RFE205 - Endodontics Midterm

What are the Characteristics of Asymptomatic Apical Periodontitis (AAP)?

*Asymptomatic Apical Periodontitis (AAP)* 1. cc: Nothing major. "Something is there." "Sometimes it acts up." 2. Always linked with *infected* pulp necrosis. 3. Radiographically, distinct PARL. - PARL only develops from infected root canal. - Sterile necrosis does not cause PARL (Moller et al., 1981). 4. Requires RCT with intracanal medication.

What are the Studies that Demonstrate that Bacteria Cause Periradicular Disease?

*Bacteria Cause Periradicular Disease* 1. Animal Models - Kakehashi et al. 1965 - Moller et al. 1981 2. Human Studies - Sundqvist Thesis 1976

What are the Bacterial Virulence Factors?

*Bacterial Virulence Factors* 1. Bacterial Lipopolysaccharide (LPS) - Present in cell wall of gram-negative bacteria - Lipid A moiety that causes severe pain and ostelysis even in the absence of viable bacteria - Use local antimicrobial agents like Calcium Hydroxide to combat this virulence factor *Safavia & Nichols 1993/1994: Inter-appointment Medicaments* 1. Calcium Hydroxide Ca(OH)2 - Ca(OH)2 is effective in hydrolyzing the lipid moiety of bacterial LPS and consequently altering (abrograting) its biologic properties - Cleaves Lipid A from rest of molecule and cause reduction in periapical lesion

What are the Classification of Pulpal Diseases?

*Classification of Pulpal Diseases* *1. Normal* *2. Reversible pulpitis* - Initial stage of inflammation *3. Irreversible pulpitis* - More extensive inflammation *a) Asymptomatic* - Patient can have pulpitis with no symptoms such as seeing a large carious lesion *b) Sympatomatic* - Most will require RCT *4. Pulpal necrosis* *5. Hyperplastic pulpitis*

What are the Classifications of Periradicular Diseases?

*Classifications of Periradicular Diseases* 1. Normal 2. Apical Periodontitis a) Symptomatic (Acute) - Tap on tooth and patient jumps b) Asymptomatic (Chronic) - Tap on tooth, patient doesn't feel any pain, but there is periapical radiolucency 3. Apical Abscess a) Acute b) Chronic 4. Condensing Osteitis - Periapical radiopacity instead, still requires endo

What are the Objectives of Cleaning & Shaping?

*Cleaning & Shaping: Objectives* 1. Remove infected dentinal walls (Cleaning) 2. Enlarge the canal walls into continuous "shape" (Shaping): - Use endodontic hand files - Rotary instruments - Without proper shape, your obturation will be difficult/impossible to fill in

What is Condensing Osteitis?

*Condensing Osteitis* 1. Symptom: none or mild discomfort 2. Etiology: *increase in bone density* in response to low- grade inflammation. Presented as opposite of AAP. 3. Endo test results: mostly necrotic 4. Radiographic findings: diffuse *radiopacity* around the apex, usually found at mandibular posterior teeth. 5. Tx: RCT. - Often in younger adults with good immune function - Only give this diagnosis if see increase in bone density (radiopacity) AND necrotic tooth from vitality test Pic: Radiopacity at apex but coronal surface is normal

What are the Characteristics of Condensing Osteitis?

*Condensing Osteitis* 1. Variant form of AAP - increase in bone density. 2. cc: Variable. Little or no pain. 3. Linked with necrotic pulp in mandibular molars. 4. Tx: RCT resolves lesion.

What are the Characteristics of Conventional RCT?

*Conventional RCT* 1. Access Opening - lateral canal opening can cause other radiolucencies besides at apex 2. Canal Cleaning/ Shaping 3. Obturation - Filling space we cleaned with rubber-based material and using root canal sealers 4. Final Restoration - Anterior teeth: direct restoration like composite - Posterior teeth: if loss of tooth structure loss, then indirect with full coverage crown

What are the Characteristics of the Coronal Leakage Studies?

*Coronal Leakage Studies* 1. Swanson & Madison 1987 2. Madison, Swanson & Chiles 1987 3. Torabinejad, Ung & Kettering 1990 4. Chong BS 1995 - Coronal leakage = bacteria coming from oral cavity - Most infections that cause endo problems are routed through carious process -> the importance of good coronal restoration should NOT be underestimated *Effect of Coronal Restoration on Outcome of Endodontic Treatmetn* 1. Safavia, Dowden & Langeland 1987 - Influence of delayed coronal permanent restoration on endodontic prognosis 2. Ray & Trope 1995 - Periapical status of endodontically treated teeth in relation to the technical quality of the root filling and the coronal restoration

What are the Characteristics of the Dentin as Highly Permeable?

*Dentin is Highly Permeable* 1. Dentin permeability increases from DEJ to pulp-dentin complex: Increase in number and diameter of dentinal tubules - Big enough for bacteria to enter - Dentin mineralization starts from DEJ and migrates pulpally - As you remove more teeth structure, permeability of dentin increases 2. Dentin permeability is higher in occusal vs. axial walls.

