergonomics

What are contraindications for endodontic surgery?

(Leubke) - Health contraindication (systemic disease, patient's emotional status) - Anatomic considerations o Surgical inaccessibility - palatal roots of molars, near the mental foramen, thick buccal cortical plate o Short root length o Poor bony support o Missing cortical bone - Operator capability

What are indications for endodontic surgery?

(Leubke) - Necessity for drainage - Postoperative failure of RCT (enlarging PARL, post-op discomfort) - Predictable failure of RCT (severely curved root, resorption) - Impracticality of conventional therapy (long post, crown, severe calcification) - Procedural accidents (separated instrument, perforation)

What is the purpose of periapical curettage?

(Lin) - Not necessary to take out all the granulation tissue, more important to take out source of irritants from root canals - Granulation tissue is the hosts response to irritation - part of the healing process - Purpose of curettage is to remove diseased periapical tissues for visibility and accessibility of root tip

What are different flap designs

(Niemczyk) - Triangular - Submarginal - Rectangular - Semi lunar

How should you position the patient and microscope for surgery

(Niemczyk), rubenstein - Tooth parallel to the floor - Microscope angle toward the tooth apex so you can see with direct vision - Patient head position - the occlusal plane should be parallel to the floor for mandibular surgery and perpendicular to the floor for maxillary surgery (Rubinstein)

Why do we remove suture in 2-3 days? Wound healing process?

(Velvart) - At 24 hours you have a fibrin clot with infiltration of PMNs - Day 1 to Day 3 there is epithelial bridging which is why it's recommended to remove suture - By day 4 there is an epithelial seal - After day 4, granulation tissue replaces the fibrin clot - And day 4-14, collagen tissue formation starts and replaces granulation tissue

What is the Biologic width?

(Velvart) - Biologic width is made of junctional epithelium and connective tissue attachment, each is about 1 mm average

What does the presence of papilla depend on?

(Velvart) - Distance between the contact point and crest of bone o When 5 mm or less, papilla present 100% of time o When 6 mm, papilla present 56% of time When 7 mm, papilla present 27% of time

Where does the blood supply for alveolar mucosa and gingiva come from?

(Velvart) - Subepithelial capillaries of the gingiva and alveolar mucosa, the vascular network within periosteum, intraseptal arteries in the bone marrow and the plexus of the periodontium Flap design you want 2:1 ratio of width to length for adequate blood supply

What are different hemostatic materials and mechanism of action?

(Witherspoon review) - Ferric sulfate coagulation - Gel-foam gelatin based sponges stimulate intrinsic clotting pathway by promoting platelet disintegration - Colla-plug collagen based products that promote platelet aggregation and activate factor XII - Bone wax purely mechanical for controlling hemostasis; not used anymore, if left, retards healing and causes chronic inflammatory reaction

What are the different zones in the pulp?

** Cell free zone is also called Zone of Weil

What are pathways of communication from periodontium to pulp?

- Apical foramen - Accessory canals - Dentin tubules - dead tracts - Root fracture - vertical or horizontal - Perforation - Dens-in-dente

7 - Bacterial Endocarditis/Endocarditis Medications/Joint Replacement

- BACTERIAL ENDOCARDITIS - Group B alpha hemolytic streptococcus viridans is the most common cause. The infection produces vegetations on the endocardium. This condition is fatal if left untreated, and the heart valve is usually involved. Rheumatic fever, a previous Hx of endocarditis, and patients on hemodialysis are definite risk factors. - Subacute Bacterial Endocarditis is the most common form of Bacterial Endocarditis with an alpha hemolytic streptococcus viridans infection of damaged valves. - Acute Bacterial Endocarditis is associated with Staph aureus and involves metastatic foci. - Chronic Bacterial Endocarditis is associated with E. faecalis. - We worry about SBE. With IV drug users there is concern about Staph aureus contamination - 50% of these bacterial endocarditis cases with drug users involve acute onset with the tricuspid valve. Only 20% of these drug users that develop endocarditis have previously damaged heart valves. Prosthetic valve endocarditis has a 1-3% incidence and the aortic valve is more common. 20-40% of patients with BE, there is no underlying heart disease. Pathophysiology: 1) Formation of nonbacterial thrombotic vegetations on valves or elsewhere on endocardium 2)Transient bacterimia 3) Colonization of the vegetations by microorganisms 4) Deposition of platelets and fibrin 5) Protected colonizations 6) Endocrditis - BE occurs in areas of high turbulence - Subacute Bacterial Endocarditis - weight loss, malaise, anemia, lethargy, and joint pain - need to determine cardiac function. Systemic involvement - hemorrhage under nails, petechial hemorrhages, osler nodules (painful lumps on fingers). With SBE you can get valve destruction and regurgitation as well as congestive heart failure. Need to Dx in susceptible patients - vague, flu-like symptoms of low grade fever, lethargy, weight loss with organic heart murmur and recent history of surgical procedure suggests infective endocarditis. Most valuable Dx - lab tests - blood culture, an increased ESR, mild anemia, circulating immune complexes. Tx SBE with bactericidal agent, IV antibiotics. Cure rate for Strep endocarditis is 90%, while 50% for Staph and Enterococcus. There are no controlled human studies to support need for premedication. If pt had rheumatic fever and heart murmur, but uncertain of which type - good idea to premedicate. Require Prophylaxis: 1) Prosthetic Heart Valve 2) Previous Infective Endocarditis 3) Congenital heart Disease a. unrepaired cyanotic CHD including shunts and conduits b. repaired CHD with prosthetic material for the first 6 months post sx c. repaired CHD with residual defects 4) Cardiac Transplant with Valvulopathy - Procedures to premedicate for include exo, endo, implants, reimplants, perio; PDLs - no need to premed. ENDOCARDITIS MEDICATIONS - Oral: 1) Amox 2g 1 hr preop, kids-50mg/kg orally - Unable to take oral - Amp 2g IV or IM, kids - 50mk/kg within 30 min - Allergy to Pen. - Clindamycin 600mg 1 hr preop, kids - 20mg/kg or Azithromycin or Clarithromycin - 500mg 1 hr preop, kids-15mg/kg - Allergic to penicillin + cant take oral- Clind - 600mg IV, kids -20mg/kg IV within 30 min - wait 10-14d btw appts or change AB to decrease chance of resistance JOINT REPLACEMENT - up to 2 years is the critical time period, although there is no scientific evidence to support the need for premedication to prevent hematogeneous infections. Premedication is not indicated for pins, plates, or screws. - Koren said AB prophylaxis should be given for the first 3 MONTHS if no post sx complications. - Those who may have a potential risk for joint infection and who may receive premedication are: 1) Immunocompromised/suppressed 2) Inflammatory arthropathies - (rheumatoid arthritis) 3) Type 1 Diabetes 4) Previous infections (joint) 5) Malnourished individuals 6) Hemophilia 7) HIV 8) Malignancy KNOW:Joint infections assoc. 1) Staph aureus 67% 2) Strep viridans 5% 3) Peptostreptococcus 2%

What are the differences between bacteria and archaea

- Bacteria and archaea both have 16s rRNA but they are different sequence - They have a difference in the lipids that make up the cell membranes o Bacteria have an ester bond between lipid and glycerol o Archaea have an ether bond between lipid and glycerol

What do you need to know about an antibiotic to know it will be effective against the infection?

- Baker - You need to know what organism is causing the infection - MIC of the antibiotic (lowest conc of antibiotic that inhibits growth of the bacteria - The blood (serum) level of the antibiotic (breaking point) (MIC and breaking point will determine susceptibility- the MIC should be lower than the breakpoint for the bacteria to be susceptible to the antibiotic)

What drugs are organ transplant patients usually on?

-Steroids, anticoag, immune suppressants

What bacteria is involved?

-Streptococcus pyogenes (beta hemolytic strep)

How do you know if a patient is in cardiac arrest?

-Unresponsive 1. no resonse 2. No circuation 3. No breathing

What is athersclerosis?

-hardening of arteries due to accumulation of plaque

How do you treat this?

-muscle relaxant (soma), analgesic, send to OS

What is coronary artery disease?

-narrowling or blockage of coronary blood vessel in the heart due to athersclerosis

Why is this a problem?

-no cardiac output

What if someone has acute heptatis how do you adjust treatment?

-no treatment unless emergency tx.

Would you use stabident on an organ transplant patient?

-no, bc you have to drill into bone and that would require more healing

What is the norm billirubin level, what is high?

-norm: 1 mg/dl -high: 2.5 mg/dl

What is Trismus?

-occurs when you inject in muscle or blood vessel. -pt not able to open wide

What does it mean if you are a carrier?

-persistent of levels of virus in liver and serum for longer than 6 months w/o liver dx.

Where is PSA injected?

-pgterygomaxillary space

4 - Addison's Disease and Cushing' Syndrome

ADDISON'S DISEASE - is PRIMARY adrenocortical insufficiency. It is due to a progressive destruction of the adrenal cortex, which must involve more than 90% of the glands before signs of adrenal insufficiency appear. The signs and symptoms of the disease are the result of deficiencies of adrenocortical hormones. The most frequent cause is idiopathic atrophy, and an autoimmune mechanism is probably responsible. The actual cause is unknown but is probably multifactorial including infections. The adrenal gland consists of two compartments - an inner adrenal medulla (products are epinephrine and norepinephrine) and an outer adrenal cortex (major products are steroid hormones consisting of glucocorticoid, mineralcorticoid, and androgen). The adrenal cortex is made up of 3 zones: 1) the outer Zona glomerulosa - produces the mineralcorticoid aldosterone (works on distal tubule of kidney to retain sodium) 2) the middle Fasciculata - produces the glucocorticoid cortisol (maintains BP, blood volume, blood sugar, feeling of well-being). It also regulates carbs, fat, & protein metabolism, and inhibits inflammation and maintains homeostasis during physical and emotional stress. Synthesis of cortisol (which has anti-insulin effects) is regulated by adrenal corticotropic hormone (ACTH which is made by the anterior pituitary) 3) the inner Zona Reticularis - produces androgen. As the major hormones of the adrenal cortex are cortisol and aldosterone, the presentation of Addison's disease is due to the lack of these compounds. Lack of cortisol results in impaired glucose, fat, and protein metabolism; hypotension; increased ACTH secretion; impaired fluid secretion; excessive pigmentation; and an inability to tolerate stress (due to maintenance of vascular reactivity and normal blood pressure). Aldosterone deficiency results in sodium loss and ultimately acidosis. For completion, although not defined as Addison's disease, insufficiency of adrenocrotical function may occur secondarily. This is more common than primary, and patients may be deficient in cortisol secretion as a result of long-term exogenous corticosteroid therapy which suppresses the pituitary-adrenal axis and causes glandular atrophy and the suppression of endogenous glucocorticoid secretion. The exogenous steroid causes the anterior pituitary to decrease production of ACTH which suppresses adrenal gland production of cortisol. Treatment of adrenal insufficiency involves replacement with corticosteroids, usually for life. The usual daily requirement of hydrocortisone is 20 to 30 mg. Due to natural circadian rhythm of the body, there is usually increased ACTH in morning. In addition, patients on steroid supplementation get more steroid in the morning. Both of these allow the patient to be better equipped to handle stress during morning appointments. STRESS is the major issue with these patients. We are primarily dealing with secondary adrenocortical deficiency. With steroid supplementation - there is anti insulin effect and decrease in immune response. INFECTION is a big problem. For most patients with adrenal insufficiency, stressful dental procedures require supplemental prednisone in the amounts of 20 to 40 mg. Some prefer to double the steroid dose pre-op, then taper off by cutting the dose in half each day until the maintenance dose is reached. Consult the physician for altering steroid dosages, and ask about steroid medication for post-op pain if needed. CUSHING'S SYNDROME - persistently elevated cortisol due to one of the following: 1) excess production of ACTH 2) elevated cortisol secretion 3) long-term exogenous steroids. Patients with connective tissue diseases, inflammatory bowel disease, autoimmune disorders, dermatologic problems, or graft transplantation are usually taking steroids. The majority of cases are caused by ACTH-producing tumors of the pituitary. Problems with this elevated cortisol are due to too much of a steroid - delayed healing mechanisms, hypertension, depressed inflammatory responses, lymphopenia, protein catabolism, adrenal suppression, and mood alteration. Cushing's syndrome typically occurs - Women:men -3:1. Moon face/buffalo hump are common physical findings. There can be steroid induced diabetes due to derangement in carbohydrate metabolism and glucose intolerance and the steroid having an anti-insulin effect (increased serum glucose). There is a need to regulate the steroid level before treatment. These patients can have weak respiratory muscles, so avoid sedatives. Osteoporosis may be a complication, so position the patient carefully. Watch out for INFECTION. Hypertension, diabetes, impaired healing are all major concerns.

12 - Angina Pectoris and MI

- Cardiovascular disease risk factors - males, menopausal women (due to decreased estrogen, increased LDL), family Hx, hyperlipidemia, hypertension, cigarettes, and diabetes mellitus. - Both angina and MI can present with chest pain, or pain in the back, shoulders, arms, neck, jaw, palate, or tongue. The pain may be associated with stress, excessive effort, or respiratory function. Gastritis (burning pain & reflux) can mimic these symptoms, as well as esophageal reflux and bronchitis chest pain. - ATHEROSCLEROSIS - thickening of intima layer due to plaque accumulation - less in women b/c estrogen decreases LDL, TG, blood clotting factors Angina - Transient ischemia of the myocardium usually with a substernal chest pain radiating to the left shoulder. - The transient chest pain may occur by: atherosclerotic stenosis, exertion (↑O2 demand), emotion, or stress (epi/norepi release) and is relieved by nitrates. The myocardium needs more O2 than the coronary arteries can provide. There is an increase in the cardiac workload and/or a decrease in O2 delivery. The result is ischemic cardiac pain with no permanent damage. - An atherosclerotic narrowing of the coronary lumen leading to insufficient O2 supply to the myocardium can eventually progress to an MI situation. - There may be an ↑in HR and BP - Stable angina (exertional angina) is usually relieved by rest within 10 minutes. - Unstable angina is either a change in the frequency or duration or pattern of anginal attacks. Also considered unstable angina is new onset angina within the first 6 months. - Printzmetal's angina is related to coronary artery spasms which may occur at rest or at night. Myocardial Infarct - Can produce chest pain like angina, but it can also be silent. - Panic and sweating are more likely to occur with an MI than angina. - ↓ BP and arrhythmia occurs. - Lasts for > 30 minutes, and nitroglycerin doesn't help. - Confirm an MI with an EKG and cardiac enzyme tests. - Most commonly due to a blood clot (thrombus) in the coronary arteries. Blood flow is retarded and an acute ischemic event occurs. This in turn causes acute dysrhythmias & impaired cardiac function. - Cells of myocardium ultimately die. Meds tx: nitrates, beta-blocers, calcium channel blockers, anti-platelet drugs and anticoagulants Surgical tx: Ballon angioplasty or coronary artery bypass Management of ASA II/III Patients: 1) stable angina 2) history of uncomplicated mi (more than 30 days) Management ASA IV patients: 1) unstable angina 2) history of uncomplicated mi (less than 30 DAys) 3) history of complicated mi (post mi disability/heart failure) Emergency Protocol Angina/MI · Cease procedure immediately · Administer Nitroglycerine (0.3 - 0.6 mg sublingual tablet or 0.4 mg sublingual spray) · Administer 100% Oxygen · Call EMS · If Nitroglycerine provides no relief after 3-5 minutes, administer again (for up to 2 more cycles) · Administer ASA 325 mg (have pt chew; quicker absorption) · Administer Beta 1 Blocker · Administer Morphine (2 mg IV or 5 mg IM) or Nitrous Oxide for pain management * Unconscious pt: A- head tilt, chin lift; B- look, listen, feel C- check circulation D-defibrilator Modifications of treatment - Call cardiologist and inquire about INR level if on blood thinners and if condition is stable - Morning appointments (pt well rested) - Limit epi to .04mg = 2 carpules of 1:100,000 - ANTB: Use Pen or Clinda (Amox is wide spectrum and may kill bacteria that facilitate absorption of vit K) Avoid Macrolides, Tetracycline, Metronidazole, Amoxicillin (interfere w/ anticoagulant metabolism and prothrombin formation) - Death from MI mostly occurs from V-fibrillation (acute dysrhythmia). If you use a defibrillator within 1 minute, there is a 90% success/survival, within 2 minutes - 80%, and each minute after that there is a further decrease of 10%.

What is the significance of doing a root-end filling?

- Christiansen - compared MTA root end filling to just smoothing gutta-percha o GP group 28% healing, 52% o MTA group 85% healing, 96% o This study had both retro-prep and filling

11 - Asthma

- Chronic inflammatory respiratory disease consisting of recurrent episodes of dyspnea, coughing, and wheezing resulting from hyper-responsiveness of the trachea-bronchial system. - The obstruction of airflow in asthma is because of bronchial smooth muscle spasm, inflammation of bronchial mucosa, mucous hypersecretion, and sputum plugging 5 Types: Extrinsic/allergic asthma: most common; triggered by inhalation of seasonal allergens; most frequently in children and young adults with fam hx. Allergens interact with IgE antibodies attached to surface of mast cells. The Ag-Ab complex cause the mast cell to degranulate and release various cytokines such as bradykinins, histamine, leukotrienes, and prostaglandins. Intrinsic asthma: Associated with endogeneous causes such as emotional stress, gastroesophageal acid reflux, or vagal-mediated responses. Mostly middle aged adults; no fam hx. Drug induced asthma: NSAIDs, ASA, b-blockers, ACE inhibitors. Aspirin and NSAIDs block the cyclooxygenase pathway leading to the buildup of leukotriene (via lipoxygenase pathway), which results in broncospasm. Metabisulfite preservatives of foods and drugs (local anesthetics containing epinephrine) is another trigger. Exercise-induced asthma: Thought that thermal changes during inhalation of cold air can provoke mucosal irritation. Infectious asthma: Infectious agents such as viruses, bacteria, dermatological fungi, and mycoplasma organisms can cause an inflammatory response of the bronchi. This results in increased airway resistance and bronchial constriction. Status asthmaticus - a severe and prolonged asthmatic attack (longer than 24 hrs) that is refractory to usual therapy; life threatening Frequency of attacks: 1. Acute asthmatic attack - characterized by wheezing, coughing, chest tightness, severe dyspnea, flushing; lasts for several minutes and resolves spontaneously following rest, or with administration of medication. 2. Intermittent asthmatic attacks - occur < 5 days/month. 3. Chronic asthmatic attacks - > 5 days/month for longer than 3 months, regardless of intensity. Pharmacological Management Acute asthma - immediate therapy with b-2 adrenergic agonist (albuterol, epinephrine, isoproterenol); produce fast bronchodilation and smooth muscle relaxation; administered orally or via inhalers. Intermitten asthma - do not required continuous drug therapy. If needed, b-2 adrenergic agonist is first, then Theophylline. Chronic asthma - managed by b-2 adrenergic agonist and theophylline. Inhaled corticosteroid is added to the therapy regime when the airway obstruction is refractory to the first two drugs * Antileukotrienes - useful in mild to moderate asthma and in ASA-induced asthmatic response Dental Management - Review patient's med hx to determine: type, severity, frequency, and duration of asthmatic attack. Find out if patient has ever been hospitalized for asthmatic condition, and how they manage condition pharmacologically. - Consultation with the physician may be necessary for more severe cases. - Anxiety is a major trigger; important to apply stress-reducing measures; Appointments should be kept short and in the morning. - Oral sedation and nitrous oxide are helpful; - AVOID: Barbituates and opiates; produce respiratory depression; Macrolide antibiotics (erythromycin and azythromycin) should be avoided in patients taking theophylline, increase serum level of theophylline by altering cytochrome p450 enzyme. - Sulfite preservatives in local anesthetics with epinephrine can precipitate an asthmatic attack. These anesthetics should be avoided in patients with acute asthmatic attack. - NSAIDs and aspirin should be avoided since they can result in buildup of leukotriene - In severe asthma using systemic steroids, a supplemental cortocisteroid therapy is recommended if procedure to be carried out is stressful to the patient. Oral Manifestation - Mouth breathing - B-agonist inhalers can decrease salivary flow - Gastroesophageal acid reflux is exacerbated by the use of b-agonist and theophylline. - Oral candidiasis is a side effect from chronic usage of steroid inhaler. - The use of antileukotriene and theophylline can cause headaches. Management of asthmatic attack If the patient has been using an inhaler for his/her condition, it should be used as a prophylactic measure prior to starting treatments. If an acute episode of asthmatic attack develops one should: 1. Recognize the problem (wheezing, respiratory distress) 2. Stop the procedure 3. Position patient comfortably (usually upright) 4. Administer short-acting bronchodilator inhaler 5. If episode continues, activate EMS, administer maximum 0.3-0.5ml Epi (1:1000K) subcutaneously 6. Provide positive-flow oxygenation and monitor vital signs (oxygen saturation if possible)

Does a tooth infection cause systemic effects?

- Dahlen: Took LPS from fusobacteria and bacteroides and put into pulp and IV in rats. Resulted in pulpal inflammation, systemic immune response and found antibodies in lymph nodes and spleen. Systemic response with IgG and IgM circulating antibodies. Used the Jerne Assay. ***Dr. Stevens loves this paper to support the notion that what you put into a root canal, or whatever is inside of the root canal, can have systemic effects. ***

What are some physical means of sterilizing?

- Heat and pressure o Boiling water temperature kills most organisms but not spore forming organisms o If you seal the pot and continue to heat past boiling temp, pressure increases with temperature spores killed in 20 min o Open heat system (dry heat, ex. Oven) turning heat up to 165 C, spores killed in 2 hours - UV Radiation - Ionoizing Radiation

Where is the bacteria in a carious pulp exposure?

- Lin and Langeland o 15 teeth with radiographic pulp exposure examined histologically o ** Bacteria observed as deep in the pulp tissue as the necrosis o Bacteria present in primary dentin, tubules, predentin and adjacent necrotic pulp tissue o Periapical pathology was found without total necrosis, nerve fiber was often found to be the last thing to go o Bacterial byproducts can cause disease because in some instances, whole bacteria was not found

What is a liner? What is a base?

- Liners - low viscosity, very flowable, produce thin layers, antimicrobial, block dentin tubules, to stimulate repair in dentin - Bases - more viscous, need to be applied with pressure, thicker layer, used to replace extensive amounts of dentin that was removed, for insulating, low heat transfer under metallic restorations

How can you classify bacteria?

- Macro approach look at grossly observable characteristics (ex. Shape, appendages, composition, growth requirements, substrate) - Micro approach quantitative molecular comparisons (ex. Sequence of proteins, DNA base composition (GC content), DNA homology, RNA homology, rRNA sequencing - Kingdom Phylum or Division Class Order Family Genus Species - Bacterial Kingdom is divided into the Phyla: Gram negative (thin skin), Gram positive (thick skin), and no skin (ex. Mycoplasma)

What are the characteristics of black-pigmented Bacteroides (BPB)?

- Maynard: o BPBs are gram-negative, strictly anaerobic, non-motile, non-spore forming rods o Use Vit. K for growth, glucose and other sugars inhibit growth rate o Breaks down red blood cells to form hemin from hemoglobin produce black color

Describe the process of how one cell can stimulate another cell to differentiate.

- One cell type produces and secretes different proteins (signal proteins) - There has to be a receptor molecule on the surface of the receiving cell - The receptor molecule is a molecule that spans through the cell membrane of the receiving cell - one end is out into the environment and another portion is inside the cell - When the signal molecule binds to the receptor - causes a conformational change in the receptor molecule, changing its function - becomes a kinase - phosphorylates another molecule (that molecule is a signal transduction molecule) - Signal transduction molecule - transmits signal from the cell membrane into the nucleus (ex. SMAD) - When the activated signal transduction molecule reaches the nucleus, it combines with another protein or activates another protein that is in the nucleus (transcription factor) - Transcription factor - regulates transcription - reading of genes in a specific way - There are specific target sites on DNA that can interact with activated transcription factor on "promotor sites" 🡪 differentiation

What are 3 factors responsible for microorganisms being able to cause disease?

- Siqueira and Rocas - review paper o Virulence of organism o The Load o Host defense

What is the difference between sterilization, disinfection, and sanitization?

- Sterilization - elimination or killing of all viable life forms - Disinfection - elimination or killing of organisms capable of infection or causing disease - Sanitization - lowering microbial content of an object - In endo, it is impossible to sterilize, but the goal should be sterilization; what we actually do is sanitize

How does blood flow in the pulp compare to other tissues in the body?

- Pulp has highest rate of blood flow in any tissue in the oral cavity - Heart and kidney have higher blood flow than pulp - Brain is about the same blood flow rate as the pulp

What are the diagnostic approaches to gain information on the status of the pulp? Status of periapical area? (Newton)

- Pulp: o Thermal (heat cold) o Electric o Laser Doppler flowmetry (LDF) Pulse oximetry: light bounces off erythrocytes (red blood cells), is returned to a receiver channel in laser probe, and is recorded as pulpal blood flow. o Pulse oximetry: oxygenated and deoxygenated hemoglobin absorb different amounts of each light, pulsating changes in blood volume cause periodic changes in the amount of light absorbed by the vascular bed before reaching the photodetector. o Selective anesthesia o Test cavity - Periapical: o CBCT - highly sensitive o PA - need sufficient bone loss (Bender), also problem with interpretation

What is the correlation between clinical signs and symptoms and the histology of the pulp?

- Seltzer 1963: o Correlations found between incidence and history of pain, previous pulpal exposure, pain to percussion, negative EPT & thermal response to histological diagnosis of the pulp o No correlation found between the severity of pain, the quality of the pain, painful responses to thermal stimuli, and histologic diagnosis of the pulp. o A poor correlation exists between pulp-test readings and the state of the pulp. In necrotic pulps, the electric pulp tester is more accurate.

What mediators affect pulpal blood flow?

- Vasoconstriction - Norepinephrine, neuropeptide Y - Vasodilation - PGE2, bradykinin, histamine, NO

How can clinical testing reveal endo vs perio etiology?

- Vitality of the tooth - problem with multirooted teeth though - Probing o Isolated case of periodontal issue (ex 10mm pocket in one area) probably means endo - Pain o Perio- Dull diffused pain o Endo- Throbbing, localized pain - Radiographic findings o Perio lesion- More horizontal bone resorption o Endo lesion- Bone loss more local and vertical - Drainage o Usually endo lesions drain from a fistula o Some endo lesions though drain through the pocket

What do you need to know about an antibiotic to know it will be effective against the infection?

- You need to know what organism is causing the infection - MIC of the antibiotics - The blood level of the drug

What are the Fish zones of tissue reaction?

- Zone of infection (PMNs) 🡪 organisms present - Zone of contamination (round cells) 🡪 dead bone cells and round cells - Zone of irritation (osteoclasts and histiocytes) 🡪 bone resorption - Zone of stimulation (osteoblasts and fibroblasts ) 🡪 defensive wall and bone and collagen fibers being formed

What does billirubin do?

-degrade hemoglobin

What is the problem with having an elevated cortisol level?

-delayed healing, hypertension depressed inflammatory response, diabetes TAKE HOME: TAKE BP THROUGHOUT, DON'T PRESCRIBE ASA OR NSAIDS

So tell me about healing with diabetes?

-diabetics dont' heal as well because everything is proinflammatory

What is Addison's disease?

-disease when adrenal glands do not produce enough of their hormones

Where does PSA anesthetize?

-distal root of Mx 1st molar to Mx 3rd molar

Where do you inject for stabident?

-distal to the tooth (no epi)

What is the Ghon complex?

-dormant TB in hiliar lymph nodes (apical lung). "calcified lymph node w/bacteria

So if you were giving an antibiotic to an organ transplant patient would there be any changes?

-dosage and interval

What is drug induced asthma?

-due to preservatives

What will lab tests show?

-elevated ALT and AST (serum transaminases)

What about a severely uncontrolled diabetic?

-emergency treatment only

What is intrinsic asthma?

-emotionally related. No known cause. females

What does the kidney do?

-excretes wastes, filters the blood, regulates fluid volume.

How is hep A transmitted? How do you treat?

-fecal or oral route typically in children and young adults. -poor sanitization -treat with rest

What if they have a joint replacement? What would you do?

-give antibiotic (Keflex)

DENTAL MANAGMENT OF HYPERVENTILATION: How would you treat someone who is hyperventilating?

-give them a paper bag to breath into -Have them hold breath for a few seconds then exhale -DO NOT GIVE O2 (they already have too much O2 in body) -Call EMS

What happens if your patient has an asthma attack? What do you do?

-give them inhaler -call 911 -epi pen (0.3-0.5ml in 1:1000)

What is bacteria responsible for Rheumatic heart disease?

-group A beta hemolytic strep (gram - anaerobe)

Tell me why is it so resistant?

-high lipid content in its cell wall

What is pre eclampsia?

-hypertension with proteinuria

What happens during adrenal crisis?

-hypotension -hyopglycemia -arrythmias

How do you treat?

-ice and pressure for 24 hrs

Angina and Athersclerosis What is Angina?

-imbalance between O2 and supply and demand due to atherosclerosis of the cardiac fibers. Chest pain

So what is hyperglycemia?

-increase in blood glucose -can lead to oxidative stress --> free radicals

So tell me what is hyperventilation?

-increased frequency and depth of respiration. -Bascially body is blowing off too much CO2. (lack of CO2 in body) "opposite of asthma"

What is the cause?

-infectious- hep virus, mono, TB) -non infectious (drugs, alcohol)

What is Tuberculosis?

-infectous dx of typicaly affecting the lungs. (Various strains of mycobacterium tuberculosis) "hyper inflammatory response"

Infective Endocarditis So tell me what is endocarditis?

-inflammation of the inner lining (endothelial lining)of the heart due to turbulent blood flow from damaged heart valves

Hepatitis What is Hepatitis?

-inflammation of the liver

How is it transmitted?

-inhalation Most TB results from a reactivation of the tubericle

What do LA's do?

-inhibit Na influx though sodium specific channels in neuronal cell membrane

What does Lipocortin do?

-inhibits phospholipase (thus shuts down both COX and LKT)

What is MI?

-interruption of blood supply to the heart, causing heart muscle cell death

What is a TTx resistant Na channel?

-it blocks Na, channel, inhibits action potential from firing.

Why not amoxicillin?

-it increases bleeding because it inhibits Vit K

So tell me, how do you get rheumatic heart disease?

-it is an autoimmune dx

So what does this prophylaxis do?

-it lowers amount of bacteria

What about Hep D?

-it occurs as a co infection with Hep B

What is methhemoglobinemia?

-it prevents O2 uptake and it holds it tight

Why don't you want to give steroids?

-it's anti insulin and can contribute to gestational diabetes *Placenta secretes CRH --> higher sugar levels due to corticosteroids

Where do you deliver gow gates?

-lateral to neck of condyle, in line with palatal cusp of mx 2nd molar

DENTAL MANAGEMENT: If you give too much anes what do you do?

-lay them supine, monitor vitals, give O2

What INR do you want if you are doing surgery?

-less than or equal to 3-3.5

What are some symptoms of hyperventilation?

-lightheaded, dizzy, anxiety

What characteristic can give anesthetic potency?

-lipid penetration

Where are amides broken down?

-liver

How does this effect our treatment?

-liver produces clotting factors and if it is compromised then bleeding is a problem. NEED INR

Why does the gland not function in secondary?

-long term steroid therapy supresses pituatary-adrenal axis and suppression of endogenous glucocorticoid secretion => anterior pitatuary has decreased production of ACTH which suppresses adrenal gland production of cortisol

What is the function of the adrenal gland

-maintain vascular tone

What does pKA mesaure?

-measures the affinity for H ions -strength of acid in solution (opposite of pH) *if you have a lower pKA you'll have a faster onset

So tell me what is diabetes?

-metabolic disorder where you have increased glucose in blood because insulin is not being produced or working properly

What is most common predispositon to SBE?

-mitral valve prolapse

What valves does rheumatic fever effect?

-mitral, aortic, tricuspid

Why Keflex?

-more geared toward Staph infections

How would you change your treatment?

-morning appts, pain control, decrease stress (valium), monitor BP, short appt

Why is smoking a risk factor?

-nicotine decreases O2 to the heart -increases blood clotting

Would you give NSAIDS?

-no Why? -NSAIDS b/c it closes DA which is a shunt from the mom to the baby so baby can get O2.

How would you treat a patient who is well controlled?

-no alteration unless complications present

What if they have pins, plates or screws?

-no premed *would give abx first 3 months after surgery to cya

Where are esters broken down?

-plasma by pseudocholenesterase to form PABA (pt's allergic to this)

Where does billirubin occur?

-plasma, urine, eyes, epithelium

What is Cushing's syndrome?

-presistently elevated cortisol due to one of the following: 1. Excess ACTH production 2. Elevated cortisol due to tumor 3. Long term steroid use

How does the intrapulpal work? Who?

-pressure, Birchfield

What is seroconversion?

-probability of getting infected

Do not give NSAIDS (aspirin). Why?

-promotes bleeding, nephrotoxic

What are some side effects of those meds?

-prone to infection, bleeding, delayed healing, imparied drug metabolism.

What does INR measure?

-prothrombin time

Where is IAN injected?

-pterygomandibular space

What is PPD?

-purified protien derivative (they inject tubericlin)

What is cirrhosis?

-replacemnet of liver tissues with fibrous scar tissue --> loss of liver function

So how is this going to change your treatment if someone is on dialysis?

-schedule treatment the day after dialysis. -don't give NSAIDS -don't give drugs metabolized in the kidney

What is Azotemia

-sign of rental disease

What is Hep E?

-similar to hep A (oral/fecal)

Why do you not want to give a diabetic steroids?

-steroids are anti insulin so it can further contribute to hyperglycemia

How do steroids function in asthma?

-stimulate T cells which release IL-10 which is anti-inflammatory

When you have a prego in the chair why do you want to avoid seating patient on back?

-suppresses IVC, so turn them to the side

What is a hematoma?

-swelling of blood vessel

What are the antibodies?

1) IgG (greatest number, classic, placenta), IgA (dimmer is secretory, J, alternative), IgM (first to arrive, J, classic), IgE (lowest concentration, parasites, allergy), IgD (lymphcytes)

Monocytes?

1) Immature in blood, when they get into tissue differentiate into macrophages. Slower to arrive at site of injury. After they become macrophages, they remove dead cells, damaged tissue, and secrete active products. (lysosomes, complement, oxygen metabolites, cytokines (IL1), and growth factors. Macrophages can ingest debri of dead neutrophil and absorb fluid from the tissue.

Endotoxin does what?

1) Induces fever, complement, activates macrophages, causes bone resorption.

Hypersensitivity reactions?

1) Type I: immediate, cell bound antibody, anaphylactic shock, histamine, IgE, eosinophils. Type II: cytotoxic, cell bound antigen, E. Fetalis . Type III: immune complex, both are free, glomerulonepritis or serum sickness, Type IV: delayed hypersensitivity, T cell, contact dermatitis.

How does shock occur?

1) When TNF A enters circulation, it can cause vasodilation, and increase vascular permeability leading to hypotension and shock.

When do you get healing?

1) When irritants destroyed, activators destroyed by enzymes, and regeneration done.

What can chronic inflammation result in?

1) loss of function

IL-2:

1) releated by T cells and can proliferate more T cells. Enhance the cytotoxic activities of T cells and macrophages.

DENTAL MANAGMENT OF DIALYSIS What if you had patient with abscess on dialysis?

1. Ask them what kind of dialysis and when is the last time they had it. 2. Treat the day after dialysis 3. Talk to nephrologist to see if they are stable and if let them know the meds you are going to use and prescribe and if they want any changes. 4. May need INR 5. Take BP on arm that does not have shunt

Can you tell me a few steroid induced protiens?

1. Lipocortin 2. Vasocortin = lowers edema and lowers capillary permeability 3. NO synthase 4. Lysosomes 5. Kinase 2

What does cortisol do?

1. Maintains BP 2. Blood volume 3. Blood sugar 4. Overall well being 5. insulin resistance and lipolysis 6. activate osteoclast and inhibit osteoblast

What are the functions of insulin?

1. Move amino acids into the blood 2. Glycogen storage in liver 3. Increase triglycerides 4. Gluconeogenesis

What are the body's defenses against TB?

1. Mucous cells/Goblet cells (trachea) 2. Alveolar macrophages (delayed type IV) 3. Lesion (Tubericle)

What receptors does lidocaine work on?