What is Asymptomatic Apical Periodontitis (AAP)?

*Asymptomatic Apical Periodontitis (AAP)* 1. Symptom: none 2. Periapical Endo tests: *non-painful response* to percussion or palpation or biting test. 3. Radiographic findings: *presence of Periapical radiolucency (PARL)* 4. Dx: Asymptomatic; PARL 5. Tx: RCT - Pulp Dx? *Always pulp necrosis*; PARL only develops from infected root canal. Picture: - #14 has distinct periapical radiolucency - There is superimposition of maxillary sinus - Non-painful response to percussion and palpation -> lack of response to cold suggest tooth is dead - Explain to patient that we need to do RCT because the tooth doesn't feel any pain, explain bone is loss due to tooth is necrotic

What are the ADA Standards for Reamers & Files?

*ADA Standards for Reamers & Files* *1. Specification No. 28 - 1976* - Fracture resistance - Stiffness - Corrosion resistance - Dimensions - Manufacturing tolerances - Established 19 different instrument sizes (#10 - #140) -> 0.1mm - 1.4mm - Established color code for files *2. Specification No. 58 - 1982* - Physical criteria for hedstrom files (retreatment of infected canal by removing previous gutta percha) *3. No specification for K-files and NiTi files as yet* - Extra: NiTi files made of 50/50 nickel titanium

What are the Objectives of Access Opening?

*Access Opening: Objectives* 1. Debride the infected tissues - Long shank, round burr - Lingual access into pulp space 2. Caries control 3. Locate all canals - Use Endo Explorer 4. Achieve straight-line access into the canal - Find Axial walls and refined with straight-papered fissure burr - Use Endo File for straight-line access

What is Acute Apical Abscess (AAA)?

*Acute Apical Abscess (AAA)* 1. Chief complaint: *swelling* 2. Symptom: *rapid onset; spontaneous pain*. 3. Periapical Endo tests: *severe pain* to percussion or palpation or biting test. 4. Radiographic findings: probably with PARL; PDL might be still intact due to rapid onset. 5. Dx: *swelling!* - Usually in cheek and jaw region 6. Tx: *Incision & drainage; Antibiotics; RCT* - Antibiotics help resolve inflammation in face - Open tooth, drain infection, put medication inside - Most urgent diagnosis, most advanced stage - Facial swelling rapidly develops in 1-2 days - Patient may describe teeth as floating -> out of occlusion - Will jump out of chair if you touch the tooth because of LOTS of pain

What are the Characteristics of Acute Apical Abscess (AAA)?

*Acute Apical Abscess (AAA)* 1. cc: Facial swelling & extreme pain 2. Always linked with pulp necrosis. 3. "Phoenix abscess" - after initial RCT of AAP 4. Radiographically, distinct PARL. 5. Tx: Incision & drainage, initiate RCT, medicate, and antibiotics.

What are the Characteristics of Caries and Pulpal Disease?

*Caries and Pulpal Disease* 1. Bacteria associated with caries: - Streptoccocus mutans - Streptoccous sobrinus - Actinomyces 2. Bacteria associated with deep caries: - Predominantly strict anaerobes (usually gram negative) - Microbial selection by the ecosystem associated with infections of endodontic orgin *Sundqvist 1976: Bacteriologic Studies of Necrotic Dental Pulps* 1. Teeth with intact crowns and periapical lesion were studied 2. Most samples contained more than one strain (mixed flora) 3. Predominance of obligate anaerobic bacteria: - Fusobacterium, Bacteroides, Eubacteirum, Peptococcus, Peptostreptococcus and Camphylobacter *Bystrom 1981, Haapasalo 1989, Sundqvist 1976/1990: Endodontic and Periapical Flora* 1. Root canal flora of *noncarious teeth* with necrotic pulp and diseased periapex is dominated (*>90%*) by obligate anaerobes, usually belonging to the genera: - Fusobacterium, Porphyromonas, Prevotella, Eubacterium, Peptostreptococcus *Baumgartner 1991: Endodontic and Periapical Flora* 1. Microbial composition of root canal of *carious teeth* with necrotic pulp and diseased periapex is less dominated (*<70%*) by strict anaerobes - There are some facultative anaerobes as well

What is a Case Example Shown?