-Alpha receptors (vessel)- vasoconstrictor -Beta 1 receptor (heart)- (use B blockers to decrease contractions) -Beta 2 receptor (lung)- vasodilation

Local Anesthesia What are the 2 classes of LA?

-Aminoamide and Aminoesters

What and how much abx would you give?

-Amox 2g 1hr prior -Clina 600mg 1 hr prior

DIALYSIS PATIENTS ARE DIFFICULT TO TREAT FOR PAIN What would you premed with if you needed one?

-Amox or Clina if allergy

What abx would you give?

-Amoxcillin but give higher dose because there is greater blood volume and conc of abx would be less. Consult with physician. Possibly 2 g or more

What abx would you give?

-Amoxcillin or Keflex

Can't take oral?

-Amp 2g IV or IM

Organ Transplants What are some drug side effects you should be worried about with organ transplants?

-Anemia (not enough RBC's in blood, thus not enough O2 in blood) -Bleeding (cyclosporine) -Infection -Liver toxicity

What block would you use to anes mx premolars?

-Anterior superior block

What is the basic lesion that occurs? What's in it?

-Aschoff bodies (collagen bits, fibrin, platlets)

What are some categories of drugs a patient with an MI could be on?

-Beta blockers, anticoagulants, anti platelet, calcium channel blocker (HTN med) TAKE HOME: MINIMIZE STRESS, GOOD PAIN CONTROL, USE BENZO'S IF NEEDED, SHORT APPTS, HAVE NITRO AVAILABLE IF YOU DO SEDATE USE 0.125MG TRIAZOLAM THE NIGHT BEFORE AND 1 HR BEFORE APPT. GIVE PEN OR CLINDA -max epi for cardiac patient: 0.04 -(max 2 carps of 1:100,000) (each carp has 0.017 epi) (0.017 x 2 carps = 0.034 epi) -Aspirin and NSAIDS are ok

What are the classes of diabetic meds?

-Biguanides "metformin" (decrease hepatic glucose production) -Thiazolidinedoines "Avandia" -Sulfonyureas (stimulates insulin secretion)

What anesthetic lasts a long time and why?

-Bupivicane (marcaine) - it has a high protien binding

What two systems are effected by LA?

-CNS and CVS

What is the Jones Criteria?

-Carditis (valve inflam), Nodules, polyarthritis, Chorea, Erythema

If allergic to Clinda what would you give?

-Cephalasporin (Keflex)

What are some symptoms of TB?

-Cough, wt loss, postive skin test

Someone who had a transplant is usually on what drugs for immunosuppressive therapy?

-Cyclosporine- bleeding, anemia. suppresses lymphocytes -Prednisone- delays healing, adrenal gland suppression -Azathioprine-inhibits immune response, greater bleeding and infection potential

How do you get gestational diabetes?

-From hormones, estrogen and progesterone. When you are pregnant all hormones increase except insulin. For this reason prego patients have increased inflammation because all hormones are increased.

What is the difference between granulomatous tissue and granulation tissue?

-Granulamatous tissue- infection still going on -Granulation tissue- healing

What are the two types of dialysis?

-Hemodialysis-filtration using AV fistula. Takes blood out of radial artery and filters it and puts it back in the cephalic vein. Disadvantage: Risk of blood born disease. Heaprin given. Bleeding

What are the different types of hepatitis?

-Hep A-G and TTV

Which hep has the highest serioconversion?

-Hep B 6-30%

Which Hep has the highest carrier rate?

-Hep C (70-90%)

What are some side effects of taking meds for TB?

-Hepatotoxicity -Bleeding -Leukopenia

What acute medical emergency could you face with a diabetic?

-Hyperglycemia- "ketoacidosis" polydipsia, polyuria, polyphagia -Hypoglycemia- (insulin shock)- they took insulin but didn't eat.

What if there is swelling?

-I would give a loading dose 1000mg loading 500mg every 8 hrs

If allergic to PCN?

-IV vancomycin

From there what do you do?

-Take a good med history -Call physician to see if patient is stable to treat

If you have a patient that is in pain what medication will you give him. Why?

-Tylenol

What would you give for pain?

-Tylenol

What would you give for pain?

-Tylenol III

What is the most common reason for death from MI?

-V-fib

What are the contents of anesthetic?

-Vasoconstrictor -Distilled water (volume) -Sodium bisulfite (preservative) -Sodium chloride (isotonic)

When treating a patient that has hepatic issues what precautions should you take?

-Watch how much anesthetic (it's metabolized in the liver) -Watch how much tylenol (metabolized in the liver)

Adrenal insufficiency So tell me what is adrenal insufficieny?

-a condition where the adreanal glands do not produce adequate amounts of steroid hormones (cortisol, aldesterone)

Tell me about Hep C

-acquired parentally and sexually RNA VIRUS -after blood transfusions

What is Chronic active hepatitis?

-active replication of virus in liver

What is a major concern within first 6 months of transplant?

-acute rejection

What is the difference between acute and chronic hepatitis?

-acute- hep A and E -acute and chronic- B, C, D

What are a few predispositions?

-age (older people tend to get it- immune system not as strong) -Male

What age group gets this disease?

-age 5-15

What are the risk factors?

-age, gender, family history, smoker, diet, diabetes

What is extrinsic asthma?

-allergin (IgE) response to foreign particle

So what bacteria are involved with endocarditis?

-alpha hemolytic strep -staph aureus -enterococcus -HACEK

What does it mean when you get burning on injection?

-contamination

What is the Duke criteria?

-criteria to diagnose endocarditis

How many carps can you give a normal patient of 1:100? What about 1:50?

1:100 = 11 carps 1:50 = 5 carps

How many carps can you give a cardiac patient?

1:100 = 2 carps 1:50 = 1 carp

Calculate how much epi you can give someone if you are using 2% lidocaine w/1:100,000 epi

1g/100,000 1000mg/100,000 1mg/100 x 1.8 = 0.018mg of epi per cartridge

Why?

1st trimester- organs still forming 3rd trimester-not comfortable (induce pregnancy) (emergency tx only)

How do you calculate how much 2% lidocaine you can give to a 200lb person?

2g/100ml 2000mg/100ml 20mg/1ml x 1.8 = 36mg/cartridge Max dose = 2mg/lb x 200/36m = 11 carpules

11 - Tuberculosis

3 important reasons to be concerned about TB: 1) it is an infectious disease - communicable - and high risk 2) may be found in the oral cavity 3) the dentist may be the 1st person to detect the patients TB. The organism responsible for TB is Mycobacterium tuberculosis, which is an obligate aerobe that likes high O2 tension areas such as the lungs. High risk groups include those in contact with TB, HIV patients, IV drug users, and health care workers. The typical transmission of TB is by infected, airborne droplets of mucous or saliva forced from the lungs. The quantity and size of the sputum and droplets influence the transmission. It may take up to weeks or years for active TB to manifest. TB can affect any organ of the body, but the lungs are most common. Typical infection starts with inhalation -> alveoli -> multiplication -> regional lymph nodes -> can get systemic dissemination. 2-8 weeks later -> hypersensitivity skin test (PPD - purified protein derivative) - goes from negative to positive. The major lesion of TB is a productive tubercle with central casseous necrosis. When it involves multiple organs it known as miliary tuberculosis which is epithelial degeneration that can go to the meninges, pericardium, kidneys, adrenal gland, spine... In the initial stage of TB there may be malaise, night sweats, fever, and cough. For a skin test to be positive without doubt it has to be >15mm. If a person has active TB - treat only in a hospital setting. If the patient has a past Hx of TB do not treat until cleared by physician (need verification that the complete drug regimen was followed [often up to 18 months]). If this complete drug therapy was not taken, the patient still may provide risk. If the patient has +PPD - often no dental treatment is given and the patient is placed on meds and x-ray is usually taken in conjunction for confirmation. Signs and symptoms of TB (non-productive cough, pleuritic chest pain, and fatigue) - definitely do not treat - refer to physician. Patients with TB often take rifampin and isoniazid. These meds are often hepatotoxic, so Rx aspirin type products may be contraindicated.

What would someone who is being treated for TB be prophylaxed with?

300mg Isoniazide for 9 months

Let's say a patient has an area of swelling and infection and you give anesthetic and it doesn't work. Why isn't it working?

1. the local pH is lowered so it's more acidic. Thus more more hydrogen ions cannot cross membrane. 2. You get more dilation --> more blood flow to the area to absorb anesthetic 3. Stimulates nocieception (decreases threshold)

What INR level do you want for minor surgery?

< or = 3.5

Uncontrolled

<70 blood glucose- maybe tx >400 blood glucose- med consult >9.5% HBA1c - em only

How should you treat perforations?

? (Fuss) - First try to treat conservatively with non-surgical treatment and then if not possible or if fails, do surgical treatment. - Non surgical treatment: o Lateral perforations: § Coronal- Should be able to seal externally w/ composite resins or glass ionomers § Crestal perforations- Difficult to manage bc of proximity w/ oral environment. Surgical intervention is usually necessary to seal off the defect. Any biocompatible material w/ short setting time should be used in these cases § Apical perforations: If small the perforation can be sealed w/ conventional RCT and sealed w/ GP and sealer. If large an apicoectomy could be considered o Furcation perforations § Author recommends using calcium hydroxide, tricalcium phosphate, HA or dentin chips to try and repair these perforations. Glass ionomers and resins could also be considered. In large furcation perforations w/ perio involvement the prognosis is poor and surgical removal of one root should be considered.

How does vital bleaching affect the pulp?

Calviedes Fugaro - Light and laser activated tooth-bleaching systems increase substance P expression in the pulp (Calviedes) - Fugaro looked at vital bleaching o Group 1 - 4 days of bleaching o Group 2 - 14 days of bleaching o Group 3 - 14 days of bleaching, 14 days recovery o Found minor histologic changes in 16/45 bleached teeth o Only significant difference between control in group 1 and 2 o Bleaching is considered safe for dental pulp

Can the tooth crack?

Cameron Cameron Guthrie Brannstrom

8 - Bacterial Endocarditis/Endocarditis Medications/Joint Replacement

BACTERIAL ENDOCARDITIS - alpha hemolytic streptococcus viridans is the cause (of subacute bacterial endocarditis). The infection produces vegetations on the endocardium. This condition is fatal if left untreated, and the heart valve is usually involved. Rheumatic fever, a previous Hx of endocarditis, and patients on hemodialysis are definite risk factors. Subacute Bacterial Endocarditis is the most common form of Bacterial Endocarditis with an alpha hemolytic streptococcus viridans infection of damaged valves. Acute Bacterial Endocarditis is associated with Staph aureus and involves metastatic foci. Chronic Bacterial Endocarditis is associated with E. faecalis. We worry about SBE. With IV drug users there is concern about Staph aureus contamination - 50% of these bacterial endocarditis cases with drug users involve acute onset with the tricuspid valve. Only 20% of these drug users that develop endocarditis have previously damaged heart valves. Prosthetic valve endocarditis has a 1-3% incidence and the aortic valve is more common (problem with infection of suture line). 20-40% of patients with BE, there is no underlying heart disease. Vegetations on valves or elsewhere on endocardium - the disease usually arises secondary to localization of microorganism on sterile vegetations composed of platelets and fibrin (form over areas of trauma or scars). Subacute Bacterial Endocarditis - weight loss, malaise, anemia, lethargy, and joint pain - need to determine cardiac function. Systemic involvement - hemorrhage under nails, petechial hemorrhages, osler nodules (painful lumps on fingers). With SBE you can get valve destruction and regurgitation as well as congestive heart failure. Need to Dx in susceptible patients - vague, flu-like symptoms of low grade fever, lethargy, weight loss with organic heart murmur and recent history of surgical procedure suggests infective endocarditis. Most valuable Dx - lab tests - blood culture, an increased ESR, mild anemia, circulating immune complexes. Tx SBE with bactericidal agent, IV antibiotics. Cure rate for Strep endocarditis is 90%, while 50% for Staph and Enterococcus. There are no controlled human studies to support need for premedication. If pt had rheumatic fever and heart murmur, but uncertain of which type - good idea to premedicate. ENDOCARDITIS MEDICATIONS - 1) Amox 2g 1 hr preop, kids-50mg/kg orally 2) if unable to take oral meds - 2g IV or IM, kids - 50mk/kg within 30 min 3) Allergy to Pen. - Clindamycin 600mg 1 hr preop, kids - 20mg/kg; Cephalexin or Cefadroxil -> 2g, kids-50mg/kg; Azithromycin or Clarithromycin - 500mg 1 hr preop, kids-15mg/kg 4) If allergic to penicillin and cannot take oral meds - Clind - 600mg IV,kids -20mg/kg IV within 30 minutes or Cefazolin - 1g, kids - 25mg/kg IV or IM within 30 minutes. Procedures to premedicate for include exo, endo, implants, reimplants, perio; PDLs - no need to premed. High risk procedures requiring premedication - prosthetic cardiac valves, previous cardiac endocarditis, surgical systemic pulmonary shunts, complex cyanotic congenital heart disease. Moderate risk procedures requiring premedication - congential cardiac malformations, acquired valve dysfunction (from rheumatic fever), hypertrophic cardiomyopathy, mitral valve prolapse with regurgitation. No risk - no premedication - pacemakers and defibrillators, rheumatic fever with no valve defects, coronary artery bypass graft, patent ductus arteriosis, isolated atrial septal defect. JOINT REPLACEMENT - up to 2 years is the critical time period, although there is no scientific evidence to support the need for premedication to prevent hematogeneous infections. Premedication is not indicated for pins, plates, or screws. Those who may have a potential risk for joint infection and who may receive premedication are: 1) Immunocompromised/immunsuppressed 2) Inflammatory arthropathies - (rheumatoid arthritis) 3) Type 1 Diabetes 4) Previous infections (joint) 5) Malnourished individuals 6) Hemophilia

Types of intracanal medicaments:

Barbosa CaOh, CHX and CMCP (Barbosa): antibacterial effect all of them

10 - Dialysis

Dialysis is the process of artificially filtering [blood], due to end stage renal disease when the nephrons diminish. There are 4 types - peritoneal, hemodialysis, equilibrium (hapten-antibody reactions), lymph. With peritoneal, a hypertonic solution is injected into the peritoneal cavity and the solution is then drawn out. With acute renal failure, this is occasionally done. It is possible to do this via ambulatory method (through catheter). For chronic treatment, hemodialysis is the preferred choice, and it is performed every 2-3 days. >90% of people get this with 3 to 5 hrs /session. The procedure is to surgically create an arteriovenous fistula that is accessible to a needle. The patient is then plugged into the machine, and the patient is also given heparin to avoid clotting. Infection of fistula is of concern, and some do premedicate to prevent endarteritis and endocarditis. With these patients, avoid drugs metabolized by the kidneys, and the patients may have abnormal bleeding factor VIII. Patients are best treated on the day after their hemodialysis (avoid treating the same day). Monitor bleeding times. Patients may also experience a thrombocytopenia and leukopenia, so look for bleeding problems and potential infection problems. Patients on dialysis may be predisposed to infective endarteritis and endocarditis as the shunt provides a portal for bacteria to enter, in addition to cardiac output increasing.

diabetes

DENTAL MANAGMENT: DON'T TREAT SYMPTOMATIC PATIENTS Ask patient when was last attack. Take prophylatic puff of albuterol Before treating make sure they brought their inhaler

Different dental stem cells?

DPSC (Dental Pulp Stem Cells) - These cells regenerate really fast. Source for reparative dentin. SCAP (Stem Cells from Apical Papilla) - Plays a significant role in root formation. Source for regular root dentin. SHED (Stem Cells from Human Exfoliated Deciduous Teeth) - PLSC (Periodontal Ligament Stem Cells) - in vivo analysis of cementum like and PDL tissues DFPCS (Dental Follicle Precursor Cells)

What if they stay numb?

DiLenarda

13 - Diabetes

Diabetes mellitus is a chronic systemic disorder with an elevation of blood glucose and disturbances in lipid and protein metabolism. There is a decreased availability or reduced activity of insulin, which is required for homeostasis and proper protein, carbohydrate, and fat metabolism. DM is the 3rd leading cause of death in the US as there are many associated problems, especially vascular problem (microangiopathy and atherosclerosis). 90% of DM pts have Type II. In general, risk factors include genetic factors, as well as destruction of islets of Langerhans caused by inflammation, cancer, surgery, or due to iatrogenic causes (too much steroids - remember - steroids have an anti-insulin effect). Glucose is a major fuel for the body - and the only fuel for the brain. Too much or too little available glucose can cause CNS dysfunction. Normally, the level is 50-150 mg/ml. The brain needs at least 50mg. If the blood glucose goes too high, the kidneys cannot absorb it all, and excess spills into the urine. Normally, insulin protein is made and secreted by the B cells of the pancreas. When there is a high serum glucose level, there is stimulation for an increase in insulin release. Insulin promotes the uptake of glucose into cells and the storage in the liver in the form of glycogen, as well as the uptake of fatty acids and triglycerides. Proper insulin levels prevent excess loss of glucose through the urine by promoting its uptake throughout the body. Basically, insulin and its metabolic affects are deficient in diabetes and with Type I (IDDM), there is no insulin production, thus leaving the cells of the body and brain impermeable to glucose. The body has to try to find other forms for energy and survival, but without insulin, one will die. The two considerations with diabetes are hypo and hyperglycemia. After a meal you get hyperglycemia. If glucose cannot be taken into the cell, then glucose and subsequently water are lost in the urine leading to frequent urination, increased thirst, and dry skin. The lack of glucose utilization ability by the body leads to the breakdown of triglycerides into free fatty acids (ketone bodies) and also the breakdown of proteins into amino acids. This leads to ketoacidosis and if this continues there will be a decrease in the blood pH leading to metabolic acidosis causing a decreased cardiac contractility. The body naturally tries to correct this through a respiratory alkalosis and ultimately the result may be diabetic coma. The most acute complication of DM is hypoglycemia - <50 mg/ml. This causes a decreased function of the cerebral cortex leading to mental confusion and lethargy. Decreased glucose leads to an increased parasympathetic and sympathetic system response causing increased epi release and in turn increased BP, sweating, tachycardia -> potential shock. Type 1 is an absolute deficiency of insulin where there is B cell lesions/necrosis leading to loss of function of this aspect of the pancreas. This is usually attributable to autoimmune antibodies. Once again, insulin is needed to avoid ketoacidosis. Type II -> target organs exhibit insulin resistance -> decreased receptor activity - genetic factors are partially responsible. Gestational diabetes - 2% of pregnant women - by the 6th to 7th month. Hypoglycemia is a bigger acute dental problem to worry about as it can lead to unconsciousness and possibly a coma. Give a little cake icing before the start of the procedure. DM affects the large blood vessels by arteriosclerosis -> MI, hypertension; s mall blood vessels by kidneys, eyes, lower extremities; overall the blood vessels being affected may lead to susceptibility to infection. This susceptibility to infection comes into play as DM impairs the inflammatory response as the body will not be able to phagocytose as well with decreased blood flow. Watch for flare-ups with these patients. The major cause of death with DM pts is renal disease. Muscle, fat, and liver are all insulin dependent. - Treatment considerations - Give morning appointments. Due to the administration of oral hypoglycemics, this time will be better for the patient. Do not give aspirin with pts taking oral hypoglycemic medications. Aspirin can potentiate the hypoglycemia as it can inactivate the meds. Steroids can also potentiate the diabetic condition, and can also contribute to the already compromised immune response in dealing with infection. Give a short acting anesthetic to diabetic patients so they can resume normal eating habits.

So tell me what is Dialysis? Why does someone need dialysis?

Dialysis is a method of blood filtration used when the kidney is not functioning properly.

How do opioids work?

Dionne

How do NSAIDs work against pain?

Dionne Dionne

Whatis dentin made of?

Dsouza Lee Fujisawa Rahemtulla

9 - Hepatitis

Essentially is an "inflammation of the liver." The ultimate problem with hepatitis is the degeneration and necrosis of liver cells - the ballooning degeneration of hepatocytes. The liver lobule becomes infiltrated with lymphocytes and macrophages. Jaundice is a common finding, as bilirubin (a breakdown product from hemoglobin) normally goes to the liver and is broken down there. If the liver is not functioning properly, it cannot do this and there is a build up of bilirubin. Hepatitis can result from an infectious or noninfectious etiology. Infectious etiologies may be viral hepatitis, infectious mono, secondary syphyllis, or TB. Noninfectious etiologies may be drug induced (excessive Tylenol) or alcoholism. Of primary concern to the dentist are the infectious etiologies, and out of these viral hepatitis is by far the most common infectious form. There are 5 distinct viruses that may cause viral hepatitis - A, B, C, D, E A B/D C E Oral/fecal transmission Predominantly parenteral, Parenteral Fecal/oral Serum contact vaccine vaccine no vaccine no vaccine RNA B - DNA RNA RNA D - RNA Blood, skin cuts, absorption blood, transfusion through eye, sexual contact environmental surfaces, saliva Hepatitis A & E are usually without complications. Hepatitis D never occurs alone. When it does occur, it always occurs in the presence of B. 5% Type B and 45% Type C develop chronic hepatitis causing persistent hepatocellular necrosis and biochemical abnormalities -> fibrosis -> cirrhosis Hepatitis B (and D) - formerly called serum hepatitis. The Dane particle is composed of outer core and inner shell (intact HBV). Outer shell is HbsAg and its antibody is anti-HBs, while the inner core is HbcAg and its antibody is anti-HBc. Any age is susceptible and it is a very serious disease with a lifetime of complications. 5-10% of patients act as carriers (all carriers must be considered potentially infectious). Dentists are most concerned with Hepatits B. [Hepatitis B surface antigen - HBsAg - protein expressed on outer surface of or coat of HBV - consists of two major polypeptides, and a number of different subtypes have been identified to aid in epidemiological markers in evaluating transmission. HbsAg is detectable in >95% of pts with acute hepatitis B. 3 types of antigens of HBV - HBsAg, HBcAg, & HbeAg. Hep C was formerly called nonA, non B hepatitis. HBC is a virus which is a virus of nonA and nonB origin and therefore the name was coined]. Possible consequences of hepatitis - recovery, persistent infections, chronic active hepatitis, fulminant hepatitis, cirrhosis, death. At first, you may get flu-like symptoms and ultimately there may be signs of jaundice. It is important to receive active immunization. With active hepatitis, no treatment should be performed. A completely recovered patient has no real specific drug considerations to worry about, but if active or carrier, may want to be careful of administering certain drugs (lidocaine, mepivicaine, prilocaine, bupivicaine, aspirin, acetaminophen, codeine, meperidine, ibuprofen, valium, barbiturates, and tetracycline). The liver is important because of its metabolic functions - secretion of bile (for fat absorption), sugar to glycogen, metabolism of amino acids, carbs, fats, bleeding factors, drug metabolism.

Whatabout diabetes?

Fouad Bender

What is decompression?

Freedland

Lets tatk apicos!

Friedman Trope, Newton Martin, Newton Dionne, Hargreaves, Jackson Kim Baumgartner Besner Lemon Jeansonne Messer Buckley Besner Torabinejad Rud Erikson Lin Phillips Torabinejad Lin Kim, DeDues Fister Gilheany Tidmarsh, Gagliany Cambruzzi Wuchnich, Baumgartner Torabinejad, Morgan Baumgartner Slaton Harrison Jeansonne Lustman Torabinejad, Thompson Andreason Jeansonne Gartner, Oynick and Oynicj, trope Chong Kim, Pecora Hartwell Velvart becker

What do you fill with?

Friedmn Sjogren Sorin Schilder Hamann Trope Shipper, Texiera Tay Kim Kim Pashley Cotton Sabeti

What about internal and external bleaching

Fugaro, Seale Baumgartner, Ritter Haywood Nutting Madison and Walton Sicher and Bhaskar Rotstein Walton Torneck Glockner

What is a normal level of GFR, creatine and BUN

GFR: 120ml/min Creatine: 1mg/ml BUN: 15mg/ml

What is abnomal GFR, creatine and BUN

GFR: 15 ml/min Creatine: 5 mg/ml BUN: 50 mg/ml

Dialysis:

Galili

How do NSAIDs work against pain?

Hargreaves Cooper

Stress reduction?

Hargreaves Dionne Kvist Cooper

Why would it not work?

Hargreaves Narhi Taylor Gold Roy Fouad Skidmore

Why should you do retreatment and surgery instead of just surgery?

Hepworth - Hepworth did a review of literature - Showed that there was 59% success rate for surgery by itself but 81% success when both retreatment and surgery was done - Hepworth also showed that retreatments due to technical reasons (no lesion) had a success rate of 95% where as retreatments due to failed therapy (lesion) had a success rate of 66%

Bleeding disorders?

Herman

What about organ transplant?

Herman

What about Pediatric Endo?

Hibbard Andreason Torneck

What are the characteristics of chronic inflammation?

Infiltration (macrophages, lymphocytes, plasma cells), destruction (eosinophils make free radicals, leukocytes digest cells, fibroblasts make proteinases), proliferation (fibroblasts make collagen stimulated by IL1, blood vessels proliferate as macrophages secrete VEGF).

1) What is inflammation? What is infection?

Inflammation is the bodies vascular and cellular response to injury. Infection is the invasion and proliferation of pathogenic microorganisms into tissue.

What are the chances of this working?

Ingle, Rotstein delta dental Toronto Sjogren Toronto, allen allen toronto, rubenstein and kim, chong, setzer perrson bender, grossman cvek, Kerekes Cvek, Schroder Kvinnsland, Benanti Fuks Doyle, kim, Iqubal, torabinejad

Steps of acute inflammation?

Injury, release of mediators (histamine, nitric oxide, prostaglandins, interleukins, bradykinin), Venule events leukocyte extravasation, phagocytosis, digestion, bacterial killing, host damage, and repair

What if the pain is not coming from the tooth?

Klausner Selden Travell Robertson Goon Moskowitz Natkin and Sandler Sessle Ratner

Can a tooth fracture?

Pitts Gher Walton Heithersay Lemon

What does a normal pulp look like in terms of immune potential? How does it respond to infection?

Pulver Jontell Falker Hahn Staquet Cohen Okiji - Pulver - used fluorescent antibodies to label IgG, IGM, IgA, complement 🡪 found no evidence for antibody producing cells in normal pulp - Jontell - Looked for dendritic cells - found dendritic cells and macrophages present in tissue of normal pulp - Falker - Looked at both normal and potentially inflamed 🡪 saw antibody production in pulp explant culture that were not serum antibodies (contradicted Pulver study) - Hahn - Detected both T and B lymphocytes in the normal pulp (less B cells); o T lymphocytes were predominant in reversible pulpitis o In irreversible pulpitis 🡪 more T4 cells than T8 cells, More B cells than T cells o This paper shows that there is a correlation between clinical symptoms and histology of the pulp - Staquet - Cultured odontoblast and fibroblast cell lines from pulp 🡪 increased upregulation of TLRs in response to stimulants (LPS, LTA, virus); odontoblasts can have immune reaction - Cohen - inflamed pulps had higher amounts of prostaglandin than normal pulps - Okiji - leukotrienes present in inflamed pulps and not normal pulps

What are some prognostic factors to endodontic surgery?

Song Von Arx Barone (toronto study) ● Song Retrospective study, prognostic factors for outcome were sex (female), tooth position (anterior), lesion type (endodontic lesion vs. endo+perio) and root end filling (MTA vs IRM) ● Von Arx Meta analysis, higher healing rates occurred when there was lack of preop pain/signs, good density of root canal filling, no PA lesion or < 5 mm, and use of endoscope over not using one ● Barone (Toronto study) prospective cohort study, 3 successful outcome predictors were ages >45 years, teeth with inadequate root-filling length and crypt size <10mm

What does a tooth with Moderate- severe caries look like histologically?

Seltzer - Seltzer - reparative dentin formation, chronic inflammation (macrophates & lymphocytes),dentin tubules decalcify, bacteria travel through tubules, pulp exposure 🡪 acute partial pulpitis in coronal pulp, can get abscess development under site of exposure 🡪 spreads to total chronic pulpitis o Remainder of pulp may be uninflamed o Pulp can convert to granulation tissue over time

What about EPT

Seltzer Fouad, Baumgartner Klein Narhi

How do you classify endodontic conditions?

Seltzer Morse - Seltzer - histologic pulp calcifications o Intact o Atrophic o Intact with scattered chronic inflammatory cells (transitional) o Chronic partial pulpitis - inflammation in coronal o Chronic total pulpitis - Inflammation everywhere and in PDL o Necrosis - dead pulp - coagulation or liquefactive (can get false + on EPT) - Morse: ● Vital symptomatic: A pulpal condition, usually called normal, in which the pulp responds to thermal and electrical tests in manner similar to normal control, Pt. doenot reports adverse symptoms. ● Hypersensitive dentin: A pulpal condition with no apparent histologic changes, in which the patients feels pain when dentin is exposed to touch from dental explorer, toothbrush and thermal or other stimuli; but the pain disappears within a few seconds after the stimulus is removed. ● Inflamed-reversible: A pulpal condition, induced by dental caries and operative procedures, in which patient responds to thermal or osmotic stimuli such as sweet or sour food or fluids, but symptoms disappear when caries or other irritants are removed, and sedative dressing is placed. No spontaneous symptoms. ● Inflamed/degenerating without radiolucent periapical area-irreversible: Deep dental caries or restoration, spontaneous pain, precipitated by thermal or other stimuli. Pain is moderate to severe and is long lasting. On xray no changes. RCT is indicated in this and following 3 categories. ● Inflamed/degenerating with radiolucent periapical area-irreversible: Similar clinical presentation & xray changes evident ● Necrotic without radiolucent periapical area: May or may not spontaneous moderate to severe pain, or pain elicited by various stimuli such as thermal, percussion or palpation. Response to testing modalities is absent. No xray changes. ● Necrotic with radiolucent periapical area: Similar clinical presentation to above & xray changes evident.

Why do flareups occur?

Seltzer Walton and Fouad, trope Walton and Fouad Svetcov Goldman Eleazor

What if I perf

Seltzer, Beavers, Jew, Lemon Trope Benananti TBJ Fuss and trope fuss Lemon Walia frank Benananti Kvinssland TBJ and Shabanhang TBJ, Baumgartner, Holland Martin Abou Rass

What about diagnostic testing?

Seltzer/reynolds Petterson Trowbridge Trowbridge Throwbridge Peters Trowbridge Cooley Wilcox Ingolfsson Friend Bystrom

Should smear layer be removed?

Sen, McComb Baumgartner Dewitt, Drake Love, Ando, Horiba Hulsmann Haapasalo Torabinejad, Pashley Econdomides Yamada, Baumgartner Cait Texieria Waltimo Schilder

What is the success rate of traditional vs modern surgery?

Setzer ● According to Setzer (systematic review of traditional and modern surgery), modern surgery has a probability of success of 1.58 times the probability of traditional surgery. Traditional 59% vs Modern 94% success

12 - Organ Transplant

Several different types: 1) Autologous (used with bone marrow transplants) - the patients own marrow is used 2) Syngeneic - identical twin transplant 3) Allogeneic - from same species 4) Haploidentical - from parent 5) Xenograft - from living, nonrelated - different species 6) Cadaver - worst match, but most available Pts with transplants usually take a triple immunosuppressive therapy: 1) cyclosporine - cyclic polypeptide fungal metabolite - suppresses CD4 lymphocytes from elaborating IL-1. Do not get bone marrow suppression; often can see gingival hyperplasia. 2) prednisone - (corticosteroid) - increases potency of cyclosporine, decreases growth factor synthesis, is an anti-inflammatory; get adrenal gland suppression so patient may not be able to deal with stress, infection, trauma, or anxiety. 3) azathioprine - inhibits DNA/RNA synthesis and immune response. Bone marrow suppression occurs - greater bleeding and infection potential. Pretransplant patients - order lab tests - want to look for potential bleeders, those prone to infection, liver/kidney metabolism problems. Want to avoid potential problems. Posttransplant patients - there is immunosuppression with an increased chance of infection. Within first 6 months - acute rejection is major concern - do not treat. Stable period - no contraindication to dental treatment, but find out if patient needs steroid supplementation, and if there is hypertension or bleeding problems. Chronic rejection stage - if this is happening to patient - no elective treatment - only emergency treatment. Cardiac transplant patients - susceptibility to infection and bleeding - anticoagulated state. Concerns about vasoconstrictors & bleeding. Liver - Protein & drug metabolism considerations, as well as bleeding problems due to clotting factors. Tylenol, ibuprofen, aspirin, and codeine are all metabolized by the liver. Bone marrow - big issues are worrying about infection and bleeding. Kidney - patients may be on coumadin - bleeding issue, also concerned about drugs metabolized by kidney (i.e. penicillin, tetracycline, cephalexin)

What is phototargeting?

Soukos

What is tissue pressure in the pulp?

Stenvik

What tissues are needed for tooth to form? Evidence?

Kollar Thesleff - You need to have an interaction of epithelium and mesenchyme (dental papilla) - Kollar showed that if you take epithelium from a different portion of the body (ex. Foot) and dental papilla, you get a tooth - Thesleff showed two epithelium and mesenchyme and cultured them separately and they used filters in between o 0.1 micron size filters 🡪 no growth o 0.6 micron size filters 🡪 odontoblast processes growing o Only when both epithelium and mesenchyme were present did basement membrane form o Only if there was basement membrane, did they see differentiation of odontoblast

What should I give the patient post op?

Krasner Reader Reader Reader, walton, fouad, keenan

Advantages and disadvantages for using ultrasonics for retroprep?

Morgan - Advantages - you can get deep, conservative preparations, parallel to long axis and including isthmuses and anatomical variations - Disadvantages - potential crack formation o Morgan - in vivo study, 25 roots, after ultrasonic retroprep, took PVS impression and SEM evaluation of casts showed only 1/25 had a crack

How do we evaluate success?

Strinberg Orstavik

Outcome of retreatments (Sundqvist)

Sundqvist - Microbial analysis of teeth with failed RCT and outcome of treatment - 74% success rate of retreatment - (+) sample 🡪 33% success - (-) sample 🡪 80% success - Initial size of lesion had influence of outcome - Length of obturation did not affect outcome

are bacteria linked to pain?

Sundqvist Griffee, Gomes Fouad Baumgartner, Jung - PCR Horiba, Jacinto

What type of microbes are found in root canals?

Sundqvist Leonardo Vianna Wilson Stevens Rocas - Primarily anaerobic bacteria - Sundqvist found that in necrotic trauma teeth, over 90% were anaerobic o Sundqvist found that there is a selective environment in the root canal - after 3 yrs, facultative anaerobes more common, after 6 years, obligate anaerobes predominated - Il-Young found Fusobacterium, Peptostreptococcus micros, P. gingivalus, Terponema and Bacteroides forsythus using PCR and rRNA probes - Bacterial biofilms resistant to antimicrobial agents (Leonardo) - Archaea in root canal was found with PCR of 16s rRNA sequence (Vianna) - 10% of the time, you will find yeast, candida albicans in root canals (Wilson) - Found virus in infected root canals, phages in E. faecalis (Stevens) E. faecalis is more associated with asymptomatic cases of primary endo and failed RCT (Rocas)

How about luxation injuries?

andreason Jacobsen Cunha Ebelder Andreason Andreason Dumsha

Irrigant interaction with other materials? Toxic effects?

baumgartner basrani - 5.25% NaOCl by itself or when mixed with EDTA and hydrogen peroxide does not release chlorine gas. But when mixed with citric acid, creates chlorine gas, which is toxic (Baumgartner) - Chlorhexidine mixed with NaOCl creates precipitate called PCA, para-chloroanaline, which is toxic (Basrani)

Why do we instrument? Who said that?

bystrom falk, card, val rodriguez, peters - Remove bacteria 🡪 Bystrom: instrumented the canals without any intracanal medication or disinfecting irrigant, just used saline. Bacteria were eliminated or reduced but grew again between appointments. Need disinfecting agent for help - To make space for GP - Enlarge the canal, especially apically to make room for irrigant to reach 🡪 Falk, Card, Val rodriguez, Peters - Maintain curvature of the canal

What are the components and properties of MTA?

Torabinejad - Components o MTA powder consists of fine hydrophilic particles o Phases are tricalcium silicate, dicalcium silicate, tricalcium aluminate, tetracalcium aluminoferrite, gypsum, and bismuth oxide (radiopacifier) - Properties (Torabinejad) o pH of 10.2 initially, which rises to 12.5 three hours after mixing o at 24 h MTA had the lowest compressive strength of 40 MPa but it increased after 21 days to 67 MPa o Set time: 2 hours and 45 min

How about restoration?

Widerman Webber Pashley Hutter Hashimoto Kozam Fujisawa Bouilliaguet Ray and Trope Iqubal Ricucci TBJ Khayat Wu and Wesselink Lynch Ran Mattison Schindler Cooley Bergenholtz

1) Hypoparathyroidism

a) Due to abnormal functioning of parathyroid glands or their accidental surgical removal b) When hypo, blood plasma hypocalcemia fails to activate feedback mechanism which stimulates the production of parathyroid hormone calcidiol does not get converted to calcitrol results in lack of calcium mobilization due to decreased osteoclastic activity neuromuscular junction reacts in convulsive state (tetany) tx with oral calcium.

1) Hyperthyroidism (thyrotoxicosis)

a) Hypermetabolic state resulting from excess secretion of thyroid hormones (T3 & T4) i) Usually due to diffusely hyperactive thyroid gland (Grave's Disease = diffuse toxic goiter) ~90% of cases (1) Autoimmune disorder due to production of thyroid-stimulating immunoglobulins (TSI) or long-acting thyroid stimulator (LATS) which mimic the action of TSH excessive T3 & T4 release causing thyroid hyperplasia, iodine accumulation in thyroid gland & excessive release of thyroid hormone (gland requires dietary iodine to synthesize T3 & T4) (2) Female > male (3) Before age 40 ii) Increases metabolic rate, heat production; pts thin, nervous, exopthalmus due to mucopolysaccharide deposits behind globe (may cause optic nerve atrophy) iii) CV abnormalities such as rapid pulse, palpitations, increased RBC mass to carry needed oxygen for increased metabolism b) Normal feedback mechanism: low blood T3 & T4 hypothalamus releases TRH (thyrotropin-releasing hormone) anterior pituitary releases TSH (thyroid-stimulating hormone) thyroid releases T3 & T4 into bloodstream metabolic rate, O2 consumption, energy production by promoting breakdown of protein, carbohydrates & lipids, ¯ cholesterol levels, potentiates epinephrine c) 2nd most common endocrine disorder; 2nd to diabetes d) Tx of hyperthyroidism: i) Antithyroid drugs - propylthiouracil, methimazole block oxidation of inorganic iodide blocking synthesis or thyroid hormones ii) b-blockers - helps control neuromuscular & CV effects of excess T4 iii) Thyroidectomy (total or partial) iv) Radioactive iodine (131I) - circulates thru body & gets trapped in gland ( ½ life of 8 days) e) Post-tx complication: inadvertent removal of parathyroid glands hypoparathyroidism f) Dental Management: No elective dental care until pt rendered euthyroid (NL thyroid fxn); avoid use of epinephrine because of its cardiostimulation & hypertensive actions; avoid anticholinergic drugs (interfere with body's heat regulating mechanism & can increase cardiac activity) & radiographic contrast solutions (contain iodine). g) Dental Emergency: Analgesics & antibiotics ok until medical consult obtained; no epi; no definitive tx until consult completed. h) Thyrotoxic Crisis (Thyroid Storm): i) Occurs in pts with thyrotoxicosis (hyperthyroidism) but is rare ~1% ii) Due to stressful dental tx, epinephrine, infection, trauma or surgery in hyperthyroid pt iii) Abrupt onset, initial symptoms (restlessness, nausea, vomiting, abdominal pain), later symptoms (fever, sweating, tachycardia, pulmonary edema, congestive heart failure), finally (severe hypotension, coma, death if tx not provided) iv) Management: medical emergency pts transported to hospital, given large dose of propylthiouracil & b-blocker to reverse the thyroxine-induced CV effects

1) Hypothyroidism

a) Insufficient levels of thyroid hormone due to: i) Destruction of thyroid gland (i.e. surgery due to hyperthyroidism more common in dental practice) ii) Dysfunction in hypothalamus-anterior pituitary axis iii) Hashimoto's thyroiditis: autoimmune disorder involving lymphocytic infiltration of gland b) Rare; female > male c) 2 categories: i) Cretinism (young children) - have thyroid hypofunction because of congenital absence of thyroid gland, hypoplasia, thyroid dysplasia, fibrous replacement, lymphocytic replacement (1) Symptoms include somnolence, hypothermia, feeding problems, slow physical & mental development (mental retardation in 1:5,000) ii) Myxedema (adults): tends to develop from: (1) surgical excision or radiation therapy (2) chronic lymphocytic thyroiditis (Hashimoto's disease) autoimmune infiltrate compresses & destroys thyroid follicles (stored thyroid hormone) goiter enlarges as more lymphocytes migrate to gland hypothryroidism results as disease progresses (circulating thyroid antibodies to thyroglobulin are present in blood throughout course of Hashimoto's thyroiditis) d) Clinical Findings: i) Slowing of all body processes due to insufficient thyroid hormone (1) Cretinism: retarded physical & mental development (a) Skin is thick, dry, wrinkle, pale (b) Nose is flat, retracted (c) Eyes are wide-set (hypertelorism) (d) Tongue is enlarged, protruded (e) Lips are thickened (f) Mouth remains open (g) Face is broad (2) Myxedema: (a) Puffy face, dull facial expression (b) Non-pitting edema of eyes (c) Loss of lateral third of eyebrows ("Queen Anne's sign") (d) Slow pulse, decreased cardiac output, weight gain (e) Mentally sluggish, drowsy (f) Cold intolerance, capillary fragility, anemia (g) Without tx or if cardiac depressant drugs used myxedema coma which includes: (i) Congestive heart failure (ii) Hypoventilation (iii)Hypothermia (iv) Unconsciousness e) Medical Treatment: replacement thyroid hormone until euthyroid state is achieved (Synthroid, T4, levothyroxine) f) Oral Manifestations: accumulation of subcutaneous mucoprotein overly large tongue, puffy lips, mouth breather (therefore, gingivitis & rampant caries), prepubertal deficiency delays eruption of primary & secondary teeth, speak is slow & husky g) Dental Management: Need medical consult although no contraindications for routine dental care. Hypothyroid pt at slight risk of myxedema coma during stressful dental tx (ppt coma include extreme cold weather, elderly, infection, surgery, use of CNS depressants {narcotics}) i) Avoid dental tx until euthyroid ii) If acute oral infection high doses of antibiotics, medical consult iii) Edematous tissues revert to normal following replacement thyroid hormone therapy

Why do you want to instrument to larger apical size?

card - Card: showed that larger apical size allows you to eliminate bacteria more. But you don't want to make it too large that you blow out the apex. They went upto size 60 in this study

are antibodies found in the pulp?

hahn okamura

What is Sargenti (N2) paste? Why don't we use it?

langeland - Made of paraformaldehyde - Langeland 🡪 showed that it was toxic and found outside the root canal into the tissues and in the bloodstream o Can cause resorption and ankylosis

What is the difference between bacteria- cidal and -static?

cidal- killing static- arrests bacteria

Miliary TB

disseminated TB = tiny lesions

What do neuropeptides do?

olegart kim taylor and byers

What if you have no breathing and a pulse, what do you do?

give breaths. CAB

What should you use for anti-anxiety?

Hargreaves

What is gluconeogeneisis?

-Fat and protien breakdown

What is Jaundice?

-accumulation of billirubin

What are these NiTi files?

Walia Haikel Li

Can you prescribe narcotics?

-hell no, could cause respiratory depression (hypoventilation)

Can you tell me the anatomy of the adrenal gland the what it secretes?

-Zona glomerulosa- aldosterone: control BP and Na and K uptake. Keeps in Na and secretes K. -Zona faciculata- cortisol -Zona reticularis- androgens

How do you know that a kidney is not functioning properly?

-abnormal levels of GFR, creatine and BUN.

What are 3 instances that you should not give epi? Why?

-if they are on MAO or TCA antidepressants- hypertensive crisis -Hyperthryroidism- can worsen condition -Cokeheads- arrhythmias *Asthma *For antipsychotic drugs you get hypotension so it's better to use epi.

What does epi do?

-increases duration, decreases toxicity, decreases absorption

Macrophage-lymphocyte interaction in chronic?

1) Macrophage are activated by the release of IFN-y/MAF from lymphocytes and that activates the macrophages. The activated macrophages can then release IL-1/TNF to activate lymphocytes or present an antigen to the lymphocytes to activate them.

3 - Local Anesthetics

A nerve impulse is propagated through the conduction process by action potentials. The action potentials are transient depolarizations, which allow for an increased permeability of the nerve membrane (increase in permeability of the ion channels). Local anesthetics function by allowing for a depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves. A neuron has 3 parts - body, dendritic zone, axon. The impulses are messages in form of action potential, and the action potential results from an increase in permeability to Na & K. Resting potential = -70mV (negative inside of nerve membrane). Na enters the nerve membrane slowly and you get slow depolarization, until it hits a certain threshold (-50mV), and then a rapid depolarization occurs (Na pours in and the inside becomes positive +40mV). Then, a repolarization occurs - as the nerve membrane becomes less permeable to Na coming in, while K rushes out. Impulses spread on an unmyelinated nerve fiber in a slow forward process called "creeping." Myelinated nerve fibers have a much faster impulse spread and the impulses leap from node to node, known as saltatory conduction. 2 theories of how local anesthetics work: - Specific receptor theory (more accepted) - anesthetics bind to specific receptors on or within Na channels, preventing the ions from rushing in and the action potential from taking place. - Membrane expansion theory - anesthetics diffuse to hydrophobic regions of the nerve membrane - expanding the membrane causing a decrease in diameter of Na channels. Basically, they decrease the permeability of ion channels to Na and inhibit neural excitation. 3 parts of anesthetic molecule - aromatic ring (lipo), intermediate amide or ester linkage; amine group (hydro) - ↑Lipid solubility - ↑ potency - ↑Protein binding - ↑ duration - ↑Ionization - ↑ diffusion/onset (↓pKa - quicker onset of anesthesia due to more free base, quicker lipid diffusion). - In high H+ concentration, which means a low pH, the anesthetic is mostly in cationic form. The cationic form of the anesthetic molecule does the actual blockading of the Na ion channels, but it is the uncharged (base) form that is necessary to get the anesthetic molecule into the nerve in the first place. Therefore, with infection, there is a low pH, more cationic form, and it is difficult for the anesthetic molecule to get in, and tough to get appropriate anesthesia. - Henderson-Hasselbach eq. - ratio of anesthetic in cationic to base form - The equation is the Log Base/Acid = pH-pKa = % of base (uncharged) and acid (charged) form - Diffusion is dependent on pH, pKa, and concentration gradient. As the lipid solubility increases, there is a more effective blockage. - Protein binding allows for increased duration, as found with bupivicaine (marcaine). - Esters - more allergies due to PABA product (paraaminobenzoic acid) metabolism by plasma esterases - Allergic reactions occur through IgE (immediate hypersensitivity); can result in anaphylaxis with signs of urticaria, erythema and dyspnea. - Management of Anaphylactic Shock: Place pt in supine position, Open airway, notify EMS, Epi 0.3 mg IM or IV every 5-10 minutes, O2, Monitor vial signs, If improvement occurs admin. Histamine blocker and IV/IM corticosteroid to prevent recurrence - Amides - more toxicity; metabolized by liver amidases - Systemic signs of local anesthetics toxicity: CNS excitation at first, but ultimately depression Cardiovascular effects - depressed conduction, decreased force of contraction. peripheral vasodilation, increases drug absorption, which is one of the reasons we use epi (for peripheral vasoconstriction). Deep depression is a sign of toxic overdose. Drug interactions to be concerned about are those with depressants as there may be potentiation of cardiac and respiratory depression. - If pt allergic to ester or amide anaesthetics, use diphenhydramine, opioids and analgesic combo - Prilocaine may cause methemglobinemia -> cyanosis - Articaine - acts as both an amide and ester b/c of thiopene ring KNOW: WHY LAs fail: 1) Inflammation 2) Varied anatomy 3) Excessory innervation 4) Anxiety 5) Central Hypersensitization 6) Tachyphylaxis (↓effect w/ ↑use) - Dental cartridge includes: LA, vasonstrictor, preservative (prevents O2 from reacting with the vasoconstrictor), sodium chloride (makes the solution isotonic) and dH2O. - Sodium bisulfite - epi preservative - Benzocaine (hurricaine) - commonly used topical; ester. - Vasoconstrictors: decrease blood flow to area, slow absorption, decrease risk of local anesthetic overdose, increase duration of anesthesia, and decrease bleeding. - Epi - works on alpha & beta receptors, but stimulates cardiac beta 1 predominantly - NE - works on alpha receptors predominantly - Levonordefrin - works on alpha receptors. - Beta 1 is the heart, Beta 2 is bronchioles - Burning sensation: 1) contaminated preservative 2) inject too fast 3) anaesthetic carp too cold - Trismus tx: 1) Muscle relaxants 2) Analgesics 3) Hot rinses 4) Slowly exercise muscle 5) Follow-up - IAN block - needle placed in Pterygomandibular space - GG block - anaesthetizes V3: auriculotemporal, IAN, long buccal, n. to mylohyoid, incisive n. , lingual n. - Enter needle distal to max 2nd molar; aim at lateral side of condylar neck below lateral pterygoid; enter parallel to line from tragus of ear to corner of mouth - Akinosi block - closed mouth technique; barrel of syringe parallel to max. occlusal plane; needle at level of mucogingival jxn of max 2nd molar; no bony cantact to provide landmark Intra-pulpal Injection: - Efficacy of saline equal to Lidocaine if given w/ back-pressure (Birchfeld & Rosenberg 1975) PDL Injection: - Strong back pressure is the most important factor in anaesthetic success (Walton 1981) - Vasoconstrictor significantly increases the efficacy of PDL injection (Kim 1986) - PDL injection anaesthetic w/ epi did not increase HR (Nusstein 2004) Intra-osseous Injection: - Stabident or X-tip: inject 1/3 carp of plain anaesthetic w/ 27 gauge 8mm long needle. - 2% Lido w 1:100K epi = 91% success in Md post teeth w/ irrev. pulpitis (Nusstein 1998) - 2% Lido w 1:100K epi = ↑HR 67% of subjects; 3% Carbo w/o epi = no change HR (Replogle 1999) - 2-15% reported mod post op pain w/ Stabidentor X-tip (Replogle 1999)

How do you detect rheumatic fever?

ASO titer (detects antistreptolysin antibodies)- to see if they have a strep infection

5 - Local Anesthetics

A nerve impulse is propagated through the conduction process by action potentials. The action potentials are transient depolarizations, which allow for an increased permeability of the nerve membrane (increase in permeability of the ion channels). Local anesthetics function by allowing for a depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves. A neuron has 3 parts - body, dendritic zone, axon. The impulses are messages in form of action potential, and the action potential results from an increase in permeability to Na & K. Resting potential = -70mV (negative inside of nerve membrane). Na enters the nerve membrane slowly and you get slow depolarization, until it hits a certain threshold, and then a rapid depolarization occurs (Na pours in and the inside becomes real positive). Then, a repolarization occurs - as the nerve membrane becomes less permeable to Na coming in, while K rushes out. Impulses spread on an unmyelinated nerve fiber in a slow forward process called "creeping." Myelinated nerve fibers have a much faster impulse spread and the impulses leap from node to node, known as saltatory conduction. There are 2 theories of how local anesthetics work: 1) Specific receptor theory (more commonly accepted) - anesthetics bind to specific receptors on or within Na channels, preventing the ions from rushing in and the action potential from taking place. 2) Membrane expansion theory - anesthetics diffuse to hydrophobic regions of the nerve membrane - expanding the membrane causing a decrease in diameter of Na channels. Basically, they decrease the permeability of ion channels to Na and inhibit neural excitation. There are 3 parts to an anesthetic molecule - aromatic, hydrophilic, and intermediate (amide or ester linkage). Lipid solubility relates to potency, protein binding relates to duration, and ionization relates to diffusion/onset. The pKa of the anesthetic molecule is a measure of the affinity for H+. Basically, a high pKa means slower onset of anesthesia. A low pKa means rapid onset of local anesthesia. In high H+ concentration, which means a low pH, the anesthetic is mostly in cationic form. The cationic form of the anesthetic molecule does the actual blockading of the Na ion channels, but it is the uncharged (base) form that is necessary to get the anesthetic molecule into the nerve in the first place. Therefore, with infection, there is a low pH, more cationic form, and it is difficult for the anesthetic molecule to get in, and tough to get appropriate anesthesia. The ratio of the anesthetic in this cationic or base form is dependent on the Henderson-Hasselbach equation. This talks about the percent of the drug that exists in either form. The equation is the Log Base/Acid = pH-pKa = % of base (uncharged) and acid (charged=cationic) form. Diffusion is dependent on pH, pKa, and concentration gradient. As the lipid solubility increases, there is a more effective blockage. Protein binding allows for increased duration, as found with bupivicaine (marcaine). The types of anesthetics include esters and amides. Esters - more allergies due to PABA product (paraaminobenzoic acid) metabolism by plasma esterases. Amides - metabolized by liver amidases [toluidine from Prilocaine may cause methemglobinemia -> cyanosis] Maximum dosages for most anesthetics is 2mg/lb up to 300mg; for vasoconstriction - .2mg epi total for the healthy patient and .04mg for the cardiac or hyperthyroid patient. An example may be: there are 1.8ml/carpule. If you are using 2% xylocaine = 36mg/carpule. If the patient is 200lbs, that would allow for 2mg/lb of the anesthetic, or 400 mg total for the patient. But, since the maximum allowance is 300mg of anesthetic for the patient, you would only use the 300mg number. You then divide 300 (the maximum number of mg of anesthetic)/36 (the number of mg in a carpule of anesthetic) = 8 carpules of 2% xylocaine. Therefore, you can safely give a 200lb patient 8 carpules of 2% xylocaine. [If the patient is above 150lbs, then just take 300 and divide it by the # of mg/carpule]. When calculating the maximum amount of epi allowed, 1:100,000 will be the example. There are .018mg epi/carpule, and a healthy patient can have up to .2mg of epi. You divide .2/0.018, theoretically allowing you to give 11 carpules of 1:100,000 epi safely, but if unhealthy - .04mg is the maximum = 2 carpules. So with a 200lb patient, you would only be allowed to give 8 carpules of 2% xylo with 1:100,000 epi, as the limiting factor is the xylocaine. The preservative with epi is sodium bisulfite. Benzocaine (hurricaine) is the commonly used topical and is an ester. To administer a Gow gates block, draw a line from the ala of nose to the tragus of ear. Systemic signs of local anesthetics include CNS ( local anesthetics crosses the blood-brain barrier) excitation at first, but ultimately depression. Cardiovascular effects (as there is a direct action on heart) include depressed conduction and decreased force of contraction. Peripheral vasodilation increases drug absorption, which is one of the reasons we use epi (for peripheral vasoconstriction). Deep depression is a sign of toxic overdose. Drug interactions to be concerned about are those with depressants as there may be potentiation of cardiac and respiratory depression. Vasoconstrictors - decrease blood flow to area, slow absorption, decrease risk of local anesthetic overdose, increase duration of anesthesia, and decrease bleeding. Epi - works on alpha & beta receptors, but stimulates cardiac beta 1 predominantly. NE - works on alpha receptors predominantly, levonordefrin - works on alpha receptors. Beta 1 is the heart, Beta 2 is bronchioles. The dental cartridge includes the local anesthetic, the vasonstrictor, the preservative (prevents O2 from reacting with the vasoconstrictor), sodium chloride (makes the solution isotonic), and distilled water. Bupivocaine = Marcaine, Etidocaine = Duranest. Both have a long duration.

Which hepatitis forms have no vaccine?

C and E

What are the forms of chronic inflammation?

Fibrous, serous, supparative, granulomatous

How about root resection?

Filipowikz Blomlof Persson

What about bacterial resistance?

Luria and Delbruke Sedgeley

Angina and MI:

Natkin and Sandler

What are the trauma classifications?

Ravn Ravn Ravn

What about viruses?

Sabeti Trope Torabinejad Stevens

Pascon

Showed that it was the zinc in the zinc oxide that is toxic

What are examples of bacterial virulence factors?

Stevens Sundqvist Okuda Killian Fletcher Sven Takada Bramanti Hanazawa Van Steenbergen Patella Kaminiski Kayaoglu Ishihara Foschi - Bacterial products are inhibitory (cytotoxic) to human cells. Tested effect of bacterial products in sonic extracts on human gingival fibroblasts -> they inhibited fibroblast proliferation, DNA synthesis and cell morphology (Stevens) - Bacteria in endo infections can attract PMNs (chemotaxis) - > abscess Used boyden chamber, positive control-> serum with chemotactic agent, negative control -> serum alone w/o chemotactic agent (Sundqvist) - Capsule of B.melaninogenicus is anti-phagocytic and protects even after phagocytosis (compared to non-capsulated strains). Since the accumulated phagocytes are unable to phagocytize these bacteria, they get frustrated and die and form pus. (Okuda) - Bacteroides and Capnocytophaga can degrade immunoglobulins IgA and IgG by action of Ig proteases. (Killian) - Protease enzyme produced by P.gingivalis is a virulent factor (it cleaves C3 complement) P. gingivalis without the prtH gene that produces protease enzyme is less virulent than the wild-type with the gene (Fletcher) - LPS can stimulate bone resorption by stimulating osteoclasts (hence it occurs only in live bone bec. it needs viable osteoclasts). LPS -> activate complement -> stimulate osteoclasts -> bone resorption (Sven). - LPS induces production of IL-1 and IL-6 in human fibroblasts (IL-1 causes thymocytes to proliferate, so when they proliferate, they incorporate more DNA, the radioactive DNA incorporated was measured) (Takada) - LPS from B. gingivalis stimulates cytokine production (PGE, IL-1, TNF) from macrophages which can cause an inflammatory response (Bramanti) - Not just LPS , fimbriae (appendages) can also stimulate cytokine production (Hanazawa) - Metabolic end products (such as ammonia) are also toxic to eukaryotic cells (chick embryo chondrocytes in this study) (Van Steenbergen) - Protein L (a cell wall protein) can activate human basophil and mass cells to release histamine, leukotrienes and prostaglandins. (Patella) - Protease from P. gingivalis can also activate the kallikrein-kinin cascade to form bradykinin (pre-kallikrein -> kallikrein -> kinin -> bradykinin) and increase vascular permeability. Spots on guinea pig skin were due to extravasation of dye from the blood vessels into the tissues due to increased vascular permeability caused by bradykinin formed from P.gingivalis protease (it activated the kallikrein-kinin cascade) (Kaminiski) - Virulence factors of E.faecalis (Kayaoglu) o Factors that enable colonization of host (adhere/ grow) - Aggregation substance (AS) enables binding to collagen type I (so E.faecalis can attach to dentin tubules as it is primarily made of type 1 collagen) o Factors that resist host defense mechanisms -i) Surface adhesins (SA) enables them to form biofilms. Biofilms resist medicaments like CaOH. ii) Sex pheromones are signaling molecules that increase conjugation /clumping b/w cells so they can transfer plasmids for antibiotic resistance and other virulence factors. o Factors that damage host tissue directly by toxins or indirectly by inducing inflammation. i) LTA (present in all gram +ves so not specific to E.faecalis) - binds to eukaryotic cells and cause them to lysis by their own complement system. ii) superoxide free radicals iii) gelatinase and hyaluronidase (E.faecalis can survive under poor nutrient conditions by producing its own food from tissue breakdown products) iv) cytolysin - destroys other gram +ve bacteria that may compete with it and shifts the flora towards gram -ve bacteria. - Virulence factors of spirochetes (Ishihara) o Spirochetes are gram -ve , highly motile long spiral shaped cells. T.denticola very common in endo infections o Factors for adherence/invasion and colonize biofilms o Factors for immunosuppression - dentilisin (chymotrypshin-like protease that cleaves at amino acids phenylalanine and tyrosine) activates C3, degrades ILs and immunoglobulins o Factors for tissue damage- dentilisin is a protease , also degrades other proteins and tissue fluids and provide food for spirochetes. Crystalysin breaks down RBCs. Induce activation of osteoclasts to cause bone resorption. (So large area od PA radiolucency may be assoc. with spirochetes bec they induce bone resorption by activating osteoclasts) o Spirochetes not only cause localized infection (severe bone destruction) but they can also spread to distant organs (brain, heart, spleen) and potentially cause systemic manifestations. Wild and immunocompromised mice infected with spirochetes alone or along with other red complex microorganisms. Even w spirochetes alone, there was sig localized and systemic disease. Decreased body weight, spleen weight. (Foschi)

What about for SBE prophylaxis?

Tzukert Waldman Glick

Tooth Morphology studies?

Vertucci (green) DeDues Kuttler DeDues Dedues Vertucci Burch Weine Vertucci Green Kuttler and Dummer Deutche Chyoaneb Hovland Hulsman Skidmore Vertucci Kulid Bone Belizzi Vertucci Sebala, vertucci Vertucci Trope Skidmore Lambrinidi Weine

What is LPS

Warfringe Schilder

How does the pulp respond to injury

Yammamura Garant Feit Stanley

1) Tuberculosis

a) Caused by Mycobacterium tuberculosis (most commonly) b) Transmitted by airborne droplets; communicable in active state c) Lung is most common site of infection but may infect affect any organ including mouth d) Typical infection - inhale infected droplets primary infection of lung begins pulmonary tuberculosis (bacteria multiply in alveoli) infection progresses locally & may involve regional lymph nodes may disseminate via bloodstream if not controlled (believed that majority of disseminated bacteria are killed by host defenses) 2 to 8 weeks post-infection, host becomes sensitized to host (conversion of PPD from negative to positive, PPD = "purified protein derivative"), most infections remain localized & self-limited because of host defenses; if not controlled nidus of infection becomes a productive tubercle with central necrosis & caseation, cavitation may occur dumping bacteria into airway for further dissemination either into other lung tissue or out of lungs by forceful expulsion once lesion is contained & interrupted, lesion heals with hardening, encapsulation & calcification, lesion is "healed" but some bacteria may remain in dormant stage; if lesion not controlled, infection spreads with multiple organ involvement (miliary tuberculosis). e) Complications - individual organ damage & possibly death (~5 to 10% die) f) Clinical Findings - relative lack of signs unless lesions are extensive, positive PPD test, radiographic findings i) Tuberculin skin test (Mantoux) - inject tuberculin (cultured extract from M. tuberculosis) 0.1 ml intradermally read test result 49 to 72 hours later, induration of 5 mm or less is negative result, area 5 to 9 mm is inconclusive (probably infected with another Mycobacterium), 10 mm or greater indicates a positive test result (1) Positive PPD - means an individual has been previously infected but does not mean pt currently has clinical tuberculosis pt needs exam & culturing ii) diagnosis of clinical tuberculosis requires physical exam, radiographic exam (upper lobes of lung usually involved) & sputum culturing g) Medical therapy - chemotherapy (9 to 12 months of isoniazid, rifampin & streptomycin), pt must comply pts taking isoniazid (INH) should avoid acetominophen-containing compounds because at increased risk of developing hepatotoxicity pts taking rifampin have increased incidence of infection, delayed healing & gingival bleeding due to leukopenia & thrombocytopenia pts taking streptomycin must avoid aspirin (toxicity) i) Most pts become noninfectious within 2 weeks after starting chemotherapy by decreasing the number of viable organisms & less coughing ii) If pt still has positive sputum cultures after 3 months, evaluate for resistant bacteria h) If pt with no history of tuberculosis with past negative PPDs has positive PPD, get physical exam & culturing & then chemotherapy i) Dental management: i) Active sputum tuberculosis: do not tx on outpatient basis, need hospital setting (ventilation); after 2 to 3 weeks chemotherapy, pt may be treated on outpatient basis ii) Past history of tuberculosis: approach with caution, get med hx, consult as needed, relapse is rare iii) Recent conversion to tuberculin-positive PPD: pt needs physical exam from physician, assume have tuberculosis until told otherwise, no current tx iv) Has signs or symptoms of tuberculosis such as dry non-productive cough, pleuritic chest pain, fatigue render no dental tx, refer to physician v) Pt with oral manifestation of tuberculosis has painful, deep ulcer on dorsum of tongue, palate, lips, mucosa, gingiva; biopsy & culture Scrofula: has enlarged, painful, possibly abscessed cervical & submandibular lymph nodes

1) Hypopituitarism

a) Dwarfism due to dysfunction of the hypophysis in the early years of skeletal development (similar clinical appearance to hypothyroidism) i) Jaws are underdeveloped ii) Development & eruption of teeth delayed

1) Pregnancy:

a) Early signs of pregnancy - absence of menstrual period, breast engorgement (due to estrogen & progesterone), nausea (due to human chorionic gonadotropin & estrogen), fatigued & abdominal bloating. b) Maternal Adaptations to Pregnancy i) Neurologic - nausea, vomiting, gag reflex, fatigue, syncope, discomfort, depression ii) Cardiovascular - aldosterone sodium retention total body water & plasma volume (~50%), cardiac output (30 to 50%), stroke volume (30%) & heart rate (15%); systolic & diastolic bp decrease; ~90% develop reversible systolic murmurs iii) Hematologic - "a hypercoagulable state" because have increased potential for coagulation & thrombosis due to in clotting factors (V, VII, VIII, X, XII), platelet counts remain normal, an increase in fibrinolytic activity to compensate for tendency to coagulate deep vein thrombosis & pulmonary embolism may begin in 1st trimester, may develop anemia as RBC volume increases but not as much as increased plasma volume (~20% of cases) iv) Respiratory - entire respiratory tract becomes edematous because of capillary engorgement makes breathing difficult; diaphragm gets elevated by uterus decreasing function residual capacity v) Renal - progesterone induces changes that increase glomerular filtration rate ~30 to 50% due to increased aldosterone & its effects ( plasma volume & cardiac output) vi) Immune - decreases in neutrophil chemotaxis, cell-mediated immunity, NK cell activity; increased levels of circulating complement, neutrophils & lymphocytes; WBC counts become elevated during pregnancy so tricky to identify infection vii) Endocrine - ed levels of glucocorticoids, estrogens, progesterone modify glucose metabolism & need for insulin; thyroid function mimics hyper thryroidism viii) Gastrointestinal - increase in uterine size mechanically displaces stomach causing intragastric pressure; progesterone may decrease sphincter tone & inhibit GI motility chance of gastric acid reflux & acid aspiration heartburn & belching are common c) Complications of pregnancy: i) HTN - primary cause of maternal mortality & morbidity (bp >140/90); must have med consult (1) Chronic HTN - had before pregnancy (2) Pregnancy-induced HTN occurs at 20 weeks gestation, most threatening condition of pregnancy (a) Preeclampsia - presence of edema, HTN, proteinuria; usually occurs in nulliparous women; manifests as generalized arteriolar vasospasm & constriction causing ischemia, necrosis & hemorrhage of involved organs; bp does not reflect severity of disease but if pt presents with bp > 135, get consult to confirm had essential HTN before pregnancy (b) Eclampsia - is the occurrence of a grand mal seizure in the presence of preeclampsia (dental emergency initiate BLS); complications include cerebral hemorrhage, aspiration pneumonia, hypoxic encephalopathy, & thromboembolic events; 25% occur before labor, 50% during & 25% after delivery (w/in 7 to 10 days) ii) Gestational diabetes - sparing of glucose metabolism by mother to provide greater amounts of glucose for developing fetus (~1 to 3%) iii) Preterm Labor (spontaneous abortion) - if pt complains of contractions, must be evaluated for preterm labor; is normal phenomenon to have these contractions often due to dehydration, give water; occur every 15 minutes; spontaneous abortion occurs in 1:5 pregnancies during 1st trimester usually due to intrinsic fetal abnormalities; dental tx performed around this time will be incorrectly assumed as the cause of abortion; ?secondary bacteremia? iv) Supine Hypotensive Syndrome - as uterus expands with growing fetus & placenta, it comes to lie directly over inferior vena cava, femoral arteries & aorta if mother supine, weight of gravid uterus may impede blood flow thru major vessels hypotension syncopal or near syncopal episode tx by positioning pt on her left side & elevating the head of the chair to avoid compression of these major blood vessels v) Infectious diseases - mother may pass infections to fetus so avoid all infections (such as exposure to children in dental office) fetal infections often cause congenital abnormalities d) Oral complications i) Pregnancy gingivitis - elevated estrogen &/or prostaglandins in gingiva may increase its sensitivity to irritants causing inflammation; perform good oral hygiene & avoid perio surgery until after labor ii) Pyogenic granuloma "pregnancy tumor" - a benign, painless gingival mass that histologically resembles pyogenic granuloma (~1% pregnancies, usually presents during 2nd trimester, resolves on own postpartum) iii) Tooth mobility - may occur in late pregnancy (uncommon); probably due to changes in lamina dura, attachment apparatus, but not from loss of calcium stores; resolves postpartum e) Treatment timing: i) 1st trimester - Embryonic period (weeks 2 thru 8 post-conception) is period of active organogenesis, fetus a great risk to teratogens no dental tx, limit radiographs ii) 2nd trimester - perform all needed dental work, organogenesis is complete, risk to fetus is low, mother has had time to adjust to pregnancy, fetus not too large to make mother uncomfortable iii) 3rd trimester - positioning of mother is important to avoid supine hypotensive syndrome, dental tx can be comfortably administered until middle of third trimester iv) Dental radiographs - no increase in gross congenital abnormalities or intrauterine growth retardation occurs from radiation exposures during pregnancy totaling less than 5 to 10 cGy (1cGy radiation exposure (=more than 1000 full mouth series with E speed film ) increases risk of spontaneous aborting 0.1%, fetal dose to 2 PA film with lead apron is 700 times less than one average day of natural radiation in US. v) Drug Administration: (1) FDA pregnancy categories: (a) A No risk to fetus in any trimester (b) B No effects on animals (c) C Adverse rxns in animals, use judgement (d) D Definite fetal risk, may be given only during life-threatening conditions (e) X Absolute fetal abnormalities (2) Commonly known teratogens (drug present during organ formation to be teratogen, which is the 2nd to 8th week post conception) - alcohol, aminopterin, androgens, ACE inhibitors, busulfan, carbamazepine, coumarins, cyclophosphamide, lithium, methotrexate, penicillamine, phenytoin, tetracycline, valproic acid (3) Recommended medication - use drugs with short ½ lives (a) Local anesthetic - lidocaine with epinephrine (B) (b) Peripherally-acting analgesics - acetominophen (B) (i) Do not use aspirin (C, 3D)), ibuprofen (B, 3D) or other NSAIDS during 3rd trimester because may prolong pregnancy & labor, impair platelet function which may prolong bleeding time, inhibit PG synthesis which may cause premature closure of ductus arteriolus increase fetal mortality; aspirin has been shown to increase cases of oral clefts & other defects (c) Centrally-acting opiod analgesics - oxycodone with acetaminophen (med consult) (i) Will cause respiratory depression in mother & fetus; both may become addicted (ii) Do not use T3 because codeine is teratogen (C, 3D) (d) Antibiotics - penicillin (B), amoxicillin (B) or clindamycin (B), cephalosporins (B), but not tetracycline or doxycycline (D) b/c tooth discoloration & inhibits bone formation (e) Sedatives/anxiolytics - nitrous oxide (not classified) for less than 35 minutes with atleast 50% oxygen (not in 1st trimester because in animal tests, inactivated methionine synthetase, a vitamin B-12 dependent enzyme caused depletion if tetrahydrofolate which is needed for DNA synthesis --> birth defects), don't expose pregnant assistant to > 3 hours per week if lack scavenging equipment because chronic exposure may cause spontaneous abortion & reduced fertility in humans; do not use benzodiazepines (D) because form clefts (4) Oral infection have potential to escalate into bacteremia serious fetal complications; acceptable antibiotics during pregnancy include penicillins, amoxicillin, cephalosporins & clindamycin; Koren days emycin is gentler than clindamycin. f) Breast Feeding - the amount of drug excreted in breast milk is usually not more than 1 to 2% of the maternal dose thus, fetus not at risk; Contraindicated drugs include lithium, anti-cancer drugs, readioactive drugs & phenindione; if mother must take medication, take just after breast feeding & avoid nursing for 4+ hours if possible. g) Overall, need consult for tx during 1st or 3rd trimesters & may perform tx during 2nd trimester

How about apexification?

frank cooke heithersay yates cvek trope andreason frank, cvek, torneck torabinejad Javlet Cvek TBJ Andreason Chosack Finukane Himel

What about pulp stones and denticles

moss

A few symptoms of asthma

shortness of breath, coughing wheezing.

What about bacteria in geographic locations?

siquiera and jung

Why is MTA a good material to use? According to who?

torabinejad Sarker Damas - MTA had cementum grow directly on it (Torabinejad) - MTA binds to dentin (Sarker) - Non-toxic to cells (Damas)

What about hypersensitivity reactions? do they happen in teeth?

torabinjad

4- DIABETES MELLITUS

· Chronic systemic disorder w/ an elevation of blood glucose and disturbances in lipid and protein metabolism Type 1 (IDDM) - pancreatic B-cell destruction (in Islets of Lagerhans) or a primary defect in B-cell function results in failure to release insulin; destruction higher in children; causes: autoimmune, cancer, surgical Type 2 - relative deficiency in insulin production and resistance of receptors to insulin; glucose transport is variable and ineffective RISK FACTORS Type 2 - Obesity, Sedentary life style, HX of Gestational DM, HTN, Ethnic grp, Family hx, >45yrs, HDL<35, TG> 250, Impaired Glucose Tolerance Test KETOACIDOSIS: Mostly type 1; lack of gluc. utilization ability leads to TG breakdown into FFA (get converted to ketone bodies) and glycerol (gets converted to glucose) and protein breakdown into AA leading to: ↓ blood pH, metabolic acidosis and ↓ cardiac contractility; could result in diabetic coma; body tries to correct this through respiratory alkalosis · Liver, muscle and adipose tissue are insulin dependent; nervous system is independent · ↓ blood glucose level: insulin ; ↑ blood glucose level: glucagon, glucocorticosteroids, epi , thyroid hormones · Cause of endothelial Basement membrane alterations: 1) Reactive Oxygen species 2) Advanced Glycosylation Endproducts (AGE); Polyol Flux pathway (Sorbitol prod) · Vascular complications: Diabetic retinopathy (cataracts) + nepropathy (renal failure) · Atherosclerosis: ↑ risk of ulceration/gangrene in peripheries, HTN, MI and Stroke · Increased Polyol levels (Aldose-reductase pathway): affect Schwann cells leading to neuropathy (parasthesia or Burning Mouth syndrome) · Major Cause of Death: renal failure Symptoms: Type 1 Cardinal signs: Polydypsia, Polyuria, Polyphagia, weight loss, loss strength, ketone breath Other signs: bed wetting, skin infections, headache, drowsiness, malaise, dry mouth, dry skin Type 2 Cardinal signs: same as in 1 but less common Usual signs: weight gain or loss, urination at night, vulvar pruritis, blurred vision, decreased vision, loss of sensation, impotence, postural hypotension Additional tests: 1) Opthalmic exam 2) Urinalysis (acetone) 3) HbA1C glycosylated haemoglobin test Glycosylated Hemoglobin level: Normal 4-5.9%; Good glycemic control 6.5-6.9%; Fair 7.0-7.9% ; Poor >8.0% 1% ↓ Glycosylated Hem ~ 40% drop in chance of microvasc complications Fasting Blood Glucose: Normal < 110mg/dl Diabetic > 126 2-hr Post Prandial: Normal < 140mg/dl Diabetic > 200 MOST PT's are on intermediate (4-10hr) insulin; morning appt best Treatment: Type 1 - diet + physical activity; Insulin; pancreatic transplant Type 2 - diet + physical activity; oral hypoglycemics; insulin; combo of meds + insulin Drugs: only for Type 2; not for Type 1 or pregnant pts Oral manifestations: altered wound healing (altered blood flow and immune cell func.), Burning mouth syndrome, increased incidence of infection, xerostomia increased inflammation due to plaque; bone loss, periodontitis · Impaiered PMN function (adherence, chemotaxisis, phagosytosis), monocyte + Macrophage (overproduction of cytokines and chemokines Dental considerations: · stress reduction, AB use, Diet modification, Appt timing, changes in meds, consult w/ physician · Profound anaesthesia - minimize release of endogen. Epi; epi in carp is insig.; give short acting so they can resume eating habits · Don't use steroids b/c ↑ blood glucose; pt is already immune compromised as well · Acute infection - AB should be rx. · AVOID ASA + NSAIDS - could induce hypoglycaemia by potentiating oral hypogly meds (Sulfonylureas) · Sched appts between peak insulin activity to reduce chance of hypoglycaemia (morning best) · Take glucose reading; if blood glucose <70mg.dL admin. oral carbs Emergencies: 1) Hypoglycemic shock: Mild stage: hunger, weakness, tachycardia, pallor, sweating, paraesthesia Moderate: Incoherence, Uncooperative, belligerent, lack of judgement, orientation Severe (<50mg/dL in CNS): unconsciousness, tonic-clonic movements, hypotension, hypothermia, rapid pulse Tx: Awake - give p.o. 15g carbs (4-6 oz OJ, 3-4 tsp sugar, hrad candy, frosting) Unconscious - IV line w/ either 25-30 mL 50% dextrose or 1mg glucagon; if cant place IV than subcut or IM 2) Hyperglycemic shock: Always assume its hypo b/c this is less likely and small amount of extra glucose has no sig effect Ask patient: · Date of diagnosis, type, severity, control, therapy, complications, last FBSs, last HbA1C, what happens if misses a meal? Is snack needed?

What are the antigen antibody reactions?

pano

What about Septocaine/Articaine?

reader haas

How do we determine the length to clean and obturate to?

ricucci radiograph: dummer, kuttler - Tactile sense - Paper point apex locator: sunada meredith rivera wilson - Ricucci showed that instrumentation and obturation to apical constriction had best outcomes, obturating long had worst outcomes, short was 2nd worst - Radiograph o Dummer - showed that apical foramen is 0.38 mm from rad apex and apical constriction is 0.51 mm from apical foramen o Kuttler - only 20% of adult teeth and 32% of young teeth have foramen at the vertex, others deviate; the older you get, the more cementum deposition; apical constriction is about 0.5 mm from foramen - Tactile sense - Paper point - Apex locator o Sunada 🡪 invented apex locators ▪ Measuring difference in electrical resistance between inside of tooth and outside of tooth at PDL ▪ 40 microA (6.5 kOhms) = 0.1 mm short of apical constriction o Meredith 🡪 dry canal is more accurate than wet canal o Rivera 🡪 recapitulating to get patent canals is more accurate. Even before you instrument, 63% of the time, your length is long and after instrumentation 30% of the time, length is long. Need to take WL film o Wilson - Apex locator and Electric pulp test are safe to use in patients with cardiac pacemaker/defibrillator

Correlation between clinical and Histology?

seltzer and ricucci - Seltzer - showed the difference - Ricucci - 94% accurate for normal/reversible pulpitis clinical vs. histology. 84% accurate for irreversible and histology

What does EDTA stand for? How does it work?

sen - Ethylene diamine tetraacetic acid - EDTA chelates calcium ions and removes inorganic material (SEN)

What is smear layer?

sen Garberogli Chailertvanikul - Sen Composed of dentin shavings, odontoblastic processes, pulp tissue, and bacteria. It can block the tubules which can protect the bacteria and prevent your sealer or medicament from going into tubules. It can leave gaps so you can get microleakage during obturation. Removed via EDTA due to chelating action with calcium ions in the dentin which helps to remove the smear layer - Garberogli showed that 3% and 17% EDTA removed smear layer as well as phosphoric and citric acid, but the two acids also caused demineralization - Chailertvanitkul - said that with or without smear layer, there was still leakage via coronal

How does CaOH work?

siqueira and tronstad - Damage to bacterial membrane - Protein denaturation - Damage to DNA - High pH helps with coagulation and helps form apical barrier - prevents osteoclasts, which work best at pH ~5 and promote osteoblasts (Tronstad)

uses of CaOH

sjorgren, bystrom, vera Wadachi Tronstad Cvek - Antibacterial - sjorgren, bystrom, vera - Dissolution of tissues, coagulation: Wadachi - Resorption by Tronstad - Pulp capping by cvek - Induce apical barrier formation

How do you remove smear layer?

yamada Best way is to use NaOCl 🡪 EDTA and then 🡪 NaOCl (Yamada)

1) Cushing's Syndrome

§ Clinical picture results from elevated blood levels of cortisol due to: 1. Excess production of ACTH by pituitary gland (major cause, 60% due to ACTH-producing tumors of pituitary gland) 2. Elevated cortisol secretion 3. Ectopic ACTH production (i.e. lung cancer tumors) 4. Iatrogenic Cushing's Syndrome due to long-term exogenous corticosteroid therapy - corticosteroids are chronically prescribed for their anti-inflammatory effects to pts suffering from: § CT diseases § Inflammatory bowel disease § Autoimmune hematological disorders § Graft transplantation § Dermatological diseases § Excess cortisol results in relentless gluconeogenesis (pt tends to diabetic despite high levels of insulin) § Pt breaks down protein throughout body muscle wasting, high levels of insulin fat distribution & redistribution § Long-standing elevations in blood levels of exogenous cortisol causes: 1. Delayed healing mechanisms 2. Hypertension 3. Depressed inflammatory responses 4. Lymphopenia 5. Protein catabolism (atrophy of bone, cartilage & muscle) 6. Mood alteration 7. Adrenal suppression § 3 female : 1 male § Clinical findings due to elevated cortisol: 1. Fluid retention 2. Hypertension 3. Hyperglycemia 4. Glucouria 5. Hypoaklemia 6. Hypernatremia 7. Truncal obesity (protruding abdomen) 8. "moon" face 9. "buffalo hump" (deposit of fat b/t scapula over the thoracic spine) 10. Atrophic skin & easy bruising secondary to collagen wasting & dermal weakening 11. Thin fingers limbs due to protein breakdown 12. Skeletal muscle weakness, usually develop osteoporosis, vertebral collapse & severe back pain 13. Hirsutism & virilism because ACTH stimulates release of androgens & cortisol 14. At risk for thromboembolisms, amenorrhea, bacterial & fungal infections 15. Likely to develop steroid-induced diabetes mellitus due to derangement of carbohydrate metabolism & glucose intolerance 16. Emotionally labile, psychiatric disturbances § Diagnosis: § Based upon elevated levels of cortisol in blood & urine on 3 separate occasions § Lab test: Dexamethasone suppression test - measures cortisol levels 20 hours post-injection with dexamethasone (steroid) pts with Cushing's continue to secrete elevated levels of cortisol after this injection § Also assay blood levels of ACTH, androgens to identify origin of dx: § Elevated ACTH only pituitary gland neoplasm § Elevated cortisol & androgens carcinoma of adrenal cortex § Medical Treatment: § Correct daily cortisol levels § Surgically eradicate any tumors or hyperplasias § Avoid permanent endocrine deficiency § Post-surgery, pts live normal lives but require supplemental cortisol § Oral Manifestations: § Face is round, swollen, reddish, acne § Eyes have conjunctival edema § Gingiva is enlarged, swollen, bleeds easily § No bony abnormalities of jaw despite osteoporosis § Periodontal & candidal infections because of suppressed inflammatory rxns enabling bacterial & fungal infections § Dental Management: § Regulation of steroid levels prior to starting treatment § Routine dental care can be provided when steroid levels stable § Pts taking corticosteroids secondary to adrenal surgery may requires supplemental dose, especially during times of infection, surgery § Avoid respiratory depressants b/c pts have weakened respiratory muscles § Bones fragile due to osteoporosis § Infections can be managed with routine antibiotics § Periodontal disease requires frequent cleanings & surgical correction of osseous defects § If pt has systemic complications of Cushing's Syndrome (hypertension, heart failure, diabetes mellitus), impaired healing will be present.

uses of CaOH

Chong - Eliminate bacteria - Reduce inflammation - Neutralize canal contents and tissue debris - Act as a barrier against leakage - Dry wet canals - stop bleeding

Which material is the best for root-end filing?

Chong Torabinejad Torabinejad Zhou - Chong - compared IRM and MTA as root-end filling materials and found that at 12 months, 84% success for MTA and 76% success for IRM; at 24 months, 94% success for MTA and 87% success for IRM no statistical difference but MTA was a little higher than IRM - Torabinejad study with monkeys - compared MTA with amalgam and found that amalgam produced severe inflammation whereas cementum layer was observed over 5/6 MTA root fillings and there was less inflammation demonstrated biocompatibility - Torabinejad showed that MTA had better marginal adaptation under SEM in comparison to amalgam, super-EBA and IRM - Zhou 2017 compared MTA to bioceramic putty; success rate for MTA was 93.1% and BP-RRM was 94.4%; no sign difference o Prognostic factors: molars, larger lesions, and inadequate root fillings had lower success rate (what are contributing factors to failure of surgery?)

What do you need for regeneration?

- Stem cells - Scaffold - Growth factors

How does bacterial killing occur?

1) Through oxygen free radicals (h202, superoxide) AND digestive enzymes (collagenase, elastase, gelatinase)

Can a bacteremia cause a root canal infection?

Robinson and Tziafas Delivanis

How do different antibiotics work and which should be used?

Cipro Baumgartner Baumgartner Yammamoto Vacek Hersh, DeRossi Harrison

History of endodontics?

- 1909 🡪 theory of focal infection - 1919 🡪 x-ray became available - 1920 🡪 first calcium hydroxide used - 1931 🡪 Rickert and Dixon hollow tube theory - 1959 🡪 Sargenti paste - 1963 🡪 endodontics became a specialty

What is gutta-percha made of?

- 20% gutta-percha - 66% zinc oxide (filler) - 11% heavy metal sulfates, ex. Barium sulfate (radiopacifier) - 3% waxes or resins (plasticizer)

What is MTA made of?

- 75% Portland cement = tricalcium silicate, dicalcium silicate, tricalcium aluminate, tetracalcium aluminoferrite - 20% bismuth oxide (radiopacifier) - 5% gypsum

What nerves cause different types of tooth pain?

- A delta nerve fiber: fast conducting myelinated. Fibers are located at the pulp dentin border zone at the pulp periphery, located in the coronal portion of the pulp o Rapid fluid movement from extreme cold generates fluid movement - excite Adelta fibers for pain - C fibers: slow conducting, unmyelinated. Located in the pulp proper, extending into the cell-rich zone 🡪 stimulated by gradual thermal change and heat, causes referred pain

What is in situ hybridization?

- A technique that uses a labeled complementary DNA or RNA to localize a specific sequence in a section of tissue - Sense strand - the strand coding for the protein - Antisense strand - the complimentary strand - You can use this technique to detect whether any of these proteins (signal molecules, receptor, signal transduction) is being produced

2 - Addison's Disease and Cushing' Syndrome

- ADDISON'S DISEASE - PRIMARY adrenocortical insufficiency - Due to progressive destruction of the adrenal cortex - Most frequent cause is idiopathic atrophy, and an autoimmune mechanism is probably responsible. - Adrenal gland- an inner adrenal medulla (epi and norepi) and an outer adrenal cortex (major products are steroid hormones)The adrenal cortex is made up of 3 zones: 1) outer Zona glomerulosa - produces aldosterone (works on distal tubule of kidney to retain Na) 2) middle Zona Fasciculata - produces the glucocorticoid cortisol (maintains BP, blood volume, blood sugar, feeling of well-being). Regulates carbs, fat, & protein metabolism, and inhibits inflammation and maintains homeostasis during physical and emotional stress. Synthesis of cortisol (which has anti-insulin effects) is regulated by adrenal corticotropic hormone (ACTH which is made by the anterior pituitary) 3) inner Zona Reticularis - produces androgens. - As the major hormones of the adrenal cortex are cortisol and aldosterone, the presentation of Addison's disease is due to the lack of these compounds. - Lack of cortisol results in impaired glucose, fat, and protein metabolism; hypotension; increased ACTH secretion; impaired fluid secretion; excessive pigmentation; and an inability to tolerate stress - Aldosterone deficiency results in sodium loss and ultimately acidosis. SECONDARY adrenocortical insufficiency - more common than primary; patients may be deficient in cortisol secretion as a result of long-term exogenous corticosteroid therapy which suppresses the pituitary-adrenal axis and causes glandular atrophy and the suppression of endogenous glucocorticoid secretion. The exogenous steroid causes the anterior pituitary to decrease production of ACTH which suppresses adrenal gland production of cortisol. - Treatment of adrenal insufficiency involves replacement with corticosteroids - The daily requirement of hydrocortisone is 20 to 30 mg. - Natural circadian rhythm and increased ACTH in morning allow the patient to be better equipped to handle stress during morning appointments. - STRESS and INFECTION are major issues with these patients. We are primarily dealing with secondary adrenocortical deficiency. With steroid supplementation - there is anti insulin effect and decrease in immune response. - ADRENAL CRISIS - precipitated when an Addison's pt is challenged by stress (Illness, infection, surgery). This is a medical emergency manifested by sunken eyes, profuse sweating, hypotension, weak pulse, cyanosis, nausea, vomiting, weakness, headache, dehydration, fever, dyspnea, myalgia, hyponatremia, eosinophilia. Immediate treatment of adrenal crisis: · 100 mg of Hydrocortisone or 4 mg dexamethasone IV, 5% dextrose sol', fluid and electrolyte replacement and immediate transportation to a medical facility. Preventive measures: 1. Schedule surgery in for morning appointments 2. Use of Nitrous oxide/Oxygen or Benzodiazepine IV sedation (plasma cortisol levels not reduced by these agents) 3. Drugs that decrease Cortisol (ie. Ketoconazole) should be discontinued 24hrs pre-surgery with physician's consent 4. Barbiturates should be used cautiously (cause an increased metabolism of cortisol) 5. Methods to reduce blood loss should be employed since it could lead to hypotension and increase the risk of adrenal crisis. 6. Anticoagulants increase risk of post surgical bleeding and hypotension 7. Long acting local anaesthetics (ie. Bupivicaine) should be used at end of procedure for pain control 8. Aspirin and NSAIDS should not be given to long term steroid users because of peptic ulceration risk 9. For surgical procedures, blood pressure monitored at 5-minute intervals and before patient leaves the office. If systolic <100mmHg and diastolic <60mmHg corrective action required. This includes patient position (head lower than feet), fluid replacement, vasopressors and evaluation of sigs of adrenal dysfunction vs hypoglycaemia. 10. For patients taking steroids on an alternative day regimen, dental treatment should be done on the same day they take the steroids. CUSHING'S SYNDROME - persistently elevated cortisol due to one of the following: 1) Excess production of ACTH caused by ACTH-producing tumors of the pituitary 2) Elevated cortisol secretion - adrenal tumor 3) Long-term exogenous steroids use - Problems with elevated cortisol- delayed healing, hypertension, depressed inflammatory responses, lymphopenia, protein catabolism, adrenal suppression, and mood alteration. - Moon face/buffalo hump are common physical findings. - Induced diabetes due to derangement in carbohydrate metabolism and glucose intolerance and the steroid having an anti-insulin effect (increased serum glucose). - Need to regulate the steroid level before treatment. - Avoid sedatives - patients can have weak respiratory muscles - Osteoporosis may be a complication - Major Concerns: Infection, Hypertension, Diabetes, Impaired healing Tx modifications: Take Blood pressure throughout appt; Don't prescribe ASA or NSAIDS b/c could increase chance of peptic ulcer when used with steroids.

What are different types of stem cells?

- Adult stem cell vs embryonic stem cell - Totipotent, pluripotent, multipotent o Totipotent - can differentiate into any of 3 germ layers and placenta o Pluripotent - cells from blastocyte - can develop into any of 3 layers, not placenta o Multipotent - have potential to differentiate in same lineage

What is the outcome of pulp capping?

- Cho Carious pulp exposures were capped with either Dycal or MTA and restored. f/u for 1 and 3 years o 1 year: 89.9% survival for MTA, 73.9% for Dycal o 3 years: 67.4% survival for MTA, 52.5 for Dycal

What are some mechanisms of virulence? (Slots paper)

- Colonization/Attachment and growth virulence factors o External appendages, capsular material, endotoxic LPS, pili or fimbriae o Growth stimulatory factors can be bacteria-derived or host derived - Mechanisms to evade host defense o Decreased chemotaxis, resistance to phagocytosis, resistance to complement, degradation of immunoglobulins, fibrinolytic activity, leukotoxin, endotoxin - Bacterial factors that destroy host tissue o Destroy tissue by direct action or indirectly by inducing inflammatory reaction unfavorable to host o Collagenase, phospholipase, alkaline and acid phosphatase, volatile sulfides

What are some mechanisms of virulence ? (Slots paper)

- Colonization/Attachment and growth virulence factors o External appendages, pili , fimbriae, capsular material, endotoxic LPS o Growth depending on synergism (eg. BBP need synergistic bacteria to form growth factors for Vit K metabolism) - Mechanisms to evade host defense o Decreased chemotaxis, resistance to phagocytosis, resistance to complement, degradation of immunoglobulins, fibrinolytic activity, leukotoxin, endotoxin - Bacterial factors that destroy host tissue o Destroy tissue by direct action or indirectly by inducing inflammatory reaction unfavorable to host o Collagenase, phospholipase, alkaline and acid phosphatase, volatile sulfides

What is the structure and function of the basement membrane?

- Consists of type IV collagen, heparin sulfate, chondroitin sulfate, laminin, fibronectin - Signal molecules (interaction between epithelium and mesenchyme) need to go through basement membrane

What are the classifications of endo-perio lesions:

- Endo only - Perio only - Primary endo, secondary perio o Treatment of endo will take care of perio lesion - Primary perio, secondary endo o Possibly perio tx will induce healing for endo without endo tx - Combined lesion o Need both endo and perio tx

8 - Hepatitis

- Inflammation of liver from infectious and non-infectious sources - Infectious Hep: Hep virus, MONO, TB, 2o syphilis - Non-infectious Hep: alcohol abuse, overuse of Tylenol, Methtrexate - 8 types: A-G + TTV (transfer transmitted virus) - Acute: A, B, E and F; Chronic: B, C (longer than 6 months) Hep A - RNA virus; replicates in the liver; found in stool; oral-fecal route - In water + found supplies; doesn't require tx; doesn't cause major complications - Jaundice common; vaccine available - No carrier form; no chronic state Hep B - DNA virus; replicates in liver & stem cells - DANE particle: outer surface (HBsAg) + core (HBcAg) - From cleavage of core particle get (HBeAg - virus is infective) - Transmission: blood transfusion, sexual contact, saliva transfer through mucosa - vaccine available; acute, chronic and carrier state Hep C - RNA virus; blood-borne infection; in post-transfusion and hemodyalisis pts - NO vaccine - Acute, chronic and carrier state Hep D - RNA virus; requires HBsAg for viral envelope - Results in fulminant infection; more severe than Hep B - Co-infection (both viruses infect cells at the same time) - Superinfection (one virus infects first, then the next virus) Hep E - RNA virus; oral-fecal route; symptoms similar to A; younger ppl - JAUNDICE common Jaundice: Mainly in A & E; Increased bilirubin in plasma, epithelium and urine because liver cannot metabolize it. Bilirubin is a breakdown product of hemoglobin; emulsifies fat in small intestine (normal level 1mg/100mL) Hep infection can result in: 1. Recovery 2. Carrier state 3. Chronic active 4. Fulminant 5. Cirrhosis 6. Carcinoma 7. Death. In carrier state, the viral antigen is present in the plasma without signs of the disease; can progress to chronic active. In fulminant cases, co/super infections lead to massive hepatocyte destruction with an 80% mortality rate S&S: - most Hep B and C pts are asymptomatic 1. Prodromal phase - abdominal pain, nausea, vomiting, fatigue, malaise, fever 2. Icteric phase - jaundice, hepatomegaly, slenomegaly 3. Recovery phase - symp dissapear; hepatomegaly and liver dysfunc continue - Chronic liver disease assoc with increased bleeding, esophageal varices, ascites, jaundice, spider angioedema, dark urine Lab test: ↑AST & ALT, ↑serum bilirubin, ↑WBC, pTT, decreased vit K factors 2,7,9,10 Serologic tests: - IgM-HBc = current infection - IgG-HBc = recovery - IgG-HBs without HBsAg = complete recovery - IgG-HBs with HBsAg = chronic Hep Exposure through needle stick injury from HBsAg (+) pt: - Vaccinated: Immediate admin of HBIG inject. + booster shot - Unvaccinated: Immediate admin of HBIG inject. + vaccine Exposure through needle stick injury from HCsAg (+) pt: - only thing we can do is monitor liver tests. Treatment: Rest and Ingestion of fluids, monitor ALT level; for chronic admin Interferon; for fulminant admin steroid; Liver transplant is last resort Dental Management: 1. Active hep - only emerg care in isolated operatory room 2. Chronic hep - consult MD regarding liver function, tx modifications and meds used 3. Past disease - w/out liver dysfunction, tx can be given - INR ≤ 3.5; pTT between 11-14 sec. - vit K injectionor platelet replacement might be necessary - minimize use of drugs metabolized in liver: Amide LA's, Analgesics (ASA, Acet., Ibuprof, Codeine); Sedatives (Diazepam, Barbituates); ANTB (Ampicillin, Tetracyclin, Metronid., Vancomycin)

What are some chemical means of sterilizing?

- For sterilization Alkylating agents (ex. Ethylene oxide and formaldehyde) - For disinfection phenolic compounds, alcohols, heavy metals, halogens, peroxides, cationic and anionic detergents - Antibiotics have higher selectivity

What microorganisms are found in endodontic infections?

- Fungi ascomycetes (yeasts and penicillium) - Archaebacteria - Eubacteria (true bacteria) - Viruses

What is the function of pulp extracellular matrix?

- Gives resiliency of pulp - relates to protection of odontoblast - Pulp is geared toward maintenance and protection of odontoblast - Space to allow nutrients to diffuse through to get to odontoblast and toxins can diffuse out

What are the ideal properties of a retrofilling material?

- Good sealing - Biocompatibility - Radiopaque - Good compressive strength - chemical properties - Low solubility

What is the difference between gram-negative and gram-positive bacteria?

- Gram-negative bacteria have an outer membrane with LPS and a thinner layer of peptidoglycan - Gram-positive bacteria do not have an outer membrane but they have a thick layer of peptidoglycan and teichoic acids that go from the inner cell membrane and pass through the cell wall and have some similar actions as LPS - Gram negative - more susceptible to proteolytic enzymes, high pH, oxidizing agents, lysis by complement - Gram positive - more susceptible to acids (low pH), detergents, organic solvents, iodine, penicillin-type antibiotics

What are the mechanisms of action of different antibiotics?

- Inhibition of cell wall synthesis o Ex. B-lactams (penicillins, cephalosporins), Bacitracin, Vancomycin o Penicillins inhibit crosslinking of glycan strands in the peptidoglycan o Beta-lactamase is an enzyme that splits the penicillin and inactivates it - Inhibitors of cell membrane function o Not common because these drugs are very toxic o Ex. Polymyxin B, gramicidin - Inhibition of folate synthesis (nucleotides) o Ex. Sulfonamides, trimethoprim - Inhibition of DNA replication o Ex. Quinolones (ciprofloxacin, levofloxacin) - Inhibition of RNA synthesis o Ex. Rifampin o Targets RNA polymerase - Inhibition of protein synthesis o Targets 30S ribosome inhibits initiation, ex. Tetracycline, aminoglycosides o Targets 50S ribosome inhibits elongation, ex. Chloramphenicol, Macrolids (Erythromycin, Azithormycin, Clarithromycin), Lincosamides (Clindamycin)

What is the difference between innate immunity and adaptive immunity?

- Innate immunity is nonspecific defense mechanisms that come to play immediately or within hours of an antigen's appearance, causes inflammation, antigens are recognized by toll-like receptors (ex. Macrophages are activated by antigens to create cytokines to bring more immune cells into the area) - Adaptive immunity is antigen-specific immune response, takes a few days to weeks, T-cells B-cells and dendritic cells, memory

12- Hyperventilation

- Is the state of breathing faster and/or deeper than necessary, bringing about lightheadedness - Can also be a response to an imbalance in body's natural levels of O2 and CO2, such as metabolic acidosis; the body uses hyperventilation as a compensatory mechanism to decrease blood acidity - Stress/anxiety are common causes - Can also be brought about voluntarily by taking many deep breaths. - Can be brought on by low oxygen levels in the blood (hypoxia), painful stimulus, ingestion of medications, increased metabolism, exercise, and hyperthyroidism. Pathophysiology - In normal breathing, gases in the alveoli of the lung are nearly in equilibrium with the gases in the blood. As patients get anxious, the body enters a fight-or flight state. Deeper/quicker breaths exchange more of the alveolar gas with ambient air and have the net effect of expelling more carbon dioxide from the body. - The resulting low concentration of carbon dioxide in the blood is known as hypocapnia. Since carbon dioxide is carried as carbonic acid in the blood, hypocapnia results in the blood becoming alkaline. This is known as a respiratory alkalosis. - 2 mechanisms that contribute to the cerebral vasoconstriction that is responsible for lightheadedness, parasthesia, and fainting seen in hyperventilation are: low carbon dioxide causing decreased hydrogen ion concentration (respiratory alkalosis), which causes blood vessels to constrict. - The other mechanism is the decrease in hydrogen ions (alkalosis) causes decreased freely ionized blood calcium, thereby causing cell membrane instability and subsequent vasoconstriction. - Increased blood level of Epi and norepinephrine cause palpitation, sweating, and trembling Dental Management - Apply stress-reduction techniques and good chair-side manner - Recognize S&S of hyperventilation: wet, cold, clammy hands, flushed or pale face - Management of hypervent. directed at re-establishing normal respiratory pattern and reducing anxiety Steps to manage hyperventilating patients: Terminate all treatments and remove all materials from the patient's mouth. Position the patient upright Calm the patient down and ask the patient to breath slowly. Direct the patient to re-breath their exhaled CO2 by placing their hands or a sealed bag over their mouth. This will increase partial pressure of CO2. (Koren likes to use the oxygen mask) DO NOT administer O2 to hyperventilation patient since this will further increase the imbalance between oxygen and carbon dioxide, causing partial CO2 pressure to drop. Once hyperventilation ceases, try to determine the cause

10 - Dialysis

- Kidneys are a pair of vital organs whose main function is to keep the blood clean and chemically balanced; every day process 200 liters of blood to filter out 2 liters of waste - The wastes and water become urine which flows to the bladder. - The functional unit of kidneys is the nephron consisting of a renal corpuscle (where blood is filtered) and successive segments of renal tubule - Glomerular Filtration Rate (GFR) - the rate at which the ultrafiltrate is produced by renal glomeruli. In health, GFR = 125 ml/min. In disease, GFR decreases, and larger molecules escape into the filtrate, resulting in the appearance of blood cells, epithelial cells, and the proteins in the urine. - Chronic renal failure (CFR) or end-stage renal disease (ESRD) is GFR < 60 ml/min for more than 3 months,. Diseases of the kidneys may lead to s: retention of metabolic waste products, accumulation of toxic levels of drugs, acid-base alterations, and fluid retention and blood pressure abnormalities. Persistent dysfunction of the kidneys eventually results in the need for Dialysis and renal transplantation. Functions of kidneys: 1. Regulation of plasma volume 2. Secretion of essential hormones: Erythropoietin, Renin, Calcitrol, PGI2 (prostacycline) 3. Excretion of nitrogenous waste products Signs of renal dysfunction - failure to remove toxic wastes, electrolyte imbalance, and fluid overload. Clinical detection of renal disease is made by measurements of the frequency, amount and color of urine, GFR, microscopic analysis of the urine, urine pH, urine protein levels, serum creatinine concentrations, creatinine clearance, and blood urea nitrogen (BUN) levels. Laboratory Findings in Renal Disease 1. Acute renal failure (ARF) - most in young, healthy adults; sudden injury to the renal tubules as result of trauma, toxic substances, ischemia, infection, severe hemorrhage, complication of major surgery (transfusion reaction), burns or shock; may cause permanent loss of kidney function, but can be reversed 2. Chronic renal failure (CRF) - irreversible and progressive disease, resulting in scarred and nodular kidneys that ultimately requires hemodialysis and renal transplantation. 3. End-Stage Renal Disease (ESRD) is total (or nearly total) and permanent kidney failure that occurs as a complication of chronic progressive renal failure. Must undergo dialysis or transplantation to survive. S & S: - Compensatory hypertophy - healthy kidney increases in size to compensate for the disease of the other kidney. - Effects of the renal failure occur when 70% of all nephrons are destroyed. - Azotemia (elevated BUN concentration) is the classic sign of renal disease seen in both acute and chronic renal failures. - Uremia is a symptom that results from chronic retention of toxic nitrogenous products and water. Appears when BUN >50mg/100ml and serum creatinine > 5mg/100ml. 4 successive clinical stages of renal failure 1. Loss of renal reserve - a decrease in kidney function without clinical manifestations; lower creatinine clearance is the only observable change. (Creatinine is a poorly metabolized breakdown product of muscle; creatinine in urine is derived from that filtered by the glolmerulus; thus it is a good indicator of glomerular function). As the nephron population declines, ↓GFR, ↑BUN levels. 2. Renal Insufficiency - mild- moderate↓kidney function; mild accumulation of nitrogenous products in the blood, decreased ability to concentrate urine and mild anemia. 3. Renal failure - kidney function deteriorated to the point of chronic abnormalities in the (azotemia, metabolic acidosis, hypocalcemia and hyperphosphatemia). 4. Uremia/ESRD - retention and accumulation of excretory products and↓endocrine and metabolic functions of the kidney. Uremic manifestations: urea frost on skin, intestinal inflammation, chronic anemia, platelet dysfunction, ↓phagocytic activity, ↓ Erythropoietin, Renin, Calcitrol, PGI2, reduced mental activity, CHF, polyuria, polydipsia, muscle fatigue, hyperkalemia Treatment - Pharmacologic therapy - For early renal insufficiencies, changes in diet and antihypertensives (to control hypertension), diuretics (to control significant fluid overload), Vitamin D and calcium (to manage secondary hyperparathyroidism), Vitamin E (for muscle cramps), Erythropoietin (for anemia), Insulin (for glucose intolerance). - Dialysis - when azotemia poses a serious threat to life or when loss of renal function is irreversible. It's an artificial means of filtering the blood and removing the toxic waste products from the blood stream. Either hemodialysis (90%) or peritoneal dialysis (10%). - Hemodialysis - accomplished by an AV fistula; pts' blood is anticoagulated during dialysis (usually heparin, duration of action ~ 4 hours) to prevent both the infusion lines and dialysis machine tubing from clotting. Blood is filtered through an external semipermeable membrane. Done in outpatient sessions every 2 or 3 days that last 3-4 hors. Advantage of hemodialysis: an effective mechanism of filtering blood. Disadvantages: blood borne infections (Hep B, C and HIV) and bleeding tendencies (Heparin, ↓platelet factor III, platelet destruction by machine). - Peritoneal dialysis - involves abdominal peritoneum as a semi-permeable membrane across which the transfer of solutes and water occurs. After a period of equilibration, the solution that contains dissolved waste products is removed and is replaced by fresh solution. Advantage of peritoneal dialysis: low cost, ease of performance, low risk of blood-borne disease transmission, no need for anticoagulation, greater patient mobility (done at home); Disadvantages: slower process, requires more frequent dialysis, has common complication of peritonitis. - Renal transplantation - treatment for pts with irreversible renal failures. Ideally from relatives with good histocompatibility profile; Immunosuppressive drugs are used to prevent rejection. Dental considerations - Koren wants ANTB prophylaxis given for 2 yrs post organ transplant to prevent IE - For hemodialysis patients receiving dental treatment: 1. Consult nephrologists regarding: Hypertension, Anemia, Bleeding abnormalities (ask for bleeding time and platelet count numbers prior to elective surgery); Need for preoperative antibiotic prophylaxis (type, dosage, and interval); Need for corticosteroid augmentation therapy; The infectious disease status for HIV and Hepatitis B and C 2. Monitor BP throughout the procedure; must never be taken on the arm involved in AV fistula. 3. Tx the day after dialysis (to prevent prolonged bleeding from Heparin) 4. Caution with meds that might build up in the bloodstream due to impaired excretion (narcotics, or meds that cause prolonged bleeding such as NSAIDs and ASA) 5. Avoid nephrotoxic medications (streptomycin, tetracycline, acyclovir, cephalosporins, ketoconazole and aminoglycosides. Tylenol is nephrotoxic at high doses, it is still a drug of choice for pain management 6. Adjust dosages (Fig 1 below) of medications according to the extent of renal impairment

What does the vasculature in the pulp look like?

- Large vessels found towards central pulp and smaller vessels in the periphery - Terminal capillary network (TCN) in the periphery - feeding odontoblasts - The smallest diameter of capillary is 7.5 microns - size of RBC - Anastamoses between arteries and veins - controls blood flow in pulp o ** Important because during inflammation, there is more blood flow and pressure, which may be detrimental to odontoblast - controlled by opening and closing shunts - Lymphatics - another way in maintaining pressure - takes excess fluid and drains - There's also a U turn loop in arteriole

What is the smear layer?

- Mjor - review article - Smear layer: debris consisting of ground components of enamel and intertubular and peritubular matrix, water, dentinal fluid, and saliva - Smear layer can decrease dentin permeability - protective effect on pulp - Damage to pulp with prep - displacement of odontoblast nuclei into dentinal tubules - A study showed, brief grinding (1 second, 3x) with a diamond bur flushed with saline caused instantaneous increase in blood flow. Grinding halfway into dentin caused a 53% increase in blood flow lasting for about 10 minutes. - Crown preps with high speed and no water have been shown to decrease blood flow. - The peripheral flow of fluid following cavity preparation allows plasma proteins to enter the tubules, clotting of these proteins can reduce the diameter of the tubules

What are differences between Prokaryotes and Eukaryotes?

- Prokaryotes (bacteria and archaea) are smaller and have nucleoid, DNA is in a single circular strand of DNA and is haploid, replicates by binary fission, DNA sequence has little repetition, one mRNA can code for multiple genes, there is linked transcription and transduction, no organelles, and has 70S ribosomes, cell wall made of peptidoglycan, and appendages are a singlet structure - Eukaryotes have a true nucleus and genetic information in in chromosomes, in which DNA is extensively folded with histones to make chromosomes, there are many repetitive and not transcribed pieces of DNA, one mRNA codes for one protein and the mRNA usually has a 5' guanosine cap and polyadenylation of 3' end, transcription and translation are separated in time and space, organelles are present, 80S ribosome, cell wall made of cellulose or chitin or mannan, and appendages are 9+2 arrangement.

What are the indications for use of antibiotics in Endodontics?

- Prophylaxis for IE - Severe spreading infection (ex. Extraoral swelling, fever, lymphadenopathy) - Cases of poor host defense mechanisms - Cases when adequate surgical and endodontic treatment could not be achieved during emergency visit - Certain traumatic injuries - Antibiotics do NOT decrease incidence of flare-ups in asymptomatic teeth (Walton) - Antibiotics do NOT decrease of post endodontic treatment pain in symptomatic teeth with necrotic pulps or with PA abscesses (Henry, Fouad)

What are the different types of protists?

- Protists are single-cell microorganisms that do not form tissues - Eukaryotic protists o Protozoa - no cell wall o Algae - cell wall made of cellulose o Fungi - cell wall made of chitin or mannan - Bacteria - Archaea - Viruses - non-cellular

How is genetic expression regulated?

- RNA polymerase binds to promoter to transcribe DNA to mRNA - There is a region within the promoter called the operator - The operator site is where the regulatory protein can bind to (either repressor or activator protein) - Negative regulation repressor protein binds to operator and prevents transcription o Ex. Lac operon presence of lactose, binds to repressor protein and allows lac operon enzymes to be expressed o Ex. Trp operon presence of tryptophane, tryptophane binds to repressor protein to allow it to bind, turns off the genes that produce tryptophane - Positive regulation RNA polymerase is only weakly bound and needs activator protein to start transcribing o Ex. Ara operon arabinose is an inducer, binds to activator protein and allows it to bind and produce enzymes

Can you use Laser Doppler flowmetry to assess pulp vitality?

- Ramsay: reliable interpretation of longitudinal measurements of pulpal blood flow obtained with laser Doppler flowmetry requires accurate repositioning of the measurement probe.

What is the technique in using ultrasonics for retroprep?

- Regrograde explorers to etch a shallow groove into dentin - CT-5 ultrasonic activated DRY to slightly deepen the groove - Featherlike brushing strokes with water - Don't apply downward force

What is the difference between Bacteroides, Porphyromonas and Prevotella

- Shah o Porphyromonas Asaccharolytic, pigmented, gram-negative, obligately anaerobic, non-spore-forming, non-motile, non-fermentative, bile sensitive, higher percentage of GC, produce trypsinase and collagenase o Prevotella Moderately saccharolytic, gram-neg, obligate anaerobe, non-spore0frming, non-motile, bile sensitive, colonies are translucent, opaque, gray, light brown or black § Prevotella differs from Bacteroides in metabolic end products and DNA (GC content) o Bacteroides saccharolytic, gram-neg anaerobes, non spore, non-motile rods

What is the structure and function on LPS?

- Structure: Lipid portion (Lipid A) interacts with phospholipid in the inner portion of the outer membrane, polysaccharide sugar sticks out into the environment ("O" antigen), Core polysaccharide attaches the "O" antigen to the lipid A - Biologic activities of LPS: Fever induction, leukopenia, hyperglycemia, diarrhea, abortion, B cell mitogenicity, macrophage activation, complement activation

What is the structure and function of Peptidoglycan?

- Structure: backbone of repeating units of N-acetyl glucosamine and N-acetyl muramic acid with peptide side chains that are cross-linked to another peptide side chain - Function: rigidity and shape of cell

Describe how tooth develops and how the dentin-pulp complex forms.

- Thickening of epithelial cells with ectomesenchyme underneath - Dental lamina (5 weeks) - Downgrowth of epithelium (bud stage) at 6 weeks - Epithelium starts for form a cap (cap stage) at 10 weeks o Ectomesenchymal cells outside the cap will form dental follicle (forms PDL) and ectomesenchymal cells inside the cap will form dental papilla (forms dentin-pulp complex) - Cells of inner enamel epithelium start to palisade - become more columnar - Basement membrane separates inner epithelium from ectomesenchyme - Bell stage (14 weeks) o Layers of enamel organ epithelium - inner enamel epithelium, stratum intermedium, stellate reticulum o Cells adjacent to inner epithelium differentiate into odontoblasts - starts forming predentin o Ameloblasts come from inner enamel epithelium - Initiation of dentin formation - starts at cusp tip - mineralization of predentin and leaves behind odontoblastic process as the cell retreats - creates dentinal tubules - There is development of vascular system, lymphatic system, and nerves within dental pulp - Ameloblasts begin to differentiate when dentin begins to mineralize

What are starling's forces?

- To determine net flow in and out of vasculature - Pressure pushing fluid out = Capillary hydrostatic pressure and interstitial fluid colloid-osmotic pressure - Pressure pushing in = interstitial fluid hydrostatic pressure and plasma colloid-osmotic pressure

How is genetic information transmitted?

- Transformation bacteria can take up genetic information from the environment o Ex. Smooth strain and rough strain of strep pneumonia - Conjugation transfer of genetic information by mating (F plasmid) through a sex pilus o Antibiotic resistance is due to conjugation - Transduction transfer of genetic information through viruses o Generalized when virus infects a bacteria and during replication and packaging of virus DNA, sometimes, bacterial DNA gets spliced and packaged into a virus o Specialized only happens with lysogenic temperate viruses; excision of the virus DNA out of the prophage is not perfect and a part of the bacteria host DNA gets packaged into the virus particle - Membrane Vesicle-mediated gram negative cells have outer membrane that can evaginate and be pinched off, sometimes it can contain pieces of DNA

9- Tuberculosis

- Tuberculosis is caused by Mycobacterium tuberculosis - Transmission is through the inhalation of infected droplets with a typical quiescent period - Infection results in a host inflammatory and granulomatous response with pulmonary and systemic symptoms. - Mycobacterium tuberculosis is an acid-fast, non-motile, intracell. rod that is an obligate aerobe. - The mode of transmission is by infected airborne droplets of mucus or expelled from the lungs by coughing, sneezing and talking. - Smaller droplets evaporate quickly leaving bacteria and solid materials as floating particles; larger droplets quickly settle to the ground. - Transmission via infected sputum during coughing could lead to inoculation of oral tissues. - Most cases of TB result from reactivation of a tubercle; only 10% of result from initial infection. - 90% of those infected have asymptomatic, latent TB infection (LTBI); 10% lifetime chance that infection will progress to TB. - Lung is the most common site of infection, although TB can affect any organ in the body. - Ghon focus is the primary site of infection in the lungs; Bacteria are picked up by dendritic cells, and transport the bacilli to lymph nodes; further spread is through the bloodstream to other tissues: kidneys, brain and bone. - Macrophages, T-lymphocytes, B-lymphocytes and fibroblasts are among the cells that aggregate to form a granuloma, with macrophages engulfing the bacteria. - The granuloma functions to prevent dissemination of the mycobacteria and also provides a local environment for communication of cells of the immune system. - Another feature of the granulomas of human tuberculosis is the development of caseous necrosis. - Miliary TB - bacteria gain entry to bloodstream and spread through the body and set up many foci of infection, all appearing as tiny white tubercles in the tissues. - In many patients the tissue destruction and necrosis are balanced by healing and fibrosis. - Treatment with appropriate antibiotics kills bacteria and allows healing to take place. Upon cure, affected areas are eventually replaced by scar tissue. SIGNS & SYMPTOMS: - Relative lack of signs and symptoms until the lesions have become extensive; positive skin test or radiographic findings are conclusive. - Symptoms: fatigue, malaise, anorexia, weight loss, fever and night sweats. Low grade fever is common in the evening and night and is accompanied by profuse sweating. - Persistent cough is associated with pulmonary TB and sputum is characteristically scanty and non-purulent and hemoptysis is common. Dyspnea is seen in the later stages of pulmonary disease. - The classic mucosal lesion is a painful, deep irregular ulcer on the dorsum of the tongue, with possible palate, lip, buccal mucosa and gingival involvement. Extension into the jaws can result in osteomyelitis. - The cervical and submandibular lymph nodes can become infected with TB which is termed scrofula. DIAGNOSIS & LABORATORY FINDINGS: - Tuberculin skin test (Mantoux) is the most reliable method of determining infection with M. tuberculosis. - + test means a person's been infected but does not necessarily have clinically active TB. - Tuberculin is a standardized PPD of culture extract from M. bovis. - The test is read 48-72 hrs later and evidence of induration is noted. - (+) test requires: physical examination, radiographic evaluation and sputum culture to rule out active disease. - Without treatment, approximately 5% of skin test converters develop TB within 2 years and another 5% of skin test converters develop it later. - For a preliminary diagnosis, microscopic examination of sputum smear for acid-fast bacilli is used because it's inexpensive and results are ready within 24hr MEDICAL MANAGEMENT: - Number and duration of drugs administered based on classification of : Non-drug resistant TB, Drug resistance to one anti-TB drug, Confirmed multi-drug resistance. - Drugs: Isoniazid (hepatotoxic), Rifampin (hepatotoxic), Pyrizinamide, Ethambutol, Streptomycin (ototoxic and renal toxicity; don't use ASA) - Within 3-6 months, approximately 90% of patients become non-infectious and their sputum cultures convert to negative. Most drug resistance cases (90%) develop in HIV-infected - The patient who has had a negative skin test result and on resting has it converted to positive is considered infected with M. tuberculosis. Once physical examination, radiographs and sputum culturing establish that the disease is not active, the patient may be given a course of chemoprophylaxis to prevent clinical disease from developing, based on his susceptibility - Prophylaxis is most commonly administered by the oral route, by giving Isoniazid 300 mg daily for 6-12 months.

What is the epi max for a normal patient and cardiac patient?

- normal patient = 0.2 mg/ml - cardiac patient = 0.04 mg/ml

Where do you give akinosi?

-closed mouth, @ MGJ above Mx 2nd M, parallel to occlusal plane, no bony landmark

What is Asthma?

-chronic inflammation of the airways that is reversible and recurrent.

What is a normal INR?

-0.9-1.2

If someone goes into adrenal crisis what do you do?

-100mg of hydrocortisone IV

What is normal PT?

-11-14 sec

How do you treat adrenal insufficiency?

-20-30mg of hydrocortisone daily *since they are on steroid supplement, there is an anti-insulin effect and decrease in immune response

If you were to give someone prophylaxis how much would you give them?

-2g amox 1 hr prior -if allergic 600mg clinda 1 hr prior -if allergic 500mg azithromycin 1 hour prior

Pregnancy When is the safest time to do treatment?

-2nd trimester

Post transplant, how long should you wait before you work on patient?

-3-6 months

How long are they unstable after an MI?

-6 months

What controls the synthesis of cortisol?

-ACTH regulates cortisol. ACTH is made in anterior pituitary

So tell me what insulin does?

-It stimulates the transfer of glucose from the blood into MLF (muscle, liver, fat)

Tell me about Hep B

-It's aquired parentally or sexually (blood or bodily fluid) DNA VIRUS -Most aquire as newborn

What are the guidelines for joint prophylaxis

-It's up to the treating doctor. The previous guidlines were 2 years after joint replacement but there was no evidence linking dental procedures with joint infection If a patient came to see me, I would take a few things into consideration. If they were immunocompromised I would give them prophylaxis. Prior to treating I would get a good medical history and consult with the physician.

Can you tell me the clinical presentation Chronic active hepatitis?

-Jaundice

So what anesthetic would you give prego?

-Lidocaine w/epi. Use epi to localize

Are there any virulence factors involved? What does it do?

-M protien protien of the cell wall that allow resistance to phagocytosis by PMN's

How does this relate to how we treat patients?

-May have be on abx If they had: RF and no carditis: 5 years up to age 21 RF and carditis: 10 years or up to 21 RF, carditis, and residual heart damage: 10 yrs or until 40 *No prophylaxis for rheumatic fever for dental treatment. If they had RHD, make sure they take their prophylatic penicillin

Is this more prevalent in men or women and why?

-Men. Women have estogen which is cardioprotective (vasodilates, anticlotting, decreases triglycerides)

Can you give erythromycin?

-No because it binds to P450 (which does drug metabolism) thus you will get an enhanced coumadin effect

Why don't you want to give Erythromycin?

-P450 is responsible for breaking down Erythromycin. Sterioids supress P450, which means erythromycin is in the blood more.

Do you give abx prophylaxis for organ transplants? What abx would you give?

-PCN + metronidazole

What if patient is on coumadin and has swelling what antibiotic would you use and why?

-Pen VK -Because it is narrow spectrum. Amox blocks vit K production. It enhances coumadin effect

What are the critera?

-Positive blood culture -Echocardiogram Minor criteria: -fever -previous heart condition

When do we need to give prophylaxis for endocarditis?

-Previous history of IE -Prosthetic valves -Cardiac transplant with valvulopathy -Congential heart defect (unrepaired or repaired within last 6 months)

Tell me about the different preparations of diabetes?

-Rapid acting -Short acting -Intermediate acting -Long acting

What would be a medication that someone w/TB would be on?

-Rifampin, streptomycin

What are the different types of endocarditis?

-SBE- alpha hemolytic strep- infection of valves -ABE- staph aureus -CBE- assoc with E. faecalis

What does that anesthetize?

-Sensory portion of V3: -IAN -lingual -buccal -mylohoid

What happens when you have an expired carpule?

-Sodium bisulfite --> sodium bisulfate (oxidation occurs and it becomes acidic)

What are the types of angina?

-Stable- exertional -Unstable- random -Prinzmetal-vasospasm of arterial wall (unstable)

What bacteria is common in joint prophylaxis?

-Staph and strep

What bacteria are involved in SBE?

-Staph, Strep, E. faecalis

What are some CVS changes in pregnant women?

-anemia, heart murmur

What other things do we need to be worried about with hepatitis and dental treatment?

-anesthetics metabolized in liver -analgesics metabolized in liver TAKE HOME: INR <3.5 PTT BETWEEN 11-14 sec. MINIMIZE DRUGS METABOLIZED IN LIVER

How do you decrease toxicity?

-aspirate -control dosage -inject slowly

Joint replacment: Why do we need to give prophylaxis for joint replacment?

-bc invasive procedures cause bacteremia

Why is Amox used over Penicillin?

-better against S viridans and S aureus and better absorption

Why?

-blood volume change affects absorption

What about Nasopalatine?

-canine to canine

What is Rheumatic heart disease?

-cardiac damage from rheumatic fever

Why not NSAID?

-causes bleeding

Why should you treat day after dialysis?

-they are usually tired the day of dialysis and because of platlet aggregation

Why does billirubin go to the liver?

-to form bile (to help digest fat) so if we have liver dx you get billirubin in plasma and get jaundice

Why no tetracycline?

-tooth staining

What is ventricular fibrillation?

-uncoordinated rhythm

Rheumatic Heart Disease So tell me what is Rheumatic fever?

-untreated strep throat that can affect the heart, joints, skin and brain

What are a few things that epi does?

-vasoconstriction -decreases toxicity -slows absorption -prolongs anesthetic -decreases blood loss in sx

What does it do?

-vasodilate

Can you give clindamycin?

-yes but be careful because it's liver and kidney toxic

So clinically if you have a patient that is type I, would you modify treatment?

-yes, would give them abx becuase they are immunocompromized and their PMN's are working as well? Make sure they eat before their appt Morning appt Sugar available Lessen stress (good pain control)

So if you don't have cortisol how does that affect the body?

-you can't metabolize fat, protien and glucose properly -Hypotension, increase ACTH, inability to tolerate stress

Would you give a patient epi?

-you could but consider not using it because: epi causes glycogen --> glucose could result in hyperglycemia

DENTAL MANAGEMENT OF ADRENAL INSUFFICIENCY So how does this effect your dental treatment?

-you want to check BP to make sure it's not low (adrenal crisis- hypotension) 1. Morning appts 2. Pain control 3. Post op anestheisa *if you are doing a major surgery you want to double daily dose of steroids

How does this alter treatment?

-you will have to change the class of abx

Tell me about PMNs?

1) Highest number and first to arrive of the granulocytes. Degranulation results in release of proteases, phospholipases, and oxygen free radicals.

Which mediators are ready to go?

1) Histamine (in mast cells and basophils), released by mechanical trauma, or C3A or allergens. Causes endothelial cell contraction, venular gaps, and increases cellular permeability. Serotonin (in platelets) causes vasoconstriction of small vessels resulting in hemostasis. Which mediators are newly synthesized? Prostaglandins (come from aa from cell membranes), Leukotrienes (same), Platelet activating factor (comes from mast, monocyte, and leukocytes), Nitric oxide (from macrophage).

What is the dosage?

0.3-0.6mg (3 times, once every 5 mins)

Tell me about some cytokines and their function?

1) IL2/IL4 are involved in regulation of lymphocyte function. IFN gamma is macrophage activating factor, IL1 is osteoclast activating factor.

What is acute inflammation?

1) Acute inflammation is short (hours to days) and has exudate, migration of PMNs, etc. Immediate early response.

1) Addison's Disease

1) Addison's Disease Adrenal gland a) Located above kidneys b) Consists of 2 compartments: i) Adrenal medulla (inner compartment) epinephrine, norepinephrine ii) Adrenal cortex (outer compartment) secretes steroid hormones, has 3 zones: (1) Outermost = zona glomerulosa: aldosterone (mineralocorticoid) acts on distal tubule of kidney to retain Na+ & excrete K+, H+ (2) Middle = zona fasciculata: cortisol (glucocorticoid) helps body adapt to stressful environment & helps to maintain bp, blood volume, blood sugar levels, appetite, feeling of well-being; also involved in regulation of carbohydrate, fat & protein metabolism, inhibits inflammation, maintains homeostasis during periods of physical & emotional stress (a) Cortisol synthesis is regulated by adrenal corticotropic hormone (ACTH), ACTH is made in the anterior pituitary (b) ACTH is regulated by CRF (corticotropin releasing factor) produced in hypothalamus (located above pituitary gland) (3) Innermost = zona reticularis: androgens (sex hormones) androgens. c) Causes of cortisol (glucocorticoid) deficiency: i) Destruction of adrenal cortex w/ or w/out destruction of adrenal medulla ii) Lack of stimulation of adrenal cortex by ACTH due to: (1) disease of pituitary (ACTH producer) or hypothalamus (CRF producer) (2) chronic suppression of pituitary or hypothalamus by exogenous steroid followed by sudden steroid withdrawal d) defective hormonogenesis (congenital or acquired enzyme deficiencies) e) Causes of adrenal insufficiency: i) Primary adrenal insufficiency: progressive destruction of adrenal gland (idiopathic=autoimmune, infection such as TB, malignancy) ii) Secondary adrenal insufficiency (more common form, dentists most concerned with this form): deficient cortisol secretion due to long-term exogenous corticosteroid therapy feedback mechanism sense elevated plasma steroid levels inhibits ACTH production suppresses adrenal production of cortisol partial adrenal insufficiency f) Etiology of Addison's disease: i) Progressive adrenocortical destruction (1) 70 to 90% used to be due to tuberculosis (2) currently idiopathic atrophy, probably autoimmune mechanism (3) probably multifactorial, but worldwide, due to infections ii) More than 90% of gland must be destroyed before signs of adrenal insufficiency appear g) Clinical Findings: i) Lack of cortisol results in impaired glucose, fat & protein metabolism, hypotension, increased ACTH production, impaired fluid excretion, excessive pigmentation, inability to tolerate stress ii) Aldosterone deficiency results in inability to conserve Na+ & eliminate K+, & H+ ions leading to hypovolemia, hyperkalemia, & acidosis iii) Muscle weakness, lethargy, fatigue for months before diagnosis iv) Feel well upon waking but tired after minimal exertion v) Females have irregular menstrual cycle & lose body hair vi) Loss of appetite, loss of weight with nausea, vomiting, diarrhea vii) Low blood cortisol hypoglycemia, dehydration, hypotension, elevated serum potassium, postural dizziness viii) If left untreated or pt severely stressed develop cardiac arrythmias & CV collapse from electrolyte disturbances & severe hypotension h) Diagnosis: i) Classic signs above + lab findings (1) Low plasma cortisol & low ACTH (2) Elevated BUN (blood urine nitrogen) due to decreased intravascular volume (3) Stimulation tests: Low response of cortisol to cosyntropin (synthetic ACTH) healthy pt would respond with significant increase in cortisol i) Treatment: i) If adrenal gland destroyed, replacement therapy with corticosteroid (hydrocortisone 20 to 30 mg) for remainder of pt's life (1) To match normal circadian rhythm, give 2/3 dose in AM & 1/3 late afternoon (normal circadian rhythm has increased ACTH in AM) (2) Also tend to take fludrocortisone to replace deficient mineralocorticoid since atrophy affects entire adrenal gland ii) If due to long-term exogenous steroid therapy, upon ceasing therapy, the hypothalamic pituitary portal axis regains its responsiveness & eventually, normal ACTH & cortisol secretion resumes. The time required is days to months (~14 days). j) Oral Manifestations: i) intraoral hypermelanosis multiple dark spots or streaks of hyperpigmentation of mucosa, tongue, lips or gingiva k) Dental Management: i) Tx with caution because steroid insufficiency poses increased risk of infection & stress-induced complications (adrenal crisis); pt has reduced ability to tolerate stress (1) physician consult to ascertain medication type, current dosage, & need to supplement dose (2) Requires increased steroid dose immediately before dental tx (usually 20 to 40 mg prednisone) which gets tapered off by half every day (or every other day) until maintenance dose is reached (3) Use stress-reducing measures: (a) Short morning appts (b) Anxiolytic agents (nitrous oxide) (c) Postpone extensive procedures (d) Deferral of oral surgery (e) Use long-acting anesthetic ii) Pt's at high risk of adrenal suppression: (1) Currently taking oral steroids for greater than 30 days (2) Receiving more than 30 mg hydrocortisone per day (3) Have taken more than 2 weeks worth in past 12 months iii) Pt's at minimal risk: (1) Taking alternate day therapy - tx pt on "off" day (2) Taking less than ½ daily dose of cortisol for less than 1 month iv) Pt's at no risk: (1) Taking topical steroids l) Dental emergency: i) Provide only conservative tx ii) Prescribed antibiotics & analgesics PRN iii) Must avoid stressful dental procedures until medical consult completed iv) May administer 100 mg hydrocortisone (give 3 times normal maintenance dose) IM 1 hour before tx, following day give twice normal oral dose of steroid if pain or infection persists & then taper over next 5 days by halving doses m) Medical Emergency: i) Chronic adrenal insufficiency (1) Pts deteriorate rapidly to acute adrenal insufficiency when: (a) Steroid therapy suddenly stopped (b) Subjected to stress (infection , trauma, blood loss) & do not increase their dose of corticosteroids ii) Adrenal insufficiency characteristics: (1) Intense abdominal pain (2) Muscle weakness (3) Confusion (4) Fatigue (5) Nausea, vomiting (6) Dehydration (7) Ultimately leads to unconsciousness & vascular collapse iii) Treatment: (1) 100 mg prednisone (2) IV saline with dextrose (3) If hypotensive, ephedrine q 5 minutes until normalizes (4) Avoid IM steroid because unpredictable absorption of drug

What is Edema?

1) An excess of fluid in the tissues or serous cavities. It can be exudate or transudate

5- Organ Transplant

1) Autologous (used with bone marrow transplants) - the patient's own marrow is used 2) Syngeneic - identical twin transplant 3) Haploidentical - from parent 4) Allogeneic - from same species 5) Xenograft - from living, nonrelated - different species 6) Cadaver - worst match, but most available Pts with transplants usually take a triple immunosuppressive therapy: · Pretransplant patients - order lab tests - want to look for potential bleeders, those prone to infection, liver/kidney metabolism problems. Want to avoid potential problems. · Posttransplant patients - there is immunosuppression with an increased chance of infection. Within first 6 months - acute rejection is major concern - avoid routine tx for first 3-6 months. Stable period - no contraindication to dental treatment, but find out if patient needs steroid supplementation, and if there is hypertension or bleeding problems. Chronic rejection stage - if this is happening to patient - no elective treatment - only emergency treatment. · Cardiac transplant patients - susceptibility to infection and bleeding - anticoagulated state. Concerns about vasoconstrictors & bleeding. Normal INR = 0.9-1.2; Sx INR ≤ 3.0 - 3.5 · Liver - Protein & drug metabolism considerations, as well as bleeding problems due to clotting factors. Tylenol, ibuprofen, aspirin, and codeine are all metabolized by the liver. · Bone marrow - big issues are worrying about infection and bleeding. · Kidney - patients may be on coumadin - bleeding issue, also concerned about drugs metabolized by kidney (i.e. penicillin, tetracycline, cephalexin) These patients usually taking Steroids, Anti-coagulants, Immune-supressants, and are more prone to experience infection,excessive bleeding, delayed healing, impaired drug metabolism and cancer. Always consult physician regarding ANTB therapy, anaesthesia (+/- epi), pain and bleeding control, supplemental steroids. ANTB prophylaxis needed to prevent subacute bacterial peritonitis. Prophylaxis for first 2 YEARS; with acute Endo infections always give prophylaxis; First choice (PCN + Metronidazole); if allergic to PCN use IV Vancomycin (Amox increases bleeding w/ anticoagulants) AVOID: Clindamycin - liver and kidney toxic (only short term); NSAIDS - may exacerbate GI disorders, gastric ulcers, acid reflux and nephrotoxic effects of cyclosporine and tacrolimus;

What causes pain?

1) Bradykinin, PGE2, histamine, seratonin

What is chronic inflammation?

1) Chronic inflammation is longer (weeks to months) and has an abundance of macrophages, lymphocytes, tissue proliferation, fibrous tissue, blood vessels, and tissue necrosis.

What is the objective of the inflammatory response?

1) Confine the area, clear pathogen, restore function.

How can infectious agents cause disease?

1) Either by directly entering the cell or releasing mediators that damage cell, tissue or blood vessels, or by inducing host cell immune and inflammatory response.

What is exudate?

1) Exudate is inflammatory fluid high in protein and cell debri content, due to alteration in permeability of small blood vessels in an area of injury.

Which mediators come from plasma?

1) Factor XII (Hageman factor) is involved in the formation of bradykinin, and the coagulation system. Complement proteins are also from plasma.

What are the systemic effects of cytokines?

1) Fever, shock, leukocytosis, leucopenia, acute phase response.

How do venule events occur?

1) First, NO and Pg cause blood vessel dilation as histamine, bradykinin, IL-1, TNF and other cytokines cause endothelial cell contraction. This allows more blood to flow into the area, and exudate to leak out into tissue. As exudate leaks out, the proteins in it cause a change in osmotic potential, this results in more fluid being leaked out into the extracellular tissue. As red blood cells accumulate in the capillaries, leukocytes are pushed to the outside in a process called margination. Then, leukocytes start to adhere to endothelium with weak interactions (sialyl lewis x and e/p selectin) then there are strong interactions (integrin and vcam/icam). Then the phospolipase c causes release of calcium which leads to alignment of actin and myosin fibers and creation of pseudopod, which pulls leukocytes through the endothelium into the extracellular matrix. When they get there the pseudopod is pulled toward chemotactic gradient. (IL8 and c5a)

What is transudate?

1) Fluid with low protein content. Permeability of small blood vessel is normal

Tuberculosis

1) Found in confined areas like schools and prison system 2) Bacteria does not cause problem it is the bodies granulamatous inflammatory response to the bacteria 3) Lack of definitive symptoms: night sweat, non purulent cough, hemoptysis 4) BCG: overseas vaccine, can give false positives on the mantoux test 5) The mantoux tests cell mediated immunity so HIV can have false negatives 6) Treatment okay under six years old 7) The tuburcle consists of giant cells, macrophages, fibroblasts, lymphocytes, which are encapsulated in a fibrous capsule. 8) Miliary: disseminated tuberculosis 9) Scrofula: in submandibular and cervical lymph nodes 10) PPD needs to be accompanied by a sputum culture and chest xray 11)Ghon complex: this is the dormant TB in hiliar lymph nodes or post. Apical lung 12)Tx: isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin 13)Prophylaxis: 300mg isoniazid for 9months

Local Anesthetic

1) Inf alveolar: Pterygomandibular space 2) GG: from corner of mouth to DL cusp of MX2m. Gets all branches of V3: IAN, auriculotemporal, mental, mylohyoid, lingual 3) Akinosi: closed mouth, mgj above mx2m,parallel occusual plane, no bony landmark 4) Nasopalatine: anterior teeth 5) Infraorbital: anterior teeth 6) PSA: mx2m, mx3m, distal of mx1m 7) Max for heart patient of epi is : .04mg for normal is .2, each carpule has .018. (limits to 2 and 11) 8) Birtchfield, Walton, Kim, Nusstein, Nusstein, Repogle, Repogle 9) Epi: we worry about arrythmia 10) pKA: the amount of free base at a given pH, lower pKA means more free base, so more can diffuse into cell. 11)XTIP: Give distal in attached gingival 12)Inflammation decreases threshold of nerve conductance due to the presence of PgE2 and Bradykinin. Also neuropeptiedes release causes vasodialtion and further increases nerve firing. 13) Baez: Nerve sprouting in inflammation leading to spatial summation 14)Why they fail: tachyphylaxis, anxiety, 15)Burning: too cold, expired, too fast, bisulfite 16)Trismus: muscle relaxants, cold compress, slow movement

What is Pus?

1) Inflammatory exudate rich in leukocytes and parenchymal cell debri

Diabetes:

1) Insulin: inhibits triglyceride break down, inhibits protein break down to amino acids, increases production of glycogen in liver, inhibits production of glucose in liver 2) Ketoacidosis: body breaks down triglycerides to fatty acids and glycerol, then fatty acids brokend own to acetyl coenzyme a and then ketones. Ketoacidosis leads to coma or death. 3) 4% gestational 4) Dx: fasting 126, post prandial: 200, hba1c: 7% 5) For hypoglycemic shock: give IV dextrose 50% or glucagon 1g 6) Asprin potentiates sulfonylureas 7) AGES in blood veseels and oxidative free radicals cause injury. In nerves there are increased polyls deposited from the aldose reductase pathway. Sorbitol in schawann cells

Where does paupain cleave?

1) It cleaves before the disulfide bond, dentaturing the whole antibody. Pepsin cleaves after the disulfide, and only removes the Fc portion.

Tell me about eosinophils?

1) Longer life in weeks. Degrade inflammatory mediators like leukotrienes, histamine, and PAF. Involved in type I hypersensitivity response.

Basophils?

1) Lowest number, contain heparin and histamine, involved in type IV delayed hypersensitivity.

What contributes to chronic inflammation?

1) No drainage, mobility, necrotic tissue, mechanical irritation.

Rheumatic Fever:

1) No prophy for rheumatic fever for dental treatment. If the patient has had rheumatic heart disease make sure that they have taken their Penicillin prophylaxis. 2) Joint infection: 67% Staph, 5% Strep, 2% peptostrepto. 3) Give abx for acute infection in mouth. 4) Joint replacement: give keflex (if no pen allergy) 5) SBE: Strep, Staph, E. Faecalis 6) Damage begins from trubulence. 7) Left side of heart more affected because of greater density of bacteria 8) Amoxicillin reduces bacteria, does not remove it 9) Mitral valve prolapse is most common predesposition to SBE 10)RHEUMATIC FEVER: Mitral, aortic, triscuspid

How does leukocytosis occur?

1) Normally 4-10k leukocytes but increases 2-3x. Occurs because TNF A and IL1 cause increased release of PMNs. But also stimulates macrophages and T cells to make CSF which induces proliferation of leukocyte precursors in marrow.

What casues adhesion of leukocytes to endothelium

1) PAF, LKB4, C5A, IL1

Why do you get chronic inflammation?

1) Resistant bacteria, remanants of dead organisms, foreign bodies, chemicals, metabolic products, immune rxn.

Types of healing?

1) Resolution (return of tissue to normal), Regenration (same cells as before) , or repair (new cells, lose function).

Types of healing?

1) Resolution, regeneration, and repair.

General effect of inflammation:

1) Rubor, Calor, Tumor, and Dolor. Redness from excess blood in tissue. Heat from IL1, IL6, and TNF alpha, LPS. Pain from increased pressure due to fluid accumulation, mediators (PGE2, bradykinin), and enzymatic destruction, Swelling from increased fluid in tissue due to hydrostatic and osmotic forces.

Hepatiis:

1) Seroconversion: B is 6-30 C is 2-8 2) Use steroid treatment to reduce inflammation 3) Increased ALT and AST 4) Chronic state is 6 mos in system with symptoms 5) Carrier state is 6 mos in system no symptoms of disease 6) Normal bilirubin is 1mg/100 mL, jaundice is at 2.5 7) Vaccine: HARAVAX FOR A RECOMBIVAX FOR B 8) Fatigue, vomiting, malaise, anorexia, jaundice, increased enzymes 9) Hepatitis B has dane particle: core antigen, surface antigen, and envelope antigen (only DNA virus) 10)Hepatitis D requires hep B surface antigen. 11)A and E have no carrier state and are self limiting, and oral fecal.

What about lymphocytes?

1) Start in bone marrow, T mature in thymus. Antibody mediated/humoral are B. (plasma: make antibody and memory: respond quickly at next encounter) and cell mediated are T (killer are cytotoxic, helper: stimulate B and T, suppressor: suppress B and T, and memory: respond quickly to next insult of same antigen)

What is acute phase response?

1) The bodies response to inflammation which causes 100x increase in liver proteins including: ceruloplasmine (scavenges free radicals), protease inhibitors, complement, CRP (kills bacteria). Results in fever, leukocytosis, decreased apatite, altered sleep.

Angina and MI

1) Thickening of intima due to accumulation of lipid plaques (LDL oxidation), results in reduced oxygen flow to the heart (less supply than demand) 2) Estrogen: reduces LDL, reduces clotting, increases elasticity, decreases artherosclerosis 3) Foam cells: macrophages in the intima, before lipid streak. 4) Levine sign: cluching chest. 5) N2: vasodilates and reduces cardiac load (.3-.5) 6) Unstable angina: refractory to N2, doesn't get better with rest, changes in frequency, duration, or intensity in last two months. Prinzmetal is in this category. 7) MI is followed by VFIB which is uncoordinated contractions, and requires defibrillation. 8) Tx: BMONA (beta block, morphine, oxygen, nitroglycerin, and asprin 325mg) Asprin stops clot formation. 9) ABC: airway, breathing, circulation (defribillation) 10)Pen VK is drug of choice, because amox will interfere with vit k dependant bacteria as it is wider spectrum.

Can you tell me about the pathophysiology of Angina? Injury

1. Accumulation of LDL 2. Oxidation 3. Macrophages and lymphocytes which release cytokines 4. Phagocytosis 5. Fibrous capsule/plaque brought down 6. MMP's cause sloughing 7. Tissue factor released that causes clotting 8. Then Thrombus 9. Then ischemia

So what is the function of cortisol?

1. Anti-immunogenic 2. Anti-inflammatory 3. controls stress

What are some ways you can diagnose

1. Culture 2. Chest x ray 3. PPD

Can you explain the process of getting infective endocarditis?

1. Damanged valve 2. "Vegitation" forms (fibrin and platlets build up on leaflets) 3. Bacterimia (from dental procedure) 4. Infects vegitation 5. Turbulent blood flow can cause vegitation to embolize *abx can't attack this vegitation because it has a bioflim

What does this tubericle do?

1. Defend 2. Communicate with inflam cells

What questions would you ask the patient?

1. Do you take meds and does it work 2. How often does it happen 3. How long does it last

What drugs do you want to avoid?

1. NSAID, aspirin Why? bc it will cause an increase in LKT which causes bronchoconstrition (NSAID and aspirin block COX pathway, which will incease LKT) (Instead for pain use Tylenol) 2. No Narcotics- it causes respiratory depression 3. No Epi (possible preservative allergy) 4. No Macrolides- Azithro, erythromycin avoid when taking ashthma meds bc it alerts p450 enzyme. So you will have less drug metabolism

What are the different types of insufficiency

1. Primary adrenal insufficieny- glad atrophies due to autoimmune response. 2. Secondary- due to continual steriod use (gland does not function)

What will you ask physican?

1. Stability 2. Pain meds 3. INR?

When you call physician what do you need to ask him?

1. Stability of patient 2. Abx (ask if you want adjust dosage) 3. Ask about INR 4. Ask about immunosuppressants (if they need adjusted)

Can you tell me about the antigens involved with Hep B.

1. Surface antigen 2. Core antigen 3. Early antigen "Dane particle" There is a vaccine

What can happen if you don't have prophylaxis?

1. Valve disfunction 2. Death 3. Embolyic event 4. Heart failure

Tell me about leukocytes?

64% granulocytes (93% PMN, 6% Eosin, 1% Baso) and 36% mononuclear (88% lympho, 12% monocytes)

1 - Asthma and Hyperventilation

ASTHMA - is an increased responsiveness of the trachea and bronchi to various stimuli manifested by widespread narrowing of the airways (airway obstruction). It is an episodic disease with acute exacerbations being interspersed with symptom-free periods. Hypersensitivity of the airways is characterized by an increased contractile response of smooth muscle, abnormal generation of secretions, and an abnormally sensitive cough reflex. An initial stimulus triggers mast cells, macrophages, and basophils to release mediators, which in turn leads to airway inflammation. Dyspnea (respiratory distress) is usually the result. There are two major types of asthma: Extrinsic and Intrinsic Extrinsic (allergic) - accounts for 50% of asthmatics - mostly due to a genetic/hereditary cause. These patients typically have an inherited allergic disposition. The concern with this type of patient is that an acute asthmatic attack may be precipitated by exposure to specific allergens. Penicillin, aspirin, sodium bisulfite preservatives (found in anesthetics with epinephrine), may precipitate an attack in a susceptible patient. Exposure of potential allergens usually results in Type I (IgE) hypersensitivity in which bronchospasm ensues within minutes (allergens interact with IgE antibodies affixed to mast cells along tracheobronchial tree causing mast cell degranulation and secretion of vasoactive amines and cytokines -> prolonged inflammatory response). Intrinsic (nonallergic, idiopathic) - usually a later onset (after 35). No family Hx, negative skin tests, normal serum IgE, no immunologic basis. Viral infections, physical exertion, pollution, and stress bring this on. Physiological and psychological stress can modify vagal efferent activity to cause airway changes. Other types of asthma are Mixed and Status Asthmaticus (most severe clinical form of asthma - wheezing, dyspnea, and hypoxia - which is a true medical emergency and is potentially life-threatening -> hypotension and respiratory acidosis). Beta-adrenergic agonists including epi offer the quickest, fastest relief -> airway dilatation. Albuterol is a common inhaled beta-2 agonist which stimulates receptors on airway smooth muscle cells. Other drug classes include methylxanthines (theophylline) -> bronchodilators, glucocorticoids -> reduce airway inflammation, and chromones (cromolyn sodium) -> inhibit mast cell degranulation. - It is a good idea to have the patient take the inhaler just before the procedure. Some dental tx may involve steroids. It is good to know if the patient needs steroid supplementation if using a steroid inhaler, and you may need to contact the physician. Minimize stress as it can bring on either Extrinsic or Intrinsic attacks. Give carbocaine whenever possible to minimize preservative interaction. 10% of patients may have aspirin sensitivity that may induce asthmatic attack. Patients taking theophylline preparations should not be given macrolide antibiotics (erythromycin and azithromycin) because it can result in toxic levels of theophylline. Give inhaler/O2 when attack happens. 0.3-0.5mL epi IM if need be. HYPERVENTILATION - increasing rate and/or depth of respiration resulting in blowing off excess CO2 resulting in respiratory hyperalkalosis (increase in blood pH) due to higher pH /less CO2. Anxiety is a major cause (stress and infection may be causes as well). Most common between ages 15 & 40. Anxiety causes increased respiratory rate & depth and an increase in blood epi. Hypocapnia (decrease in blood CO2) produces vasoconstriction in cerebral vessels -> lightheadedness, dizziness, giddiness. Hyperventilation causes increase in vascular resistance which may cause chest pain. Anxiety gives higher catecholamine blood levels causing palpitations, trembling, sweating. As the pH in blood increases, the level of ionized calcium in blood decreases. This hypokalemia results in neuromuscular irritability which can give tingling & paresthesia of the hands & feet. Tell the patient to breathe slowly, using a paper bag (not plastic because it collapses) or hands to rebreathe CO2 to decrease the pH. Do not give O2 - it will worsen the situation. Remember that hypocapnia leads to hyperalkalosis leading to hypokalemia. In addition, anxiety causes discharge of epi. All of these cause signs and symptoms of hyperventilation. Let the patient get the lost CO2 back into system. If this does not work you may consider giving 10-15mg of oral diazepam.

Should you use ultrasonic to clean the canal too?

Ahmad Reader, Burleson Burleson Archer

What kind of medication do people with asthma take?

Albuterol- fast acting B2 agonist- smooth muscle bronchioles Inhaled steroids Singulair (LKT modifier) Mast cell stabilizer

What materials should you use for root perforation?

Alhadainy Lantz Lee ● Alhadainy - compared light cured glass ionomer and calcium hydroxide (Vitrebond/Prisma Dycal) with chemically cured glass ionomer and calcium hydroxide (Ketac Fill/Dycal) and measured leakage ○ Light cured materials proved a better seal than chemically cured materials ○ Flow of material is an important property - to seal apical ends of perforation ● Lantz histologic study with dogs; made peforations and either waited to surgically repair or repaired immediately with GP or amalgam ○ Favorable healing when repaired immediately vs. later ○ GP had less irritation of the tissues than amalgam ● Lee in vitro study - made lateral perforations in extracted teeth and repaired with IRM, amalgam, and MTA and measured leakage by dye penetration MTA had significantly less dye leakage than IRM or amalgam

How much abx prophylaxis would you give kids?

Amox- 50mg/kg orally Cinda- 20mg/kg orally Azithromycin 15mg/kg orally (1lb = 0.45kg)

What if they can't take it orally

Amp- 50mg/kg IV if allergy Clinda- 20mg/kg IV

What is all this about calcific metamorphosis or PCO?

Andreason Walton Andreason

When should you do recall?

Andreason, Orstavik, Reit Murphy

What is autograft, allograft and xenograft?

Auto- self Allo- same species xeno- diff species

Endovac?

Baumgartner

What is a sinus tract?

Baumgartner Harrison

Can a root canal cause bacteremia?

Baumgartner Seltzer Carmona Tzukert

What are different irrigants? How do they work?

Baumgartner bystrom Spangberg Senia Leonardo Jeansonne - Antibacterial, tissue dissolving - NaOCl o Hypochlorous acid breaks down proteins into polypeptides and amino acids o Baumgartner showed that 5.25%, 2%, 1% removed all organic debris, 0.5% didn't remove as much as the other concentrations. Tissue dissolving property. o Bystrom showed that 0.5% NaOCl removed more bacteria than saline in teeth with necrotic pulps and AP. Antibacterial ▪ Spangberg also said 0.5% NaOCl is recommended as irrigant. Removes necrotic but not vital tissues o Senia talked about the efficacy of NaOCl in isthmus in apical third. It was better than saline in removing pulpal tissue in the isthmus area in apical third. Significant difference occurred higher than 5mm from apex. 5.25% - Chlorhexidine o Leonardo 🡪 effective in removing mutans (100%) and anaerobes (78%) ▪ Chlorhexidine has substantivity o Jeansonne: 2% CHX is as effective as 5.25% NaOCl in antimicrobial but does not have same tissue dissolving capability

Vitamin D Resistant Rickets?

Bender

How about an intentional replant?

Bender Grossman Nimzick Kling Andreason

- Siqueira and Rocas - review paper o Virulence of organism o The Load o Host defense

Bender and Seltzer Sjogren Fabricius Naidorf - Anti-microbial testing: o Bender and Seltzer 🡪 they did not see any difference in outcome depending on whether they detected bacteria or not; no information in their study on how they cultured bacteria - Pro-microbial testing: o Sjogren 1997 - Took samples before obturation; success rate of no detectable bacteria was 94%, success rate of detectable bacteria group was 68% o Fabricius - monkey model, had known infection inside teeth 🡪 97% failing when there were organisms, 100% healing when there was no organisms o Naidorf - argues that every study where they did sterility testing, there was increase in success rate 🡪 Pro-microbial testing; Pulp necrosis is accompanied by a cessation of blood circulation in and out of the canal, resulting in a "privileged sanctuary" from which bacteria, toxins, and protein degradation products can emanate and which is itself insulated from the normal clearing processes and immune mechanisms of the body

Tell me abouttrismus?

Benoit Hinton

How do I get posts out?

Berbert Abbot

What is the inflammatory response?

Bergenholtz Levin

Can you use a periapical radiolucency as indicator for infection?

Bergenholtz Sundqvist - Bergenholtz looked at traumatically devitalized teeth 🡪 teeth with periapical areas, 50/60 had growth from sampling root canals; teeth without periapical area did not have any detectable bacterial growth 🡪 shows us radiograph and vitality test can indicate infection without microbial testing o This paper also looked at length of time between trauma and treatment 🡪 Conclusion: in intact devitalized teeth, the longer it has been since trauma, the greater likelihood of infection - Sundqvist also showed that teeth without periapical radiolucency rarely have microorganisms and that the larger the lesion, the higher density of bacteria

Should I clean it with THE LASER?

Bergmans Soukos Meire

How does aging affect the root canal?

Bernick Rusting Dard

How does aging affect the pulp?

Bernick Tranasi Brannstrom Stanley Moss and Hendricks Toneck - Bernick o Decreased pulp chamber size o Decrease in blood vessels and nerve bundles o Increase in fibroblasts o Presence/increase in diffuse calcification o Ground substance remains the same - Tranasi - more apoptosis in older pulps, more growth factors, cell proliferation and differentiation in younger pulps 🡪 older pulps don't react as well to vitality tests - Brannstrom - Teeth with attrition. Tubules viewed under SEM. Teeth also placed in dentures to show attrition without vitality. Saw dentinal sclerosis and obliteration of tubules, but no vitality of teeth so saliva may contribute. Following attrition you will see dentinal tubules occlude. - Stanley - Sectioned extracted teeth with caries 🡪 responses: 1) dentin sclerosis (produce zone of translucent dentin), followed by 2) reparative dentin (slower response to prolonged stimuli) and then 3) dead tracts. Dead tracts is the air space above blockage from sclerotic dentin. - Moss and Hendricks - describe pulp stones vs denticles o Pulp Stone: Initial calcification of pulp tissue components serve as nidus. Nontubular. Develop throughout life. o Denticles: Inductive interaction between epithelium and pulp tissue. Epithelia from enamel organ isolated in the dental papilla. Tubular dentin surrounding epithelial cell remnants. Form only in root development. - Torneck -only small amount of teeth with obliteration will need endo tx; most obliterated canals have patent canals,

Can you tell the difference between granuloma and cyst?

Bhaskar Shrout

What is the incidence of cyst vs granuloma?

Bhaskar Spatafore Rubenstein and Kim Nair

What about the scope?

Bowers

What causes bone resorption?

Bradykinin, IL1, TNFA

What causes pain?

Bradykinin, PGE2, histamine, seratonin

How does the pulp respond to different restorative materials?

Branstrom About Fujiwasa Hanks Kaga Mandel Jones - Silicates? 🡪 it was believed that silicates were toxic to the pulp but the study by Branstrom showed that it was bacteria, not silicate that was responsible; the silicates didn't' seal that well - About looked at surviving odontoblasts with different materials: o Calcium hydroxide (100%) > polycarboxylate (82.4%) > ZOE (81.3%) > Composite (75.5%) > Enamel bonding resin (49.5%) > RMBI (42.8%) o The biggest difference regardless of what material, was the remaining dentin thickness between dentin and pulp. - Composites o Photosensitizers (9-fluorenone, benzil, di-camphoroquinone) - caused hemolysis of RBCs with these photosensitizers and light, dose dependent; radicals produced from these chemicals damages cell membranes (Fujiwasa) o Bonding agents - Methacrylate and glutaraldehyde in bonding agents (Hanks) ▪ As glutaraldehyde and HEMA exposure increases, the production of DNA and protein made decreased ▪ The level of toxicity was 2.5 micromolar or more for glutaraldehyde and 80 micromolar or more for HEMA ▪ 1 mm dentin thickeness 🡪 less than critical level ▪ 0.5 mm dentin thickness 🡪 more than critical level - Amalgams o Zinc containing amalgams had higher toxicity to fibroblasts, copper didn't affect toxicity (Kaga) o Mercury toxicity of amalgams? (Mandel - review paper) ▪ There is more mercury from food and air than amalgam ▪ Under a certain level of urinary mercury concentration (<25 mmHg), no health effect ● The upper limit of mercury from amalgam filling is < 4 mmHg ▪ Mercury toxicity causes: Kidney failure, neurologic complications, still births, immune damage o Jones - advantages of amalgams over composites ▪ Composites are less stiff than tooth enamel - unable to support tooth structure at margin ▪ Composites take up water ▪ Amalgam has similar wear characteristics to teeth ▪ Composites retain more plaque than amalgam - need to be replaced more frequently

TeIl me about Radiography?

Brynolf Slowey Bender Messer Yamasaki Sundqvist Soh Nair Mistaak and Loushine Lozano Lamus Kaffe Foursberg Goldman Degering Bhaskhar Shrout Brynolf Walton

What should I irrigate with?

Bystrom Eleazor Yang Sedgley McDonnell, Baumgartner Chang Clegg, Kishen Spanberg, Pashley Baumgartner Hand Siquierra Gomes Sirtes Shipper Gomes, Siquierra Jeansonne Williamson, Ringel Henessey Russel Waltimo Basrani Rosenthal Baumgartner Tay

Should I use an intracanal medicament?

Bystrom Sundqvist Friedman, Walton, Trope Heithersay Nerwich Evans, Stevens Andreason Hasselgren, Trope Sjogren Bystrom Holland Safavi Law Trope Andreason rosenberg Baumgartner, evans Barbin, Zerella Brooks Voet Imlay and Lin Kim Hapasallo, Stevens Madison Waltimo Oliet, Peters, Penesis Waltimo Eleazor Nair Shuping, Siquiera Trope Baumgartner

Why irrigate?

Bystrom lee - Bystrom 🡪 instrumentation alone did not remove all bacteria in 7/15 cases even instrumenting to size 80 - Anatomical anastomoses and lateral canals (Lee)

What causes chemotaxis?

C5a, IL1, IL8, PAF,

-Periotneal dialysis- filtration using a catheter in abdominal wall.

Chronic abulatory- put in your gut. 3-4 times Continuous cycle- 7-8 times *Prone to staph infection (could lead to infective endocarditis)

3 - Pregnancy

Cardiac output is increased by 30-50%, and over 90% develop reversible systolic murmurs. Pregnancy is considered a hypercoagulable state because of increased potential for coagulation and thrombosis. There is an increase in clotting factors V, VII, VIII, X, and XII (although factors IX and XII decrease, and platelets stay the same). The entire respiratory tract becomes edematous so breathing can become more difficult. There is decreased neutrophil chemotaxis and adherence, cell-mediated immunity, and natural killer cell activity. There is an increase in serum complement levels. This may explain why pregnant patients may develop fulminant, multiple space infections. Thyroid function mimics hyperthyroidism. Hypertension is the primary cause of maternal mortality and morbidity. The incidence of hypertension (>140/90) is 5-10% in the obstetric population. Preeclampsia and eclampsia are the most life threatening antepartum conditions in the obstetric patient. Preeclampsia is condition of edema, hypertension, and proteinuria. The general pathogenesis is generalized arteriolar vasospasm and constriction. A subcategory of preeclampsia is HELLP syndrome - characterized by hemolytic anemia, elevated liver enzymes, and low platelets. Delivery is the treatment choice for preeclampsia. Make sure the BP is < 140/90 on initial patient evaluation, or consult OB/GYN. Eclampsia is the occurrence of a grand mal seizure in the presence of preeclampsia, and it is an acute and true medical emergency. This can happen before, during or within a week after labor. Blood pressure and seizure control is the management. A severe hypotensive syncopal episode may happen during dental treatment. -Lay patient on their left side. This is referred to as Supine Hypotensive Syndrome - the blood pressure drops secondary to the impeded blood flow through the major vessels (i.e. inferior vena cava) which causes a syncopal or near syncopal episode. -The 1st trimester (2-8 wks) is the formative phase - no dental treatment at all. The 2nd trimester is the safest. The 3rd trimester should have only emergency treatment performed due to patient comfort/discomfort and the patient should be monitored for proper positioning. Animal and human data clearly support the conclusion that no increase in gross congenital abnormalities or intrauterine growth retardation occurs as a result of radiation exposure totaling less the 5 to 10 cGy. The maximum risk attributable to 1cGy (which is more than 1000 full mouth series) of in utero radiation exposure is 0.1% (1000 times less than risk of spontaneous abortion). The fetal dose of 2 PA films using a lead apron is 700 times less than one day of average exposure to natural background in the United States. Post pregnancy considerations - give drug right after breast feeding. Aspirin can cause pre and post partum hemorrhage and can cause closure of ductus arteriolus - can cause fetal death. You can give N2O (but minimize to <30 minutes and with 50%O2), acetaminophen with codeine, lidocaine with epi, but do not give benzodiazepines. Penicillin/clindamycin are OK, but give penicillin first because clindamycin can penetrate the bone. Remember: no aspirin, treat during the second trimester, preclampsia/eclampsia are true pregnancy concerns, and lay the patient on the left side during a hypotensive crisis.

6 - Angina Pectoris and MI

Cardiovascular disease - risk factors - males, menopausal women (due to decreased estrogen, decreased flexibility of arteries, and increased LDL,), family Hx, hyperlipidemia, hypertension, cigarettes, and diabetes mellitus. Both angina and MI can present with chest pain, or pain in the back, shoulders, arms, neck, jaw, palate, or tongue. The pain may be associated with stress, excessive effort, or respiratory function. Gastritis (burning pain & reflux) can mimic these symptoms, as well as esophageal reflux and bronchitis chest pain. Angina is a transient ischemia of the myocardium usually with a substernal chest pain radiating to the left shoulder. The transient chest pain may occur by exertion, emotion, or stress and is relieved by nitrates. The myocardium needs more O2 than the coronary arteries can provide. There is an increase in the cardiac workload and/or a decrease in O2 delivery. The result is ischemic cardiac pain with no permanent damage. An atherosclerotic narrowing of the coronary lumen leading to insufficient O2 supply to the myocardium can eventually progress to an MI situation. Stable angina (exertional angina) is usually relieved by rest within 10 minutes. Unstable angina is either a change in the frequency or duration or pattern of anginal attacks. Also considered unstable angina is new onset angina within the first 6 months. Variant angina is related to coronary artery spasms which may occur at rest or at night. Syndrome X is associated with exertional chest pain and normal coronary arteries. Nitrates are typically treatment for angina as they relax vascular smooth muscle. Relief of nitroglycerin is usually within 1-2 minutes, and O2 (5-6L/min) can also be administered. If this fails, give another dose after 5 min and call EMS. If there is no prior Hx of chest pain, do not take any chances and call the EMS first, then give O2, nitroglycerin, aspirin, and monitor vital signs. An MI can produce chest pain like angina, but it can also be silent. Panic and sweating are more likely to occur with an MI than angina. There is a decrease in the blood pressure and arrhythmia occurs. An MI may last for greater than 30 minutes, and nitroglycerin doesn't help. It is essential to confirm an MI with an electrocardiogram and cardiac enzymes. An MI is most commonly due to a blood clot (thrombus) in the coronary arteries. Blood flow is therefore retarded and an acute ischemic event occurs. This in turn causes acute dysrhythmias & impaired cardiac function. Cells of myocardium ultimately die. Myocardial ischemia is an imbalance between O2 supply & demand of the myocardium. Atherosclerotic stenosis, an increased demand for O2, and catecholamine release (stress may cause the sympathetic nervous system to releases catecholamines) may all be causes. There may be an increase in heart rate and blood pressure creating an increase in myocardium demand. Modifications of treatment with "cardiac" patients include making appointments in the morning as the patient is well rested. With angina and MI Hx, do not give more than .04mg epi = 2 carpules of 1:100,000 Pain is present in 80% of MIs, and the quality is pressing or crushing rather than sharp or stabbing as with angina. With an anginal attack, the patient usually feels the need to rest. With an MI attack, the patient is usually restless. For an MI, you can give nitrates and aspirin. Death from MI mostly occurs from V-fibrillation (acute dysrhythmia). If you use a defibrillator within 1 minute, there is a 90% success/survival, within 2 minutes - 80%, and each minute after that there is a further decrease of 10%. Do not treat post MI patients within 6 months of the MI. Make sure the INR is <3 if on anticoagulants.

Does prepping a tooth damage the pulp?

Carson Dahl Turner Searls Eda and Saito Kogushi Seltzer - Heat generation during preparation (Carson) o Teeth were prepared with air-water coolant or air-only coolant o Temp increase was 1 to 8 degree range o Thermal insult first appears around 5-7 degree celcius increase - Dahl: Crown prep at ultra high speed. Histologically examined pulp near the dentin. Odontoblastic nuclei found in dentinal tubules, odontoblastic layer was seperated from predentin, and RBC's were extravasated and in the tubules. Severe pulpal reaction resulted from crown preparation. - Turner: normally there are tight juntions between odontoblast, you can use horseradish peroxidase as visible marker; but when teeth are prepped, HRP penetrated predentin and dentin immediately beneath cavity preparation - Searls - Rat teeth prepped and amount of uptake of proline analyzed (indicator of protein synthesis) 🡪 label uptake significantly reduced in area of odontoblast immediately adjacent to the cavity - During dry cavity prep - saw rod-shpaed bodies in dentinal tubules - contained odontoblast nuclei, neutrophil and erythrocytes (Eda and Saito) - Prepping a tooth without water damages blood vessels 🡪 leukocyte extravation (Kogushi) - Seltzer - crown preps w/ and w/out water and impressions o Impressions 🡪 odontoblasts sucked in or pushed out o Heat increased capillary permeability, lots of plasma in pulp o Leukocyte adhesion o Odontoblasts reduced in #, disarranged, altered o Hemorrhage seen in pulp

Is caries progression effected by pulpal necrosis?

Chirnside, Pashley, vongsavan

Should we remove smear layer?

Chairlertvanitkul Ng - According to Chailertvanitkul, there was no difference in leakage between removing and not removing smear layer - Ng systematic review showed that removing smear layer with EDTA improved outcomes for retreatments

Types of complement activation?

Classic (antigen antibody), and alternative (LPS) but stabilized by propedrin, mannose lectin (mannose is sugar in fungi).

What is a co infection and a superinfection?

Co infection- both viruses infect at the same time Super infection- one virus infects first then next virus (worse than co infection)

Do I really need a rubber dam?

Cochran Cohen Admad

Tell me about biofilms?

Costerton Tronstad, Ricucci, Leonardo Nair, Kishen Duggan

What if I break a file?

Crump, Eleazor, Messer Fox Spill

What is cvek pulpotomy?

Cvek - Partial pulptomy treatment in complicated crown fractures - diamond bur - Cvek 1987 - treatment was successful in 96% of cases 🡪 barrier formation

What are cytokines?

Cytokines are chemical mediators that are released from macrophages, lymphocytes and endothelial cells. They are involved inflammation.

What are anatomic considerations for maxillary surgery?

Eberhardt - Zygomatic process usually overlies MB root of 1st molar - Exostoses - High muscle attachments - Sinus - Palatal aspect - greater palatine nerve and artery - Eberhardt o molar apices are closer to sinus than premolar - closest was 0.83mm for MB root of second molar o Buccal bone overlying apices ranged from 1.63 mm over first premolar to 4.45 mm over MB root of second molar o Palatal bone overlying apices was 5.42 for 1st premolar, 3.01 mm for 1st molar, and 2.76 mm for second molar palatal roots for molars should be approached from palatal but for premolar should be approached from buccal

How is fever induced?

Either IL1 creates prostaglandins which work on hypothalamaus or IL6 and TNF A work directly on hypothalamus.

Air ephysema?

Eleazor

What is lesion is not endo related

Eliasson Spatafore and Kuc

What are the 5 diff types of asthma

Extrinsic Intrinsic Drug induced Exercise induced Infectious

How were peptococcus species reclassified?

Ezaki Murdoch - Ezaki four species of Peptococcus got moved to Peptostreptococcus, main difference was GC content - Murdoch Peptostreptococcus magnus turned into Finegoldia magna, Peptostreptococcus micros turned into Micromonas micros

How were peptococcus species reclassified?

Ezaki Murdoch - Ezaki -> earlier Peptococcus and Peptostreptococcus were grouped on morphology. Peptococcus were found in clumps, Peptostreptococcus were in chains. When DNA (G+C) content were checked and DNA-DNA homology done, four species of Peptococcus got moved to Peptostreptococcus because of different DNA content. (P. asaccharolyticus, P. indolicus, P. prevotii, P.magnus) - Murdoch -> reclassified Peptostreptococcus magnus to Finegoldia Magna, and Peptostreptococcus micros to Micromonas micros (due to difference in rRNA homology).

What are some of the symptoms of endocarditis?

FROM JANE -Fever, Roth spots, Osler nodes, Murmur -Janeway lesions, Anemia, nail-bed, Emboli

What are the characteristics of E. faecalis?

Facklam Stuart - Facklam o Gram positive, facultative anaerobes, optimal growth temp 35 C o Able to survive in extreme temp, extreme pH, hypotonic solution and bile o S. faecalis and S. faecium are separated from streptococcus to form the genus enterococcus - Stuart o E. faecalis can be found in 4-40% primary endo infection, asymptomatic cases o Failed RCT, 9 times more likely to contain E. faecalis o Virulence factors: endure nutritional deprivation, invade tubules, suppress lymphocyte, resist CaOH2, biofilms

What are the characteristics of E.faecalis?

Facklam, Stuart o Facklam o Gram positive, facultative anaerobes. o Very hardy, can survive in extreme environment (high pH, large range of temperature 10-45 deg C - optimal growth temp- 35 C. high salt conc. and bile. o They produce aminopeptidase - so can digest proteins as well as sugars (so can grow in a variety of conditions) o E. faecalis and E.faecium - found in root canals. ( are separated from streptococcus to form the genus enterococcus) o Stuart o E. Faecalis can be found in 4-40% primary endo infection, asymptomatic cases. o Failed RCT - 9 times more likely to contain E. faecalis o Virulence factors : endure nutritional deprivation, invade tubules, resistant to CaOH, form biofilms, suppress lymphocytes.

What material should we use for pulpotomy?

Faschin Sonmez Fuks Cunningham Tagger - Faschin - Corticosteroids used to be used with formocresol 🡪 corticosteroid paste inhibits chemotaxis of neutrophils and macrophages to the injured area o Most to least effective in inhibition of chemotaxis: triamcinolone > betamethasone > hydrocortisone - Sonmez - different materials for primary tooth pulptomy and measured success rate o 76.9% for formocresol o 73.3% ferric sulfate o 66.6% MTA o 46.1% CaOH2 - Fuks - Meta-analysis on vital pulp therapy for primary teeth o MTA > Ferric sulfate = Formocresol >> CaOH2 - Glutaraldehyde > Formaldehyde o Cunningham - Glutaraldehyde >> Formaldehyde to fixate the pulp and allow the tissue to remain and stop reparative CT replacement of the pulp o Tagger - Glutaraldehyde was better at maintaining vitality and preventing apical involvement

Allerry to anesthetic?

Finder

What are the barriers to infection in the tooth?

First the enamel and dentin, then the pulp, then the pdl.

What cells are found in the pulp?

Garant Holland Bishop Feit Stevens/Barnett Killouth Jontell and Okiji Farnoush Bernick Matsumoto Pimenta - Odontoblasts o Garant - described odontoblast; nucleus is at one end and rough ER, golgi apparatus, and vesicles o Holland - described odontoblastic process - little or no major organelles in odontoblastic process but you do find vesicles o Bishop - found evidence for tight junctions between odontoblasts by injecting lanthium into blood stream of animal; stopped at the odontoblast cell layer at tight juntions o Feit - rat pulps were exposed and closed with CaOH2 and labeled thymidine was injected 🡪 saw proliferation of fibroblasts replacing the damaged odontoblasts; this indicates that odontoblasts are post-mitotic (do not divide to replace but is newly formed) o Stevens/Barnett: Odontoblasts are post-mitotic (non-dividing) cells, cells with characteristic of odontoblasts can still be grown from the dental pulp in vitro. Pulp tissue on the floor appeared more fibroblastic while pulp cells growing on basement membrane produced overgrowth w/ long cell processes. They produced dentin specific proteins. - Fibroblasts (Killouth) - Inflammatory cells (macrophages, t cells, dendritic cells, plasma cells) - Jontell and Okiji - Mast cells (Farnoush) - Lymphatics o Bernick - morpholotical methods o Matsumoto - enzyme 5' nucleotide phosphatase 🡪 only lymphatic cells produce this enzyme o Pimenta - used immunohistochemical approach to detect an antigen on lymphatics

How many dentinal tubules are there?

Garberaglio

What is the structure of dentin?

Garberoglio and Brannstromm - Garberoglio and Brannstromm - SEM of dentin o in periphery, ~20,000 tubules/mm2 o near pulp, ~45,000 tubules/mm2 o Size near DEJ = ~1 micron o Size near pulp = 2.5 microns

Do you use warm or cold?

Goldberg Gulabivala Baumgartner Reader Pitts Baumgartner Erikson Baumgartner, Walton Seltzer, Brady Krell Keane Naracott

How about Russian red?

Gound Hartwell Krell

How big should I instrument?

Green Abou Rass Falk Card Sjogren, Orstavik Brilliant Siquierra Yared

Why obturate?

Gulabivala - Gulabivala 🡪 entomb bacteria in canal, prevent coronal leakage, prevent egress of bacteria. He also compared different techniques and there was no difference in apical leakage between technique. Only in curved canal, thermofill was better

Should we remove smear layer or not?

Gutmann, McComb, Olgart, Lester and Boyde, Michelich, pashley - Gutmann measured amount of smear layer left after retroprep with slow speed bur and ultrasonic - Found that ultrasonics were able to remove more superficial debris than bur. Both techniques create smear layer and is not removed without irrigation with acid or chelating agents - Smear layer - contains inorganic particles of calcified tissue, tissue debris, blood cells, and potentially microorganisms o Support for removal: Contains bacteria (McComb) may support growth of bacteria left in tubules (Olgart), prevent adequate seal of materials (Lester and Boyde) o Support to keep: block dentinal tubules, block bacteria within canal (MIchelich, Pashley)

2 - Hyperthyroidism and Hypothyroidism

HYPERTHYROIDISM - cells of the thyroid follicle (the functional unit of the thyroid gland) produce T3 (triiodothyronine) and T4 (tetraiodothyronine). Hyperthyroidism is a hypermetabolic state resulting from excess secretion of T3 and T4 most frequently caused by a hyperactive thyroid gland, known as a diffuse toxic goiter or Graves' disease. Synthesis of these hormones requires dietary iodine. T3 is 3-5 times more metabolically active than T4, but T4 is produced 15x the amount of T3. Both hormones are released into the blood where they are bound to plasma proteins (most notable thyroid-binding protein - TBG). Approximately 1% floats in free unbound form and is metabolically active and available to cells. Thyroid hormones control growth and metabolism, as well as potentiating catecholamines, and promoting protein, carbohydrate, and fat metabolism. Infection and stress on body may increase the response of thyroid gland. The hypothalamus releases thyrotropin-releasing hormone (TRH) which controls the release of thyroid stimulating hormone (TSH) by the anterior pituitary. TSH by the anterior pituitary gland controls the release of T3 and T4 by the thyroid gland. In essence, there is a feedback-control mechanism. Hypo & hyperthyroidism are more common in women. Grave's disease is an autoimmune disorder where thyroid-stimulating immunoglobulins (TSI), which are autoimmune antibodies, are produced to stimulate the thyroid gland at the TSH receptor. The TS1 levels increase while TBII levels (inhibitory to TSH receptors) decrease. A rapid pulse, palpitations, heat intolerance, tremors, and increased red blood cell mass to carry additional O2 all characterize hyperthyroidism. Tx is with antithyroid drugs (propylthiouracil and beta-blockers), radioactively, or surgically. NO DENTAL Tx should be performed until the patient is euthyroid (normal thyroid levels). Be careful of stress and avoid epi as these may potentiate the hyperthyroid state. Drugs administered to a hyperthyroid patient will be more rapidly metabolized. Infection and "too much for patient to handle" can cause thyroid storm that is a thyroid crisis which may result in hypotension, coma, or death. It is possible that there may be RL where teeth are not necrotic due to the hypermetabolic state. Remember: avoid stress, epi, and avoid tx. HYPOTHYROIDISM - most common in WOMEN- 30-60yrs old. Hypothyroidism is a hypometabolic disorder that is divided into two categories based on onset. In children -> cretinism. In adults -> myxedema. This disorder may be caused by the destruction of the thyroid gland, dysfunction of the hypothalamus-anterior pituitary axis, or Hashimoto's thyroiditis (chronic lymphocytic thyroiditis). Hashimoto's thyroiditis is an autoimmune disorder involving lymphocytic infiltration of the gland followed by compression and destruction of the thyroid follicles. It is common to see a goiter with Hashimoto's. - In general, bodily processes are slowed with hypothyroidism. A child may have physical and mental impairment with a flat/broad face. Adult patients typically have a puffy face, nonpitting edema of the eyelids, and a loss of the lateral 1/3 of the eyelids (Queen Anne's sign). Pulse is slow, cardiac output is decreased, and weight gain is common. Without treatment, the person may have myxedema coma (congestive heart failure, hypoventilation, and hypothermia). Dx is made by clinical signs & symptoms and low free circulating T4. Treatment is generally with replacement thyroid hormone until a euthyroid state is achieved. Levothyroxine (Synthroid) is the most common treatment medication. While there are no contraindications to routine dental tx, keep appointments short. Stress, cold weather, infection and surgery can precipitate myxedema coma. Stay away from narcotics & sedatives because you already have CNS depression. Be careful with depressants. Acute oral infection is best managed with high doses of antibiotics to minimize the spreading of infection. Remember: avoid stress, sedatives, narcotics, long appointments, and closely monitor any infection. Hypothyroidism is more common than hyperthyroidism

What do you need in your drug kit?

Haas

How does bradykin get activated?

Hageman XII to XIIA, then prekalikrien to kalekrien (feeds back to convert more XIIA), then kininogen to bradykinin. (which works on BEN)

What cells are found in the pulp?

Hahn, torabinejad Farnoush Bernick Jontell Von Amerongen Sakamoto Bouvier Falker, Okamura

How do bacteria become resistant?

Harrision Luria and Delbruk - Harrison o 4 major mechanisms that mediate bacterial resistance to antibiotics: · Production of enzymes that inactivate the drug · Production of modified targets against which the drug has no effect · Alter cells permeability to the drug · Cause efflux of the drug so that it cannot reach an effective intracellular conc. o Bacteria achieve antibiotic resistance by genetic changes either by mutations (spontaneous or induced) or by genetic transfer (conjugation, transformation, transduction) of plasmids or transposons carrying the antibiotic resistance gene (ARG) o Overuse of antibiotics cause selective pressure. (more susceptible bacteria are destroyed and more resistant bacteria survive, so selectively increasing the more resistant bacteria) - Luria and Delbruk - fluctuation test o The development of resistance to virus or antibiotics is not due to exposure to the antibiotic but rather by spontaneous mutation Adaptation hypothesis - presence of the virus induces bacteria to adapt itself -> there will be no large fluctuation in the number of resistant bacteria from culture to culture Spontaneous mutation hypothesis - cells mutate spontaneously regardless of whether the phage is present or not -> there will be large fluctuation in the number of resistant mutants between cultures. They found that spontaneous mutation hypothesis was correct.

When should you use antibiotics?

Harrison Henry Fouad - Harrison o Rapid onset (1-3 days) o Soft tissue swelling large intraoral swelling with poorly defined borders o Regional/systemic involvement: extraoral swelling, lymphadenopathy, fever, trismus o Assessment of patient's host defense o ** Pain is NOT a good criteria to use antibiotics (Henry, Fouad) § Henry penicillin did not reduce pain or swelling in symptomatic necrotic teeth § Fouad penicillin did not reduce symptoms in patients with localized acute apical abscess

What about postsurgical healing?

Harrison Melcher

When you should or shouldn't use antibiotics?

Harrison Walton Henry Fouad o Harrison o Rapid onset of signs and symptoms (1-3 days) o Spreading swelling- diffuse, large intraoral swelling with poor definedw borders o Systemic involvement (fever, lymphadenopathy, trismus, malaise, fascial space involvement) o Immunocompromised pts with poor host defense o Pain is NOT a good criteria to use antibiotics o Walton - penicillin had no sig. effect on post-op pain and swelling in asymptomatic teeth compared to placebo o Henry- PCN did not reduce post-op pain and swelling in symptomatic necrotic teeth compared to placebo (lactose) after initiating RCT. (treatment was not completed) , eval for 7 days. o Fouad - PCN did not reduce post-op symptoms in pts with localized acute apical abscess . no sig difference b/w PCN vs. placebo vs. no med. Eval 3 days. Why not? · Abx needs to reach infected tissue in sufficient conc. and act on susceptible bacteria. There is a lack of vascular supply in an apical abscess due to necrosis. Also LAAA may be primarily inflammatory/ immunologic phenomenon causing pain and edema

Dentin chips?

Holland Tronstad

What types of selaers? What sealer is best?

Holland and Soares Holland Sipert Erikson Chailertvantikul Safavi Friedman - ZOE sealers - CaOH sealers - Epoxy-resin sealers - Bioceramic sealers - Holland and Soares both showed that there was no difference in response of eugenol sealer with CaOH sealer 🡪 both had inflammatory response - Holland: ZOE more toxic than CaOh - Sipert showed that all sealers (ZOE, CaOH, MTA) had antimicrobial response except resin sealer - Erikson showed that there was no difference in healing between different sealers used (chloroform, ZOE, epoxy) - Chailertvantikul: tested 3 sealers, resin, calcium hydroxide and ZOE and all of them showed leakage. - Safavi: looked at the toxicity of the sealers. Tubli seal had less toxic because it sets faster. Faster it sets, the less toxic it is. - Friedman: BC sealers cause less leakage, than roth sealers

What about Regenerative Endo?

Hoshnio's Hargreaves Windley Banchs and Trope Nygard Ostby Hargreaves Thibodeau Petrino Trope Hargreaves Petrino and law Grontos Sonoyama Casagrande

Dental anomlies?

Hulsman yang, melton weine lambrinidis himel cvek TBJ

Does topical do anything?

Hutchins Johnson

Hyperglycemia

Hyperglycemia --> get oxidative stress --> oxidative protiens --> AGES which binds to RAGES (in macrophages and endothelial cells) --> cause inflam mediators to be produced (IL-1, TNF-a) *This is why they don't heal well and they have destruction

List everything that can cause fever?

IL1, IL6, TNFA, PGE2, LPS

What temporary filling to use?

Imura Suanders - IRM or cavit, according to Imura, IRM or cavit was better than GP; both leaked within 22 days - Suanders 🡪 Ketac and amalgam and less leakage than GP or no filling

Tell me about nerves in the pulp?

Johnson Johnson Reader Byers, Johnsen Johnsen Olegart Byers Brammstrom Holland, Brannstrom

Do you need pulp exposure for pulpal pathology to occur

Kakehashi Mjor and Tronstad Iserman Bergenholtz Reeves and Stanley - First you need bacteria - even if you have a pulp exposure, with no infection of bacteria, there is no disease (shown by Kakehashi - with germ free rats) - Second, you don't need bacteria in the pulp or exposed pulp to get a pulpal response o Mjor and Tronstad - Prepped class V in monkeys, sealed carious dentin, saw inflammatory reaction in pulp o Iserman - used bacteria alone, not carious dentin - acute inflammatory reactions occurred due to live bacteria in cavity preps of unexposed pulps o *Bergenholtz - no viable bacteria, bacterial products only in class V preps - severe inflammatory response 🡪 viable bacteria not necessary, just bacterial byproducts o Reeves and Stanley - evaluated carious human teeth 🡪 minimum pulp inflammation observed until bacteria got to around 0.5 mm of pulp; there a relationship between closeness of infection of dentin and degree of pathology in pulp

What bacteria are found in the infected pulp

Kakehashi, Moller, Fabricious Hoshino Munson Sundqvist, Bystrom Siquierra Baumgartner Foaud Jung, Fouad, Trope Mjor Baumgartner Warfringe Baumgartner Tani-ishi Sundqvist Kaminishi Hanazawa Okuda Fletcher Sundqvist

What obturating technique is best?

Khayat Dalat Goldberg Molvydas - Khayat compared leakage of human saliva between lateral and warm vertical o No statistical difference o Leakage in 25-28 days. About 30 days everything was contaminated - Dalat: apical leakage occurred regardless of what technique was used - Veis measured dye leakage between lateral and warm vertical o Lateral was better up to 1.2 mm from foramen while warm vertical was better for the rest of the canal o No difference between two - Goldberg 🡪 thermoplastisized is better at filling lateral canals - Molvydas 🡪 warm techniques cause inflammatory reaction only in apical delta but not at the side of roots

What is the difference between traditional surgery and modern surgery?

Kim

Lets tatk apicos!

Kim Friedman Kvist, Seymour Moore Malmstrom, Khan Dionne

Why root resection at 3 mm and at a minimal bevel?

Kim Gilheany Gagliani Tidmarsh - Kim you remove 98% of apical ramifications and 93% of lateral canals when resecting 3 mm of root - Gilheany there is an increase of leakage with increased angulation of root end resection and decrease of leakage with increased depth of retrograde filling. He showed that for a 45 degree resection, optimal depth is at least 2.5mm deep, for 0 degrees, 1 mm deep filling had no leakage. - Gagliani resected at 45 degrees and 90 degrees and measured dye infiltration, there was less infiltration at 90 degree - Tidmarsh SEM study of resected roots - measured number and size of exposed tubules and found that although the number of tubules diminishes closer to the Dentine-cementum junction, there are still 13,000 per mm^2 in this area conclusion: filling should be beyond the most coronal part of bevel

Where do you fill to?

Kuttler Dummer, Burch Chugal and Spanberg Ng Ricucci Sjogren Lin, Seltzer, Sabeti

How far does the odontoblastic process extend into tubules?

Lafleche, Sigal Weber and Zaki, Thomas- lamina limitans Pashley - 1/3

Do perio and endo have a relationship?

Langland Seltzer Tanner Bergenholtz, Mazur, Czarnacki Hattler Latlme, Plackova Simon Trope Dunlap Filipowickz Kogan Garjewlo

What makes up pulp extracellular matrix?

Lechner Van Amerongen Tsuzaki Sajamoto Van Amerongen - 90% water - 10% collagen and proteoglycans and glycosaminoglycans, fibronectin o Collagen - 45% type III collagen, 55% Type I collagen (Lechner) as opposed to dentin which is mostly type I collagen (Type I collagen has no cysteines but type III has cysteines in it which has the capacity of making disulfide bonds) ▪ Lechner also found how much collagen there was out of the dry weight ~30% ▪ Van Amerongen - split collagen with CNBr digestion and found different types of collagen in pulp ▪ Tsuzaki - found tiny amounts of type V collagen o GAGs - polymer of disaccharide consisting of hexose amine n-acetyl sugar and uronic acid 🡪 negatively charged, makes it very hydrophilic ▪ Sakamoto - found GAGs in pulp o Proteoglycans 🡪 GAGs attached to protein o Fibronectin - glycoprotein ▪ Van Amerongen identified fibronectin in dental pulp

What is the composition of dentin?

Lee and Veis Mcdougall Linde Butler - 70% inorganic (hydroxyapatite), 20% organic. 10% water - 90% of organic component is collagen - mostly type I collagen o Collagen - triple helical fibers of amino acid strands, glycine in every third position, rich in proline and hydroxyproline (rigidity), cross-links between lysine amino acids - 10% of organic component is noncollagenous proteins o Dentin Phosphoprotein (DPP) ▪ Lee and Veis - found that DPP binds calcium; DPP is made of aspartic acid and phosphoserine 🡪 highly negatively charged 🡪 binds calcium ▪ Mcdougall - found that protein is only found in newly formed dentin and odontoblasts, not in predentin ▪ Linde - showed the protein causes mineralization in calcium phosphate o Dentin Sialoprotein (DSP) - Butler ▪ Highly glycosylated protein w/ glutamic acid and sialic acid - anionic ▪ Specifically found in dentin and odontoblastic process, not in predentin o Dentin Matrix Protein

How does presence of microbes affect success of treatment?

Lin Verma/Kim/Fouad Molander Sundqvist Stevens Sedgley Vidana Sukawat Mutsuo Peters Siqueira Liljestrand o Lin found stainable bacteria in 67% of failed cases. (biopsy samples from failed cases were stained with H&E, Brown and Brenn), therefore persisting bacterial infection (either by inadequate debridement or leakage) can lead to failure. o Presence of infection (residual bacteria) and intracanal inflammation can cause failure of regen endo (Verma/Kim/Fouad - immature canines in ferrets) o Microflora of failed endo teeth w AP is different from that of untreated necrotic teeth. Untreated necrotic teeth - both gram +ve and -ve, mostly obligate anaerobes. Failed endo- mostly gram +ve , can be both facultative and obligate anaerobes). 69% of failed endo has enterococci (E.faecalis- gram +ve facultative anaerobe) and most of the times, they are only 1-2 strains. (Molander- cultured samples from failed endo undergoing re-treats) o Sundqvist - also looked at microflora in failed endo teeth w AP , did retreat and followed up for 5 yrs with strict Strindberg success criteria - only completely healed cases as success. and 1) found same results as Molander ( failed cases have mainly single species of predominantly gram +ve bacteria with both facultative and obligate anaerobes. E.faecalis present in 38% of failed endo. 2) overall success rate of retreat - 74% (5 yr f/u) so ¼ cases dont heal. If -ve culture before filling - 80% success. If +ve culture before filling - only 33% success. 3) size of pre-op lesion made a difference in outcome (smaller lesions had better success rate than larger lesions). Conclusion: 2 factors affect success of retreat 1) presence of infection at time of root filling. 2) size of PA lesion o CaOH medicament is not effective against E.faecalis. (Stevens) CCP (camphorated chlorophenol is effective against it) o E.faecalis shown to survive for as long as 12 months entombed in dentinal tubules, can survive with limited or no nutrients and provide long term nidus for subsequent infection(Sedgley - inoculated teeth , filled and cultured) o E.faecalis found in failed endo is not derived from pt's own microflora (tested saliva- no EF, faeces - had different EF strains), so indicates exogenous source. (Vidana) (cheese?) o CaOH + CMCP (phenol) is effective against. E.faecalis (Sukawat). Compared w CaOH + 0.2% CHX or water. CaOH + CMCP -> Ca Paramonochlorophenolate (PMC) salt. -> PMC + OH - (both are bactericidal) o More than 50% of the times, bacteria invades deep into dentinal tubules (beyond 2/3 of the width of root dentine) Matsuo - 75% of untreated teeth had bacteria invading dentinal tubules, while even instrumented teeth had bacteria in tubules 65% of the time. More in coronal dentinal tubules than apical. Did immunohistological study using species- specific antisera. Peters - Also found that in more than half of the infected roots, bacteria are present in deep dentinal tubules close to cementum. His study was more sensitive - did anaerobic culturing of ground dentin to detect viable bacteria) o Siqueira review - Reasons for failure (even good looking endos) : microbial and non-microbial factors. Microbial factors include intraradicular bacteria in isthmus, ramifications, dentinal tubules, extraradicular bacteria in biofilms, and coronal leakage. Endo infections are associated with coronary artery disease. (Liljestrand

Why are E. faecalis resistant?

Love Son Evans Portnier Sedgley distal facklam

How to bacteria become resistant?

Luria and Delbruk Harrison - Luria and Delbruk fluctuation test o Adaptation hypothesis - presence of virus induces bacteria to adapt itself there will be no large fluctuation in the number of resistant bacteria from culture to culture o Spontaneous mutation hypothesis - cells mutate spontaneously regardless of whether the phage is present or not there will be a large fluctuation in number of resistant mutants between cultures o They found that spontaneous mutation hypothesis was correct - Harrison o 4 major mechanisms mediate bacteria resistance to abx: § Bacteria produce enzymes that inactivate the drug § Bacteria can synthesize modified targets against which the drug has no effects § Bacteria can alter their permeability § Can effectively efflux the drug so that an effective intracellular concentration is not achieved o Antibiotic resistance is the result of genetic changes in the organism either by mutation or genetic transfer o Overuse of abx cause selective pressure

Does internal bleaching cause ECR?

Madison Rotstein rotstein - Madison - three bleaching techniques were used: with and without acid etching, thermocatalytic blaching, walking bleach, or combination. o 2 teeth with thermocatalytic bleaching had resorption/ankylosis in cervical area o None of the teeth with walking bleach (30% H2O2 and sodium perborate) had ECR o Heat drives hydrogen peroxide in tubules - Rotstein - showed hydrogen peroxide can penetrate through radicular dentin in teeth with intact cementum but penetration is significantly higher in teeth with cementum defects Rotstein - also showed that after three treatments in 14 days, there was no significant difference between any of the sodium perborate preparations (sodium perborate and 30% H2O2, sodium perborate and 3% H2O2, sodium perborate and distilled water

What about if you see replacement resorption in primary teeth?

Malmgren

What about sealer?

Marshall Grossman Walton Briseno, Yesilsoy Siepert Chailvervanitkul Erikson Keane, Peters Baumgartner Peters

Bisphosphonate associated ONr?

Marx Edwards Sah Jez Dah Licata

Are endo teeth more brittle?

Masser, Sedgley Huang Schilder

Do endo and ortho have a relationship?

Mattison Mah Reitan Butcher Kvinsland

Does periodontal disease affect the pulp?

Mazur Czarnecki Hattler Filipowicz Kobayashi Langeland Bergenholtz Jannson - Mazur - looked at caries free teeth with severe perio and looked at histology of the pulp 🡪 changes in periodontium were not related to changes in the pulp - Czarnecki - Also found that severity of periodontal disease does not change the pulp status in intact teeth - Hattler - root planing in rat teeth caused reparative dentin formation, but not inflammation - Filipowicz - Vital resection doesn't work because it's for dummies. 59% vital in 6 mos, 33% in 1 yr, 13% in 5 yrs. - Kobayashi - pulp infection can come from retrograde perio lesion in non-carious vital tooth - *Langeland - perio teeth examined - perio disease can cause calcification, resorption, or inflammation and pulpal damage through lateral canals, but will only cause total necrosis if apical foramina are involved - Bergenholtz - Induced plaque on roots using ligature. Histo, plaque causes pulpal changes but no disintegration. 57% found irregular dentin in coronal portion. - Jannson - teeth with periapical radiolucency had deeper pockets

What is the focal infection theory?

Miller, Rosenow Fish Siquierra Torabinjad

What are the maximum dosages?

Moore

What is in a granuloma

Nair Stern Perrini Pulver Torabinejad Bergenholtz

But why do failures occur?

Nair, Ricucci, Tronstad, Sjogren, Nair, Leonardo, Nymzick, Siquierra

Does antihistamine work for pain?

Nevins

What factors influence outcome?

Ng - No PA lesion, Small PA lesion - No sinus tract - Patency - Canal cleaning as close to apical terminus - EDTA before final rinse with NaOCl 🡪 for retreatment cases - No using chlorhexidine with NaOCl - No perforation - No interappointment flare-up - No root filling extrusion - Good coronal restoration

What is a normal INR? What do you want the INR to be under?

Normal: 0.9-1.2 Treat if: <3

Whatabout CBCT?

Peters Trope Bronstein Low Patel

What is the sensitivity, specificity, positive/negative predictive value, and accuracy of endo diagnostic tools? Clinical testing and correlation to histology?

Peters Petersson Iqbal Mendoza Ricucci Mejare - Peters 1994 o Cold test etter when you place on cervical area, not occlusal o EPT frequently have false positives - can conduct to gingiva, breakdown products of pulp necrosis can conduct electric current, can conduct to adj tooth o False positive to cold were in multirooted teeth, or partially necrotic teeth o Reasons for false negatives 🡪 young patients (<10 years), traumatized teeth, elderly - Petersson 1999 o Sensitivity- the ability of a test to identify teeth that are really diseased. o Specificity- the ability of a test to identify teeth without disease. o Positive predictive value- the probability that a positive test result really represents a diseased tooth. o Negative predictive value- the probability that a tooth with a negative test result really is free from disease. o Accuracy- the overall rate of agreement between the diagnostic test and the gold standard. o Results: ▪ The sensitivity was 0.83 for the cold test, 0.86 for the heat test and 0.72 for the electrical test ▪ The specificity was 0.93 for the cold test, 0.41 for the heat test, and 0.93 for the electrical test ▪ The positive predictive value was 0.89 for the cold test, 0.48 for the heat test and 0.88 for the electrical test and the negative predictive value was 0.90 for the cold test, 0.83 for the heat test and 0.84 for the electrical test. ▪ The accuracy was 86% for the cold test, 71% for the heat test and 81% for the electrical test. - Iqbal o Conclusions: Sharp pain was more likely associated with pulpal pathology, whereas dull pain was more likely associated with periapical pathology. Percussion and palpation tests were powerful in differentially diagnosing between pulpal and periapical conditions - Mendoza: looked at histology of teeth with irreversible pulpitis o There are individual variations of moderate to severe changes that occur in the nerves, vasculature and connective tissue of the apical pulp in the clinical condition of irreversible pulpitis. We cannot predict, based on the clinical tests and radiographs, the exact histological condition of these structures - Ricucci o The clinical diagnosis of normal pulp/reversible pulpitis matched histology in 96.6% teeth o The clinical diagnosis of irreversible pulpitis matched histology in 84.4% cases - Mejare: o Signs/symptoms as indicators for inflammatory status: There is insufficient evidence to determine whether the clinical symptoms accurately represent the inflammatory status of the pulp. o Sensibility and vitality testing: there is also insufficient evidence to determine the accuracy of tests used to assess pulp vitality

What instrument technique is the best?

Pettiete Weine Beeson Barbizam Barnett Walton Sequeria Imura - Pettiete 🡪 NiTi was better at maintaining shape of the canal and had less strip perfs and better outcomes. Study by dental students. Concluded NiTi had more successful outcome than SS - Weine 🡪 rotary better than hand-filing; hand filing has more tendency to straighten canal and cause zipping and tear drop shape - Beeson 🡪 more apical extrusion of debris with hand-files than rotary. Apical plugs will be present when you instrument 1mm short of apex. Rotary had more irrigant extrusion when instrumented to the foramen - Barbizam 🡪 oval canals, hand files were better at removing debris than rotary - Barnett 🡪 no difference between sonics/ ultrasonics and hand instrumentation on removing bacteria - Walton- Step back was more efficient than just filing and reaming alone and cleaned more walls - Sequeria- tested 5 different technique and looked at histology. All techniques left untouched walls. No perfect system. - Imura- looked at 4 rotary and hand instruments for removal of GP in retreatment. All 4 left material behind in the canals.

What are anatomic considerations for mandibular surgery?

Philips and Frankl - Muscle attachment high muscle attachments in premolar area will affect flap design, tissue replacement, suturing - Mental foramen o According to Phillips anatomic study, the mental foramen is about 4 mm in diameter and if you draw a line from the cusp tip following the long axis of crown, is on the line 62.7% of the time, and exited superior-posteriorly 68.7% of the time o According to Phillips radiographic study, the mental foramen was usually mesial and inferior to the apex of the second premolar (avg 2.18 mm mesial and 2.41 mm inferior) - Thickness of buccal cortical bone o Frankl distance from buccal cortical plate was 4.2 mm for first molar and 7.2 mm for second molars - Inferior alveolar canal o Frankl § position of IA nerve was in the lingual half of mandible 81% of time and 16% in the buccal half in the 1st molar region § Vertical distance from nerve to root apices were 5.3 mm for first molars and 3.6 mm for second molars § Radiographically, the vertical distance between mesial apex and superior border of IA canal in 1st molar is 6mm and 2nd molar is 3.7mm

Tell me about cytokines?

Stashenko

7 - Rheumatic Fever and Rheumatic Heart Disease

RHEUMATIC FEVER - The associated bacteria is Group A beta hemolytic Streptococcus (gram-, facultative anaerobe). It is an autoimmune inflammatory disorder following infection caused by the previously mentioned bacteria. The bacteria attacks the oropharynx, the body produces type-specific antibodies to the antigen, and complexes form. These complexes cross react with tissue proteins which can then cause a vasculitis and inflamed lesions of the heart, joints, nervous system, and skin. Major problems are cardiac and pulmonary. With the 5-15 yr old age group, rheumatic fever accounts for 95% of all heart disease. These group A Strep have M proteins, which are proteins of the cell wall that allow for resistance to phagocytosis by PMNs. Rheumatic fever can be detected by an anti-streptolysin titer. There are 5 major manifestations of rheumatic fever: 1) Carditis - valvular inflammation - may have organic heart murmur or be asymptomatic. Mitral valve is the most frequently affected valve by rheumatic carditis 2) Chorea 3) Erythema margination - rash for usually 4 days 4) Polyarthritis - inflammation of large joints 5) Subcutaneous nodules The Dx is based on 2/5 of these major manifestations and a Hx of preceding throat infection and an increased anti-streptolysin-O titer (although this is not particularly definitive). A C-reactive protein test can be done as well, although it is not specific. Valvular lesions may heal completely or progress. Treatment is with salicylates and corticosteroids, and antibiotic coverage is usually given for 5 years. With rheumatic fever, look for Hx of symptoms, AP chest x-ray, and electro/echocardiogram. A patient with rheumatic fever can be asymptomatic with a murmur or can be symptomatic with dyspnea. Look for potential for congestive heart failure. (An aside about murmurs - an innocent murmur can be due to an increase in blood flow during systole). RHEUMATIC HEART DISEASE - this is the cardiac damage from rheumatic fever. 30-80% of rheumatic fever patients develop this. Rheumatic heart disease can have a latency period. Lesions of R.H.D. include valvular changes, myocardium changes, and pericardium changes because of sensitization and immune mechanisms. With the valve problems the outcome is scar tissue and valve deformity. The mitral valve is more common than aortic. Patients with a presentation of rheumatic heart disease history are more susceptible to infective endocarditis. Myocardium changes include aschoff nodules (fibrinous degeneration of collagen surrounded by granulomatous tissue). Pericarditis may occur with serofibrinous inflammation. Factors to consider are the severity of rheumatic inflammation and the amount of scarring.

6 - Rheumatic Fever and Rheumatic Heart Disease

RHEUMATIC FEVER - The associated bacteria is Group A beta-hemolytic Streptococcus (gram-, facultative anaerobe). It is an autoimmune inflammatory disorder following infection caused by the previously mentioned bacteria. The bacteria attacks the oropharynx, the body produces type-specific antibodies to the antigen, and complexes form. These complexes cross react with tissue proteins (antigen mimicry) which can then cause a vasculitis and inflamed lesions of the heart, joints, nervous system, and skin. Major problems are cardiac and pulmonary. With the 5-15 yr old age group, rheumatic fever accounts for 95% of all heart disease. These group A Strep have M proteins, which are proteins of the cell wall that allow for resistance to phagocytosis by PMNs. Rheumatic fever can be detected by an anti-streptolysin O (ASO )titer. Jones' Criteria 5 major manifestations of RF: 1) Carditis 75% of time - valvular inflammation - may have organic heart murmur or be asymptomatic. Mitral valve is the most frequently affected valve by rheumatic carditis. 2) Chorea - erratic jerky movements 3) Erythema margination - rash for usually 4 days 4) Polyarthritis - inflammation of large joints; reversible 5) Subcutaneous nodules 5 minor manifestations of RF: Fever, Arthralgia, Prolonged P-R, High Erythrocyte sedimentation rate, ↑C-reactive protein The Dx is based on 2/5 of these major manifestations or one 1 major + 2 minor, and a Hx of preceding throat infection and an increased anti-streptolysin-O titer. A C-reactive protein test can be done as well, although it is not specific. Valvular lesions may heal completely or progress. With rheumatic fever, look for Hx of symptoms, AP chest x-ray, and electro/echocardiogram. A patient with rheumatic fever can be asymptomatic with a murmur (MVP) or can be symptomatic with dyspnea. Look for potential for congestive heart failure. Treatment: - At initial diagnosis: 10 day regimen Penicillin G - ASA in anti-inflammatory doses; - Digoxin, diuretics, O2, sodium and fluid restrictions (Tx of CHF) Prophylaxis: - Pts w/ RF without carditis: AB prophy for 5 yrs or until 21 yrs of age (whichever is longer) - Pts w/ RF with carditis but no heart disease: AB prophy for 10 yrs or until 21 yrs of age (whichever is longer) - Pts w/ RF with carditis and heart disease: AB prophy for 10 yrs or until 40 yrs of age (whichever is longer) RHEUMATIC HEART DISEASE - this is the cardiac damage from rheumatic fever.30-80% of rheumatic fever patients develop this.Rheumatic heart disease can have a latency period.Lesions of R.H.D. include valvular changes, myocardium changes, and pericardium changes because of sensitization and immune mechanisms.With the valve problems the outcome is scar tissue and valve deformity.The mitral valve is more common than aortic.Patients with a presentation of rheumatic heart disease history are more susceptible to infective endocarditis.Myocardium changes include Aschoff nodules (fibrinous degeneration of collagen surrounded by granulomatous tissue). Pericarditis may occur with serofibrinous inflammation.Factors to consider are the severity of rheumatic inflammation and the amount of scarring.

How aboutgetting the patient numb?

Reader Reader Malamed Clark Frommer Birchfield Reader Walton Reader, Kim Musstein Roberts Reader Repogle and Reader

How about some instrumentation techniques?

Rhone Wu and Wesselink McKendry Mullaney Goerig Abou Rass Yared Gabel Stabholz Walton Buchannan Mullaney Goldberg Peters Baumgartneer Pettite Beeson Tepel Barbizam Peters Trope

Whats hollow tube theory?

Richert and Dixon Torneck Goldman

What is the history of ultrasonics?

Richman, Carr - Richman 1957 was the first one that introduced ultrasonics in endodontics - Carr introduced retrotips for surgery in the 90s - Historically, the retropreparation with round burs had limitations o Not placed down long axis o Lacked sufficient retention form o Lacked proper buccolingual extension o Unable to include isthmus o Unnecessary enlargement to weaken tooth - Ideal prep is a class 1 preparation at least 3.0 mm into root dentin with walls parallel to and coincident with the anatomic outline of the pulpal space (Carr)

What is the hollow tube theory?

Rickert and Dixon Goldman and Philips - In 1931 Rickert and Dixon claimed that hollow tube causes inflammation - Goldman and Phillips disproved that theory and showed that sterile hollow tubes do not cause disease or inflammation by implanting sterile tubes in rats and 1 week to 5 months there was no inflammation at the open ends of the tubes o There was formation of a capsule around the open ends

Why is coronal sealing important?

Ricucci Gillen Ray and Trope - Ricucci 🡪 after exposure to oral environment for > 3 months, bacteria remained in coronal 1/3 and not apical 1/3 - Gillen 🡪 systematic review showed that both coronal restoration and quality of endo is important - Ray and Trope 🡪 coronal restoration may be more important than endo for better outcome. Radiographic study

What is the significance of molecular methods (PCR) in endodontic infections?

Rocas and Siqueira Siqueira Sakamoto Canale-Parola Fenno o Rocas and Siqueira o Found Dialister species (gram negative, obligate anaerobic , non-sporing, non-motile, asaccharolytic - so can be confused with Porphyromonas) which was difficult to culture but now can be identified by PCR. o Found in 50% of primary infections with apical periodontitis. o Siqueira o Pseudoramibacter Alactolyticus (saccharolytic) - another species that was difficult to culture but now can be identified by PCR method. o Found very frequently - 56% of RCT with asymptomatic infections o Sakamoto o Renaming B. forsythus to Tannerella Forsythia (gram -ve, obligate anaerobes, non-motile fusiform) o As bacteroides, they have same enzymes for fermentation. Difference - require NAM for growth (cell wall synthesis) so it is co-dependent on other species for survival , produce trypsin, bile sensitive, different G+C content. o Very hard to grow, very fastidious. But by molecular methods, found that it is one of the most commonly found organism in endo infections. o Canale-Parola o Spirochetes - Obligate anaerobes, highly motile, highly proteolytic organisms. o 2 groups are pathogenic - treponema (syphilis) and Borrelia o Spirochetes are very fastidious , so difficult to culture. With molecular methods, they are commonly found in endo infections ( T. denticola) o They have a number of virulence factors (very motile, proteases) - Fenno

How should I treat a flare up?

Rosenberg August Creech Reader Seltzer Hargreaves Harrison

Do you need to sterilize all this stuff.r

Roth Senia Hilt and Hicks

How much blood is lost during surgery?

Selim ● According to Selim, an average of 9.5ml of blood is lost in an avg 47 min of surgery ● Duration of surgery has the greatest influence in blood loss than any other variable ● Palatal surgery had rate of blood loss 3x average

How do you calculate magnification of microscopes?

Rubenstein) - Focal length of binoculars - Focal length of objective lens - Power of eyepiece - Magnification change factor - Calculation: (Focal length of binoculars X power of eyepiece X magnification) - (Focal length of objective lens) - Head position is perpendicular to floor for maxillary and parallel to floor for mandibular

What is the radiographic criteria for success in surgery?

Rud ● Rud's criteria: Complete, incomplete, uncertain and unsatisfactory healing ○ Complete healing- reformation of the periodontal space, bone cavity filled w/ bone, width of the PDL is less than 2x normal ○ Incomplete healing (scar tissue)- A radiolucency (w/ irregular periphery) still exists that is either decreased in size or stationary. Asymmetric around the apex. Bone may or may not be present in the rarefaction ○ Uncertain healing- Some degree of bone regeneration (so radiolucency might be smaller), but periphery of radiolucency is circular and symmetric ○ Unsatisfactory healing (failures)- Same as uncertain healing except that the radiolucency in this group is either enlarged or unchanged

How long do you want to follow up after surgery?

Rud Halse and Molven ● According to Rud, with longer observation time, complete and unsatisfactory groups increased while incomplete and uncertain groups decreased ○ Most of the changes occured in the 1st year and not much changed after 4 yrs ○ Changes were mostly toward the better groups after 1 year ○ Minimum 1 year follow-up and ideal is 4 years ● According to Halse and Molven, cases can be diagnosed with confidence at the 1 year mark as completely or incompletely healed because long-term follow-ups after that showed that they stayed in the groups or improved. ○ Cases with uncertain healing also stayed in the same group after 1 year ○ Uncertain healing cases, after 1 year did either go to success or failure.

Where do interleukins come from?

Stashenko Damme Sasaki Safavi Torabinejad, Stashenko Huang

Do you use Sargenti Paste?

Sargenti Spanberg Langeland Pitt ford Safavi

Trigeminocardia Reflex

Scully, brown

What is cementum made of?

Sicher and Bhaskar Bartold Miki Pitaru McAllister Ivanocski

What about apical resorption?

Stashenko Trope Trope Boyce Sasaki Saito, Farr Stashenko Stashenko Stashenko Wang Hou and Stashenko Stashenko Torabinejad

What about in failed root canals?

Siquierra Molander, Rocas Sedgley Fouad Sundqvist Molander

So why not culture before you fill?

Sjogren Naidorf Seltzer, Peters Kaufman Sedgley

Why use intracanal medicament?

Sjogren Sjogren Bystrom Vera Tronstad - Sjogren showed that in one visit, 40% still had remaining bacteria. So if you do root canal in one visit, it is very important to get negative culture which is not possible with just one visit. So the use of intracanal medicament can help to lower the culture and increase the success rate o 68% success for (+) cultures o 94% success for (-) cultures - Sjogren showed that after 7 days with CaOH, no culturable bacteria even after 1-5 weeks - Bystrom recommended leaving for 1 month, CaOH > CMCP in killing bacteria - Vera 🡪 2 visits w/ CaOH was better than 1 visit to reduce bacteria load in canal - Tronstad: with CaOH you get pH changes to a more alkaline environment which can help to inactivate the osteoclast and stimulate repair processes of the tissues Inhibit resorption

One visit or two?

Sjogren Sjogren, Bystrom Siquierra, Nair, DeSouza Safavi Strella Waltimo Trope Peters, Penesis, Oliet Eleazor, Rhone Trope

Is gutta-percha toxic? Who said?

Sjogren Wolfson Tavares - Sjogren showed that large particles weren't toxic because a capsule forms around it (low inflammation and fibrous capsule) but small particles or dissolved had intense inflammatory response because harder to form capsule around the GP - Wolfson - GP not toxic to tissues because it was able to form a thin layer of fibrous capsule - Tavares - GP not toxic to tissues by testing different companies of GP

How about avulsion?

Soder, Van Hassel Blomlof Lindeskog Cvek Kling and Cvek Selvig, Kling Iqbal Dumsha, Skoglund Andreason Trope Selvig Trope Andreason Blomlof

What are examples of bacterial virulence factors?

Stevens Okuda Fletcher Sven Takada Killian Kaminiski - Sonic extracts of different bacteria had cytotoxic effects: inhibited human gingival fibroblast proliferation, DNA synthesis and cell morphology (Stevens) - Capsulated B. melaninogenicus compared to non-capsulated strain had antiphagocytic antichemotactic effects (Okuda) - P. gingivalis without the prtH gene (protease that cleaves C3 complement protein) had less virulence than the wild-type with the gene (Fletcher) - LPS can stimulate bone resorption by stimulating osteoclasts (Sven) - LPS induced production of IL-1 and IL-6 in human fibroblasts (Takada) - Capnocytophaga and Bacteroides species degraded immunoglobulins IgA and IgG (Kilian) - P. gingivalis protease can stimulate the kinin system to increase vascular permeability (Kaminiski)

What would you give if pt had chest pain?

Stop proceduure, call 911, check BP, if not low then -nitroglycerin -Give O2 -aspirin under tongue

How does presence of microbes affect success of treatment?

Sundqvist Lin Sjogren Siqueira - The larger the lesion, the higher the density of bacteria (Sundqvist) - Sundqvist studied previously root filled teeth with bone lesions and took samples; success was 33% with positive cultures and 80% with negative cultures; The size of periapical lesion made a difference in outcome (smaller lesions healed more than larger lesions), if E. faecalis was present, it was the only species isolated the microbial flora is different in failed cases than untreated cases - Lin found stainable bacteria in 67% of failed cases - Sjogren took bacterial samples of primary root canal treatment - 94% success rate for negative cultures and 68% success for positive culture (one visit) - Siqueira review - reasons for failure: microbial factors and non-microbial factors o Microbial factors include intraradicular bacteria in isthmus, ramifications, dentinal tubules, extraradicular bacteria in biofilms, and coronal leakage

What bacteria are found in acute abscesses

Sundqvist Siquierra Kettering

What are these retrofill materials?

Super EBA MTA

Tell me about the apex locator

Suzuki Sunada Kobayashi Baumgartner Shabahang Fouad Lost Schindler Dunlap Goldberg Nguyen Rivera Fuss Baumgartner

How about Formocresol for pulptomy?

Sweet Ranley Pashley, block sipes fuks trope cvek heide coll

Tell me about the pulp vasculature?

Takehashi and kim Vongsavan Krell Olegart Kim Kogushi Kim Van Hassel, Tonder

How do I get gutta percha out?

Tamse, Kaplowitz Chutich, Kaminski McDonald Walcott Hicks, Hunter

What about cysts?

Ten Cate Seltzer Torabinejad Nair Pulver Nell Harvey Bhaskar Bender Lin Nair

The endothelium becomes hyperpermeable

The endothelium becomes hyperpermeable --> decreased healing and decreased PMN response

What is a phoenix abscess:

This is an area of suppurative inflammation that arise within a granuloma. There is pus.

Barodontalgia?

This was described by Senia and Hodges.

What is more successful: retreatment or surgery?

Torabinejad Hepworth ● According to Torabinejad (systematic review), surgery rates decreased with time while retreatment rates increased with time. Surgery has higher initial success rate. ○ Surgery success rates decreased with increasing follow-up time: ■ 2-4 years: 78% ■ 4-6 years: 72% ■ 6+ years: 63% ○ Retreatment success rates increased with increasing follow-up time: ■ 2-4 years: 71% ■ 4-6 years: 83% ■ 6+ years: No data ● Hepworth Showed that there was 59% success rate for surgery by itself but 81% success when both retreatment and surgery was done ○ Hepworth also showed that retreatments due to technical reasons (no lesion) had a success rate of 95% where as retreatments due to failed therapy (lesion) had a success rate of 66%

Is there bacteria in periapical lesions?

Tronstad Abou Rass Siquierra Yamasaki Walton, Nair

TeII me about resorption?

Tronstad Gartner Wedenberg Turkun Stamos Trope, fuss trope suda trope johnson heithersay Heithersay

Can you do a pulp cap?

Tronstad Langeland Stanley COX Holland, pitt ford massler reeves, about stanley

What happens to exposed dentin?

Tronstad and Langeland Whitokite Pashley - Tronstad and Langeland - looked at vital teeth with attrition and found crystals inside tubules: rhomboid (whitlokite) and needle shape - Pashley - measured fluid movement inside tubules; cold and osmotic pressure causes fluid to move outward; heat causes fluid to move inward

How can pulp get infected in traumatically devitalized teeth?

Tronstead Langeland Pashley Peters Kerekes Robinson Bashker Love and Jenkinson Kerekes and Olsen Robinson and bioling Tziafas Horiba Exposed dentin (Tronstead) Dentin Caries (Langeland) Enamel and Dentin Cracks (Pashley) Restoration (Peters) Lateral Canals (Kerekes) Anachoresis, attraction of blood borne bacteria to the site of inflammation (Robinson) 10% of teeth have exposed tubules between cementum and enamel. (Bas ehkar) - Love and Jenkinson - review article - describes how bacteria can penetrate carious dentin and also the tubules of non-carious dentin exposed to the oral environment - streptococci can attach to walls of tubules and grow in chains, which allows them to extend through the length of the tubule 🡪 release acids causing caries - Kerekes and Olsen - review article - describes invasion of lateral canals by bacteria in perio pockets, organisms found in perio lesions are similar to that of found in endo lesions - Robinson and Boiling - anachoresis - blood-borne bacteria is attracted to area of inflammation - placed irritants in cat teeth, injected special bacteria through vein and found these bacteria in the pulp (72%) o Tziafas also showed anachoresis in dog dental pulps capped with Dycal, - Horiba - endodotoxin can travel outward from root canal into root dentin up to 300 microns outwards

How does the pulp respond to deep carious insult and pulpal exposure?

Trowbridge Reeves, About Hoshino Stanley

Should we use GTR in surgery?

Tsesis Pecora Rankow Artzi - Purpose of GTR is to protect the space to prevent the faster growing epithelial cells from entering the space - Tsesis - systematic review of outcomes of GTR o A trend of better outcome was found but not statistically significant o GTR was better for large PA lesions, through-and-through lesions o Resorbable membrane was better than non-resorbable o Pooled healed, incomplete healing and uncertain into success - Pecora - GTR in large lesions (>10 mm) - 10 cases for each group w/ and w/out GTR o Success rate was zthe same after one year but faster healing with GTR o The quality and quantity of bone regeneration was better and less scar tissue - Rankow - demonstrated use of GTR for cervical resorption, dehiscence, palatal groove o GTR can be successful in some perio bone loss, can be used in endo related bone loss § Ridge augmentation § Oblique root fracture § Cervical root resorption § Dehiscence § Proximal bone loss § Development grooves o Can use when buccal cortical plate is missing showed a case where they re-established buccal cortical plate (Abramowitz) o If replaced by epithelium you get long junctional epithelium o If connective tissue, root resorption o If bone, ankylosis o If PDL, new connective tissue attachment (that's what we want) - Artzi - Bone graft or membrane in cats o There was more bone formation when membrane was used compared to bone graft only or not grafted o Membrane is more important than bone graft to enhance tissue regeneration

How does microscope affect outcome and post-op pain?

Tsesis Setzer - Tsesis - compared post-op quality of life through surgery for the first 7 days after surgery between traditional and modern surgery o Modern surgery with microscope took 40 min and traditional took 20 min o Both groups had difficult mouth opening, mastication and speaking ability but modern surgery was more significant. o Modern surgery had more difficulty with mouth opening, mastication and ability to speak on days 1 and 2 post-op but had faster decrease in pain levels - Setzer - Compared use of higher magnification (> 10X) to no or low magnification o 88% success for contemporary surgery with no magnification or loupes o 94% success for higher magnification o The difference in probability for success was only significant in molars

What is the difference between type 1 and type 2?

Type 1- autoimmune disorder. they are dependant on insulin. they have a complete destruction of beta cells. You get ketoacidosis Type 2- beta cell receptors not functioning properly. Usually obese people over 40, genetic, diet related.

What nerve fibers are sensitive to LA?

Type B (sympathetic) Type C (pain) Type A (delta)- temp Type A (gamma)- prioproception Type A (beta)- sensory Type A (alpha)- motor

What are the different types of diabetes?

Type I, II, gestational

What are the different types of sutures?

Velvart - Monofilament (nylon, gut, steel, chromic gut) vs multifilament (silk, polyester, cotton, linen) o Monofilament produces less inflammatory reaction than multifilament because multifilament has wicking action where they draw bacteria - Absorbable (gut, vicryl) vs nonabsorbable (silk, nylon, polyester, Gore-Tex)

What are the advantages and disadvantages of different flap designs?

Velvart, Kramper ● Intrasulcular full-thickness flap - loss of papilla or possible recession in esthetic zones - best visibility of surgical site ● Triangular flap has advantage of minimal disruption of blood supply and easy reposition ● Rectangular flap has advantage of easy reposition and wound closure but disadvantage is possible gingival recession ● Submarginal (Ochsenbein Leubke) flap had advantage of leaving marginal gingiva untouched and reducing recession but disadvantage is possible scar formation ○ Needs minimum 2mm of attached gingiva - measure from base of pocket to mucogingival junction ○ You can't make incision over the lesion ● Kramper evaluated wound healing in dogs based on histology of three different flaps: intrasulcular, semilunar, submarginal Submarginal wound was the best for epithelial closure of the wound- least inflammation; intrasulcular had the least scarring formation. ● According to Velvart, PBI showed predictable recession-free healing of interdental papilla in comparison to standard sulcular papilla incision. Intrasulcular show creeping within 3-12 months

Is there any systemic effect or local adverse effects hemostatic agents?

Vickers Lemon Jeansonne - According to Vickers, there were no significant changes in blood pressure or pulse at any time period when using ferric sulfate or epi pellets - Lemon,Jeansonne demonstrated that ferric sulfate produces an intense foreign body reaction and delays healing if left in site

Articles that measure efficacy of hemostatic agents?

Von Arx Vickers - Von Arx drilled holes in skull of rabbits and measured hemostasis of different agents o Expasyl (aluminum chloride) with Stasis (ferric sulfate) and Expasyl alone provided most efficient hemorrhage control § Aluminum chloride is very acidic and chemically reacts with blood proteins to induce hemostasis - Vickers adequate hemostasis was achieved in 15/16 cases using ferric sulfate and all 17 cases using epi pellets

NiTi vs SS?

Walia - Walia - Showed that NiTi is 2-3x more flexibile and more fracture resistance than SS. More predictable in curved canals

When do flare-ups happen?

Walton - Walton 🡪 most important factor is pre-op pain or swelling, 20% had flare-ups - Overall incidence of flare-ups was 3.17% - Sinus tract never correlated with flare-ups

Does odontoblastic process go all the way to the DEJ?

Weber/Zaki La Fleche - Weber/Zaki - found odontoblast process only in the inner half - La Fleche - placed in liquid nitrogen to freeze everything 🡪 found odontoblastic process through the whole length, without liquid nitrogen only in the inner third because the odontoblastic process is a retractable suspensor system.

HIV?

Wenckus and Johnson

What is ketoacidosis?

When body cannot use sugar as a fuel because there is no insulin to break it down. You get breath that smells like acetone, fruit/nailpolish remover smell.

Your patient walks in and has recently had a MI. What do you ask him?

When did it happen

What is the evidence that shows these molecules (signal, receptors, signal transduction, transcription factors) are being produced during development?

Wilkinson Karanove Vainio Li Dong - Wilkinson - found INT2 expression (signaling molecule) in early development in the dental papilla - Karanova - found EGR-1 (transcription factor) in developing tooth in both epithelial and mesenchymal cells - Vainio - took agarose beads soaked in BMP4 (signal molecule) and exposed them to mesenchyme cells 🡪 differentiated ; when they covalently bonded BMP to beads, mesenchyme cells did not differentiate - Li - found SMAD (signal transduction molecules) is necessary for differentiation of odontoblasts by making SMAD knock-out mice 🡪 knock-out mice didn't produce DSPP (protein that odontoblasts make) Dong - detected receptors in the tissue

Are there fungi in lesion or teeth?

Wilson Waltimo Waltimo Waltimo Baumgartner Vickerman

What types of microbes are found in the root canals?

Winkler Sundqvist Ozok Vianna Wilson, Waltimo Stevens Hernandez o Winkler - looked at over 1000 teeth (4000 cultures), More than 60% were Streptococci (gram +ve facultative anaerobes). Limitations in this paper with culturing technique and sample collection, therefore results not accurate and showed facultatives as main organisms in infected root canals. (contamination of root canals during access- chance of carrying bacteria from the carious cavity into the root during opening of the canal. Many organisms maybe chance contaminants eg. S.mitus, micrococci) o Sundqvist - looked at infected root canals of non-vital teeth with intact crowns (trauma teeth) - 32 teeth. - over 90% were anaerobic. · Used anaerobic glove box - to put the anaerobic samples in it immediately · 19/32 trauma teeth had PA radiolucency (AP) - 18/19 were infected. No infection found in non-vital trauma teeth w/o lesion. Therefore, if you see a radiolucency in a non-vital tooth, almost always it is infected! (95% of the time) · Bigger the radiolucency - more complex the infection (>5mm - 6+ strains) · More pain - more complex the infection · Pain typically assoc. with Bacteroides melaninogenicus, Prevotella intermedius, Porphyromonas) · 90% were strict anaerobes (compared to Winkler - which were facultative) · as length of time increases, there is increasing chance of tooth becoming infected (1 yr - more chance of infection. Increased from 44% to 70% after 1 yr) · source of bacteria in teeth with intact crowns - gingival crevice. o There is a difference in microbial flora in apical part and coronal part. Apical microbial flora is more diverse and more anaerobic. Done by pyrosequencing of 16s rDNA (Ozok) o Archaea in root canals were found with PCR of 16s rRNA sequence . 2.5% have Archaea (Vianna) o 7-10% of the time, we find yeast (Candida albicans) in root canals (Wilson - 7% , Waltimo - 10%) may play a role in persistent root canal infection where apical periodontitis persists after endo treatment. o Viruses also present in infected root canals. (E.faecalis was isolated from failed endos undergoing retreats. Phage induction was done with mitomycin C. 4 out of 10 E.faecalis strains were lysogenic and resulted in inducible bacteriophages). Significance of presence of virus in infected root canal is not known, but we know that viruses can alter the virulence of the bacteria and transfer genetic info b/w bacteria (transduction). (Stevens) o Herpes virus group (HSV, CMV, VZV, EBV, HHV 6,7,8, HPV) - are mammalian viruses, these viruses are not in bacterial cells, they need mammalian cells. Therefore, not found in AP periodontitis because there are no viable cells in necrotic pulp. These viruses were found in pulp and PA inflammation (but not necrotic tissue) - mainly EBV (40%), CMV (Hernandez)

Which antibiotics should we use for endodontic infections?

Yamamoto Matto Dalhen - Yamamoto showed that penicillins were the most effective for Eubacterium Peptostreptococcus, and Bacteroides - Matto showed that beta-lactamase production was common in some Prevotella species; all these species were susceptible to Amoxicillin-clavulanate - Dahlen showed that enterococcus species were susceptible to vancomycin and erythromycin - AAE guidelines recommend using Amoxicillin 500 mg TID or clindamycin 300 mg QID if patient has a penicillin allergy; if persistent infection, can consider using Augmentin (Amoxicillin + Clauvulanic acid)

Which antibiotics should we use for endodontic infections?

Yamamoto Matto Kononen Andres Dahlen Jacinto Wexler Livermore Pavaskar - Yamamoto showed that penicillins are most effective for Eubacterium, Peptostreptococcus and Bacteroides (indicating that penicillin is suitable for treating acute apical periodontitis as these bacteria (Finegoldia magnus, P.intermedius, P.gingivalis) are commonly found) (this paper had MIC levels but were missing the attainable conc/ breaking point conc. in serum) - Matto showed that beta-lactamase producing bacteria (Prevotella) are not susceptible to penicillins, but by adding clavulanate to Amox, we can achieve the MIC level that is effective against most beta-lactamase producing bacteria. - Kononen shows that penicillin is not always effective in all endo infections (because of beta-lactamase production). This paper looked at F.nucleatum which is commonly found in endo infections, even in children. About half of the strains they isolated had gene for resistance to penicillin (beta-lactamase), so the beta-lactam antibiotics will not work abt half of the time. (NCCLS breakpoint and MIC was used for sensitivity testing). - Andres showed the MIC and breakpoint of different antibiotics against Porphyromonas and Prevotella which are common in endo infections. If the MIC is above the MIC breakpoint, it will not be sensitive to the antibiotic. The table shows why we use a particular antibiotic depends on how sensitive a bacteria is to the antibiotic. - Dahlen shows enterococci is not susceptible to Clindamycin and Metronidazole. So it may not make sense to give clindamycin or metronidazole in most recurrent infections since enterococci (E.faecalis) is often found in recurrent infections. Enterococci is susceptible to Vancomycin and Erythromycin. - Jacinto looked at obligate anaerobes common in apical periodontitis (F.nucleatum, Peptostreptococcus, Porphyromonas) and which antibiotics they are sensitive or resistant to. Amoxicillin , amox + clavulanate, cephalosporins, clindamycin, metronidazole, erythromycin are effective against all obligate anaerobes. (Clindamycin and metronidazole are very effective) - Wexler shows that another generation of quinolones was developed in an attempt to broaden the range of effect on bacteria that for eg. Ciprofloxacin was not effective against. This drug was effective but later withdrawn due to hepatotoxicity. This paper shows that they made efforts to make more effective antibiotics. - Livermore looked at a new class of antibiotics effective against gram +ve cocci. Enterococci strains have become resistant to most antibiotics, last antibiotic it was effective against was Vancomycin, but resistance to Vanco is also developing. Linezolid (bacteriostatic) is a new class of drug shown to be effective against enterococci. Linezolid is effective against gram +ve, not gram -ve. (Linezolid is effective against gram +ve organisms, including vancomycin-resistant EF) - Pavaskar looks at using linezolid as intracanal medicament in endo infections. Linezolid alone and in combo with CaOH is shown to be effective against EF.

Would you have to modify the antibiotic dose?

Yes, do loading dose and take medication more often because dialysis machine is making drug less effective

How does CaOH affect pulp tissue?

Yoshiba Seux - Yoshiba - 20 teeth with pulp exposures capped with CaOH2 and composite 🡪 Fibronectin associated with newly formed calcified layer may stimulate pulp cells to become odontoblasts and make reparative dentin - Seux - Pulp explants were placed next to microcrystals from CaOH 🡪 found odontoblast-like cells in the pulp; Calcium from dycal induces differentiation of pulp cells into odontoblast-like cells - Calcium hydroxide: Causes dentin bridge formation (FRANK 1966). There is a zone of obliteration, a zone of coagulation necrosis, and a line of demarcation before the pulp. Initial effect: It causes a superficial three layered necrosis mediated by hydroxyl ions. The firm necrosis causes a slight irritation and stimulates pulp to defense (inflammation) and repair (matrix formation and subsequent mineralization to calcified hard barrier). ***Effect of Calcium Hydroxide on pulp: Irregular Mineralized Layer > Extensive Dystrophic mineralized tissue > Mineralized areas around macroparticles of TCP and BCP mineralized tissue.

How do you deal with horizontal fracture

Zachrisson, Cvek Zachrisson Jacobson Jacobson, Cvek Andreason Andreason Cvek Heithersay Lemon Cooke

How does the pulp respond to heating or operative procedures?

Zack Trowbridge, peters Eda, Seltzer, Dahl Kogushi Bishop and Turner Searls Baumgartner Felton Abou Rass

1) Diabetes

a) "a disease complex with metabolic & vascular components, the metabolic component involves elevation of blood glucose associated with alterations in lipid protein metabolism resulting from a relative or absolute lack of insulin, vascular component includes accelerated onset of nonspecific atherosclerosis & microangiopathy that particularly affect the kidneys & eyes"

1) Local Anesthetics

a) "loss of sensation in circumscribed area of the body caused by depression of excitation in nerve endings or an inhibition of the conduction process in peripheral nerves"

1) Joint Replacement Prophylaxis

a) Antibiotic prophylaxis is not indicated for dental patients with pins, plates & screws. b) Not usually indicated for pts with total joint replacements (most critical period is up to 2 years after joint placement) c) Patients at risk of hematogenous total joint infection, thus consider Ab prophylaxis: i) Immunocompromised pts (rheumatoid arthritis, systemic lupus erythematosus) ii) Immunosuppressed pts from disease, drugs, or radiation iii) Insulin-dependent (Type I) diabetics iv) 1st 2 years following joint replacement v) previous prosthetic joint infections vi) malnourishment vii) hemophilia d) Suggested antibiotic prophylaxis regimens: i) Pt not allergic to penicillin: amoxicillin, cephalexin or cephedrine 2.0 grams 1 hr prior to tx ii) Unable to take oral meds, NKDA: ampicillin 2 gm IM or IV 1 hr prior iii) Allergic to PCN: clindamycin 600 mg 1 hr prior iv) Allergic to PCN, unable to take oral meds: clindamycin 600 mg IV 1 hr prior e) Procedures with higher incidences of bacteremias: i) Dental extractions ii) Scaling & root planing iii) Implant placement iv) Endodontics past the apex v) Placement of ortho bands (not brackets) vi) PDL injections vii) Cleanings where bleeding is anticipated f) Medical consult - if pt presents with physician recommendation that does not comply to above recommendations; dentist is ultimately responsible for pt

1) Vitamin D Resistant Rickets

a) Autosomal recessive b) Due to failure of renal conversion of calcidiol to calcitriol kidneys fail to resorb phosphorous hypophosphatemia increased blood serum alkaline phosphotase increased osteoblastic activity large quantities of osteoid is made but not mineralized affects teeth & causes large pulp horns to DEJ, hypoplastic enamel, 18% lose lamina dura detection in radiographs without periapical disease

1) Osteoporosis

a) Is due to disturbance in bone matrix formation "osteoid", osteoid must be present for bone to form (mineralize) b) Defined "a disorder characterized by progressive loss of bone mass until the skeleton is inadequate for mechanical support", all bones are affected (especially spine, wrists, hips) c) Manifests from imbalance where rate of bone formation is less than bone resorption due to an aberration in the calcium homeostatic mechanism, which is dependent upon parathyroid hormone & thyrocalcitonin d) Risk factors: age (rate of bone formation & resorption slows down), women > men, white > blacks e) Complications: fractures due to reduction in bone mass f) Post-menopausal Osteoporosis (most common form) i) Deficiencies in estrogen result in development of osteoporosis because estrogen is a known stimulator of osteoblastic activity decreased bone formation while bone is resorbed at normal rate by osteoclasts increased urinary output of calcium & phosphorous g) May be reason Seltzer found less favorable healing in older patients following endodontic therapy in menopausal women, a periapical rarefaction from pulp inflammation &/or necrosis does not heal as readily because osteoblasts are not stimulated to elaborate bone matrix h) Deficiency of vitamin C reduces collagen synthesis (ascorbic acid stimulates the hydroxylation of peptide-bound proline osteoblast dysfunction decreased matrix formation osteoporosis) i) Vitamin C (ascorbic acid) is required for the formation of the collagenous material of all fibrous structures (bone, dentin, cartilage & all non-epithelial cementing structures such as vascular epithelium)

Other diseases (not covered): 1) Hyperpituitarism

a) Pituitary gland influences secretions of all other endocrine glands i) Anterior pituitary secretes hormone which influences skeletal growth b) Disease etiology - hyperactivity of anterior pituitary results: i) Acromegaly - disproportionate enlargement of mandible (prognathic, malocclusion), crowns of teeth normal ii) Gigantism - general, symmetrical overgrowth of the body, size of teeth disproportionately larger

1) Hyperparathyroidism

a) Primary due to benign adenoma or hyperplasia of parathyroid gland b) Secondary due to disturbances to other organs such as kidneys c) Affects all bones of skeletal system d) Causes elevation serum calcium levels & alkaline phosphotase increases osteoclastic & osteoblastic activities with osteoclastic activity exceeding osteoblastic activity generalized demineralization of bone negative bone balance, increased serum calcium excreted thru kidneys but damages them & forms stones for further damage cyst-like cavitations in bone resulting in von Recklinhausen's disease bone defects filled with fibrous tissue radiographically teeth really stand out due to generalized mineral loss in bone e) Treatment - removal of diseased tissue, normal healing Functional Effects of Steroids: 1. Interfere with lymphokines 2. Interfere with antibody synthesis 3. Decrease wound healing 4. Anti-insulinogenic Thus, steroids better for tx vital teeth rather than non-vital teeth

1) Hepatitis (liver disease) - "inflammation of the liver"

a) Results in impaired metabolic function including abnormalities of the metabolism of amino acids, ammonia, protein, carbohydrates & lipids & alters the biochemical functions of coagulation & drub metabolism b) Primary causes i) Drug-induced - alcohol (a direct hepatotoxic drug) (1) Chronic alcoholism liver dysfunction cirrhosis (10 to 15% alcoholics) (2) Pathophysiology - early change is "fatty infiltrate" where hepatocytes become engorged with fatty lobules enlargement of entire liver (reversible) alcoholic hepatitis, a diffuse inflammatory condition with destructive cellular changes (somewhat irreversible), may be due to dietary deficiencies cirrhosis (irreversible damage) characterized by progressive fibrosis & abnormal regeneration of liver architecture = end-stage condition (3) Cirrhosis - results in progressive deterioration of metabolic & excretory functions of the liver leading to hepatic failure with accompanying abnormalities (malnutrition, weight loss, protein deficiency {affects coagulation factors - bleeding tendency}, impaired urea & glucose synthesis, renal failure, portal hypertension...) (4) Dental management (a) Bleeding tendencies (b) Unpredictable metabolism of drubs ii) Toxic hepatitis - halothane iii) Viral hepatitis - acute viral hepatitis is caused by > 5 distinct viruses, each with their own antigenic properties but similar clinical expressions (1) Hepatitis A - formerly called "infectious hepatitis" because infected water or food supply has led to epidemics, RNA virus, test for anti-HAV antibodies, transmitted fecal-oral by fecal contamination of food or water, primarily affects children, usually mild disease, rarely has complications, new vaccine present, no carrier state, recovery usually conveys immunity against reinfection (2) Hepatitis B (& D)- formerly called "serum hepatitis", DNA virus, Dane particle is composed of outer & inner shell (intact HBV), outer shell is HBsAg & its antibody if anti-HBs, inner core is HBcAg & its antibody is anti-HBc, transmitted parenteral by needle, skin cuts, mucous membranes (mouth, eye), saliva or semen contacting mucous membranes, or infected blood but not transmitted via fecal - oral or airborne droplet, any age susceptible, very severe disease, lifetime of complications, vaccine is available, 5 to 10% of pts act as carriers (all carriers must be considered potentially infectious), dentists most concerned with hepatitis B (3) Hepatitis C (Non A, Non B) - common in post-transfusion patients, transmitted parenterally, any age susceptible, occasionally severe disease process, frequent complications, no vaccine, probably has carrier state, 85% acquire disease thru transfusion of blood products or hemodialysis, at risk include health care workers, pts. (4) Hepatitis D - caused by a defective RNA virus that requires presence of HBV for infection, detected serologically by anti-HD, parenteral transmission, common in drug addicts & hemophiliacs. (5) Hepatitis E (enteric form of Non A, Non B) - transmitted fecal - oral, affects young adults, mild disease, complications rare, no vaccine, no carrier state, similar to hepatitis A, not common in USA but is common in 3rd world countries c) Pathophysiology of viral-induced hepatitis i) Degeneration & necrosis of liver cells, entire liver lobule is inflamed & consists of lymphocytes & mononuclear phagocytes ii) Symptoms include jaundice (icterus) due to accumulation of bilirubin in the skin, bilirubin is degraded product of hemoglobin, is a major component of bile, normally carried to liver via plasma but liver disease decreases metabolism & allows it to accumulate in plasma d) Complications of viral hepatitis (common to type B (+/- D), C) i) Most resolve without complications, especially type A ii) 5% type B & 45% type C develop chronic hepatitis causing persistent hepatocellular necrosis & biochemical abnormalities fibrosis cirrhosis; rarely leads to "fulminant hepatitis" which is massive hepatocellular destruction with 80% mortality rate iii) carrier state - 5 to 10% of hepatitis B e) Medical Management i) No specific tx for acute viral hepatitis (true for most viral diseases), thus palliative care only ii) Avoid drugs metabolized by liver which include lidocaine, mepivicaine, prilocaine, bupivicaine, aspirin, acetominophen, codeine, meperidine, ibuprofen, valium, barbiturates, ampicillin, & tetracycline. iii) Corticosteroids probably ineffective iv) Prophylaxis with preexposure or postexposure hepatitis B vaccine (vaccine effective for about 9 years) or postexposure immunoglobulin injection f) Needle stick protocol i) If pt known to be infected, test the vaccinated dentist for adequate titer of anti-HBs if levels inadequate or unknown, inject with HB immunoglobulins & vaccine booster dose, if titer adequate, no further tx required g) Dental Management - no tx planning modifications needed for recovered pts i) Pts with active hepatitis (1) Elective dental care not performed ii) History of hepatitis (1) Medical history fails to identify 80% of carriers of hepatitis B (or D, or C) (2) Universal precautions (3) Minimize use of drugs metabolized by the liver (because pt may have undetected chronic hepatitis) iii) Hepatitis carriers (1) Follow recommendations of CDC to avoid transmission of infection (2) Some have chronic active disease leading to compromised liver function which interferes with hemostasis & drug metabolism (3) Pt has sign or symptoms of hepatitis (a) No elective dental tx, refer to physician for evaluation h) Emergency treatment i) Consult physician ii) Obtain prothrombin time if surgery is planned iii) Strict universal precautions iv) Use isolated operatory v) Minimize use of drugs metabolized by liver vi) Use rubber dam to minimize contact with saliva & blood vii) Minimize aerosol production (use slow speed, avoid high speed & air/water syringe) viii) Perform only absolutely necessary work i) Oral complications i) Potential for abnormal bleeding due to significant liver damage (1) Prothrombin time should be checked & should be less than 2 ½ times normal (35 seconds), if greater than 35 seconds, severe bleeding may result if surgery necessary, injection of vitamin K by physician needed (2) Platelets also diminished, check count (if pt bleeds longer than 20 minutes, platelet replacement needed) j) Secondary causes i) Infectious mononucleosis ii) Secondary syphilis iii) Tuberculosis

1) Organ Transplants:

a) Types: i) Autologous: "self", such as bone marrow removed prior to chemo or rad tx & then returned ii) Syngeneic: identical twin to twin iii) Allogeneic: within the same family (siblings) iv) Haploidentical: donor is parent v) Xenograft: from another human, not related vi) Cadaver organs: largest organ pool; typically just kidneys & bone marrow b/c donors need the other stuff to remain alive b) Immunosuppresive therapy: functions to suppress all immune responses including infections, malignancies i) Regimen: (note: all antirejection drugs predispose pt to infection which is major cause of death in cardiac pts) (1) Cyclosporine: cyclic polypeptide fungal metabolite immunosuppressive by suppressing the ability of T helper (CD4+) lymphocytes to elaborate IL-2, thus blocking an early phase of the immune response (a) Does not suppress bone marrow (b) May cause severe liver & kidney problems HTN, anemia, bleeding problems, gingival hyperplasia (2) Azathioprine: inhibits synthesis of DNA & RNA & thus the immune response; also causes bone marrow suppression leukocytopenia, thrombocytopenia & anemia, therefore at greater risk for infection & excessive bleeding (3) Prednisone (corticosteroid): (a) Increases potency of cyclosporine (b) Suppresses synthesis of growth factors (c) Anti-inflammatory (d) Side effects: (i) HTN (ii) Diabetes (iii)Impaired healing (iv) Adrenal gland suppression which makes pt unable to produce & release amounts of corticosteroids at times of stress (infection, trauma, surgery, anxiety) (v) Thus, steroid increases susceptibility & masks signs if infection c) Dental Management: Get consult rejections & complications must be considered i) Pre-transplant pt: (1) Consult aids in risk : benefit ratio (2) In general, no additional need for prophylactic antibiotics so follow AHA guidelines (exceptions include low WBC count, infection in operative field, those being prepared for bone marrow transplant) (3) Lab tests needed: kidney, liver, pancreas, bone marrow (to identify potential bleeders, prone to infection, inability to metabolize drugs) (4) any potential source of infection over next 12 months she be eliminated oral infection can contribute to rejection of graft... (5) perform preventive dental tx to help combat cyclosporine-induced gingival hyperplasia ii) Post-transplant pt: (1) Med consult (2) Due to immunosuppressives, at increased risk of oral infection may now decide to prophylactically premedicate pt to protect from bacteremias (3) 3 phases of treatment: (a) Immediate post-transplant period (1st 6 months): routine dentistry not indicated, oral hygiene measures are continued (b) Stable transplant period: confirmed by med consult, most dental tx ok, may alter drug selection to avoid drugs toxic to the liver or kidney, consider steroid supplementation, monitor bp b/c cyclosporine & prednisone may cause HTN (c) Chronic rejection period: has signs & symptoms of rejection, refer to physician, only emergency dental work (4) Major concerns are steroid supplements, HTN, bleeding, infections iii) Specific organ considerations (1) Cardiac transplants: anticoagulants, HTN, drug interactions, antiplatelet therapy, angina (2) Bone marrow transplants: prevent infection tx in hospital setting with prophylactic antibiotics, high prevalence of xerostomia, dental caries,, osteoradionecrosis, mucositis (3) Liver transplants: altered drug & protein metabolism, bleeding problems, infection (4) Kidney transplants (often due to renal failure from cardiac arrhythmia): pts on coumadin bleeding problems, drugs metabolized or excreted by kidney should be avoided, platelet dysfunction associated with anemia, pts receiving renal dialysis have shunt that makes them at risk for infective endocarditis antibiotic prophylaxis?

What do we use to diagnose?

fuss klein bender hill - Cold test with CO2 snow (-78.5 C), endo ice or Dichlorodifluoromethane DDM (-50 C)- Fuss - EPT 🡪 Klein showed that EPT is less accurate in younger patients o Plexus of Rashkow is not developed in immature teeth, the more open the apex, the less the response to EPT - Radiographs 🡪 Bender showed that you need 7.1% mineral bone loss in path of x-ray beam and bone loss of the cortex to see radiolucency of a lesion - Transillumination - Hill showed that you can use it as an adjunct for diagnosis

What are the characteristics of black-pigmented Bacteroides (BPB) ?

o Maynard: o BPBs are gram-negative rods, strict anaerobes, non-motile, non-spore forming o They are asaccharolytic (do not use sugars for fermentation), use amino acids (arginine, cysteine etc) hence can survive in necrotic pulp which contains a lot of degraded protein. Require Vit K and hemin for growth. o Breaks down hemoglobin from red blood cells to form hemin. Stores it as protohemin (which gives its black color) o Like other gram -ves, they have inner and outer cell membrane and cell capsule. But they also have vesicles/blebs in the outer membrane (sets them apart) These blebs can break down proteins and agglutinate RBCs.

What are the characteristics of Peptococcus and Peptostreptococcus?

o Murdoch o They are gram positive anaerobic cocci present in normal flora of mouth, skin, upper respiratory and GI tracts. o P.magnus, P micros - in plaque and gingival sulcus, cause periodontal disease, abscesses. o Virulence - synergistic with facultatives, form capsule, proteolytic activity

What is the difference between Bacteroides, Porphyromonas and Prevotella?

o Shah: o Porphyromonas -> gram negative rods, obligate anaerobes, non-motile, non-spore forming. Difference b/w Porphyromonas and true bacteroides: Porphyromonas have i) higher G+C content ii) asaccharolytic (true bacteroides are saccharolytic) iii) bile sensitive (true bacteroides are bile resistant so they can survive in the gut) iv) produce different metabolic end products (n-butyric and acetic acid) Species: P. asaccharolyticus, P. gingivalis, P. endodontalis (differ within species by mobility, produce different enzymes (P. gingivalis produce trypsin- cuts at amino acids lysine and arginine) , produce different metabolic end products. (P. gingivalis-> phenylacetic acid) o Prevotella -> gram negative rods, obligate anaerobes, non-motile, non-spore forming Colonies are translucent, opaque, grey, light brown or black. Hemolysis is variable. Difference b/w Prevotella and true bacteroides: i) different G+C content ii) moderately saccharolytic iii) different metabolic end products Species -> P. intermedia , P.nigrescens. (they have different DNA sequence after looking at DNA homology) o True bacteroides -> saccharolytic, bile resistant, gram -ve anaerobes, non-sporing, non-motile

1 - PREGNANCY

· B.V. ↑ 40-55%; RBC ↑ 15-20%; > 90% develop benign revers. murmurs · B.P ↓ 100/70 during 2nd trimester ↑ WBCs (neutrophilia); ↑ clotting factors 7,8,9,10, fibrin slit products · ↑ need for oxygen b/c 1) enlargement of uterus 2) progesterone decreases airway resistance ↑ respiratory rate · Spontaneous abortion in 15% of pregnancies; Caused by: sepsis, febrile illness · Gestational diabetes in 1-3% of preg women; hormonal changes cause insulin resistance Pre-Eclampsia · 5-8% of pregnancies; ↑ BP, proteinuria, edema · Symptoms: blurred vision, headache, weight gain Eclampsia: · grand mal seizures, coma, death; unknown cause · BP and seizure control is the main management Supine hypotension: · Pressure on IVC causes ↓ return to heart, ↓ BP and syncope, THIRD TRIMESTER, TURN ON LT SIDE Deep vein thrombosis: · Due to ↑ clotting factors; advise pt to move legs Fetus: · 1st trimester (2-8 wks) - formation of organs and systems- avoid elective tx; acceptable OHI, SRP; emerg tx under strict conditions; fetus susceptible to malformations. · 2nd trimester - safest for non-emerg care · 3rd trimester - only emergency tx due to patient comfort/discomfort; induce preganancy · Fetal dose of 2 PAs using lead apron is 700 times less than 1 day of background radiation AVOID: 1) lithium 2) anti-cancer 3) radioactive 4) anti-coagulants 5) tetracycline · Post preg. considerations - give drug right after breast feeding (1% drug transfer to fetus) · NSAIDS: cause post partum hemorrhage and can cause premature closure of ductus arteriosus · Opioids: Associated with congenital defects; use w/ caution · N2O in 2nd and 3rd trimester (but minimize to <30 minutes and with 50% O2), · Benzos: increase chance of clefting · Barbiturates: resp depression · Steroids: anti-insulin; don't use USE VASOCONSTRICTOR TO LIMIT SYSTEMIC ABSORPTION

Why not NSAID?

ç-When patient is on corticosteroid, it is blocking the formation of mucous and now the stomach is more prone to an ulcer. If you give them NSAID you are compounding the problem