*Case Example* 1. 42-year-old man reported that tooth #19 received PFM crown about 2y ago. 2. Severe pain rapidly started last night. Noticed extra-oral swelling on the lower left quadrant in the morning. 3. Referring pain to the left ear. Ibuprofen does not relieve the pain - This is Acute Apical Abscess (pain started last night, had swelling nextmorning -> patient presents urgently) Testing 1. Dx: Tooth #19- Pulp necrosis and Acute Apical Abscess - Very sensitive to pressure (finger pressure denoted by ++) 2. Emergency Treatment: Pulpectomy; Incision and Drainage; Antibiotics 3. Definitive Treatment: Non-surgical root canal treatment 4. Alternative: Extraction 5. Prognosis: Favorable (with proper treatment) 1. Pulpectomy: open the tooth, instrument, and medicate - *Pus discharged noted upon access* - Relieves some of the high pressure - Leave tooth open for about ~10mins to drain, but HAVE to close it to prevent food debris and bacteria from coming in 2. Incision and Drainage (I & D) - Antibiotics is usually required for systemic involvement - Consider if there is pus underneath - If swelling is firm and you cut open = will only see blood come out - If swelling is fluctuant and you cut open = will see a lot of pus

What causes Pulpal and Periradicular Inflammation?

*Causes of Pulpal and Periradicular Inflammation* 1. Microbial - Mainly Bacterial Irritation 2. Chemical Irritation - Pulpal - Restorative Materials - Periradicular - Root Filling Materials 3. Thermomechanical

What are the Characteristics of Symptomatic Apical Periodontitis (SAP)?

*Characteristics of Symptomatic Apical Periodontitis (SAP)* 1. cc: Main issue is with pressure. Cannot chew. Throbbing pain. Extremely painful to touch or air. 2. Always linked with pulpal disease (IP = Irreversible Pulpitis or NP = Necrotic Pulp). 3. Radiographically, highly variable - thickened PDL or PARL. 4. Requires RCT and ensure full occlusal reduction. - Reduce occlusion so patient doesn't bite down on affected tooth *SAP = symptomatic terminology, not radiographic* - Symptomatic apical periodontitis could potentially have no periapical radiolucency

What are the Characteristics of Chemical Irritation to Pulp and Periapical Tissues?

*Chemical Irritation to Pulp and Periapical Tissues* 1. Restorative materials (resin monomers, eugenol, & chemicals) cause pulpal injury. 2. Pulpal effects are directly related to dentin thickness and permeability. 3. Root canal sealers and gutta percha points cause chronic inflammation. 4. End result is post-op sensitivity or pulp necrosis. *Unemori Study: Composite Resin restoration and post-operative sensitivity: clinical follow-up in an undergraduate program* 1. Studied the relationship between composite resin placement and post-op sensitivity. - Incidence of postoperative sensitivity (IPS) in composite restoration placed in shallow, medium and deep cavities 2. PS is directly proportional to depth of cavitation and types of material used. *Whitworth Study: Endodontic Complications after plastic restorations in general practice* 1. Investigated pulpal disease after direct restoration (602 cases with composite or amalgam) in posterior teeth (3 year recall). 2. Major findings: - Preop pain, cavity lining, or rubber dam use had no effects on the outcome. - What mattered the most: remaining dentin thickness and use of composite vs. amalgam (composite has chemical irritants).

What are the Characteristics of Chronic Apical Abscess (CAA)?

*Chronic Apical Abscess (CAA)* 1. cc: Nothing major. "Something is there." "Sometimes it acts up." 2. *Always* linked with pulp necrosis. 3. Radiographically, distinct PARL. 4. Requires RCT with intracanal medication.

What is Chronic Apical Abscesses (CAA)?

*Chronic Apical Abscesses (CAA)* 1. Chief complaint: *sinus tract*/ "fistula", "blister", "bump", "cold sore" on the gum 2. Symptom: *none...* 3. Periapical Endo tests: non-painful response 4. Radiographic findings: *presence of PARL* 5. Dx: *Sinus tract ("Draining fistula").* - Weird taste in mouth due to pus draining 6. Tx: RCT with intracanal medication; Complete RCT when sinus tract resolves. Do not give antibiotics. Do not perform I &D. - Do RCT, then wait for sinus tract to heal itself before completing treatment (~ 7 days) to know infection has resolved - Pulpal Dx? Always Pulp necrosis. *When you see the sinus tract, always trace it with gutta percha and take another radiograph* - Can put perioprobe in carefully if not causing any pain -> create pathway for gutta percha to flow into furcation area Ex: CAA is Asymptomatic -> True Ex: Different than AAP because of sinus tract *Definitions* 1. Fistula: A fistula is an abnormal connection between two hollow spaces, such as blood vessels, intestines. 2. Sinus Tract : a narrow opening underneath the skin that can extend in any direction through soft tissue and results in dead space with potential for abscess formation & drainage. - When press on sinus tract, can see pus coming out Pic 2: Location of Sinus tract: suggestive of vertical root fracture - If related to endo, will be located at root apex - If at margin, could be vertical root fracture Pic 3: Not very open, hard to get pus to drain out, patient may describe it as an ulcer - If take antibiotics it will resolve, if stop it will come back

Why does Classificaiton of Pulpal & Periradicular Diseases Matter?

*Classificaiton of Pulpal & Periradicular Diseases* - Why does it Matter? 1. To determine the treatment plan: - Perform RCT or not - Retreat vs. apical surgeries - One vs. multiple visits - Need for antibiotics and adjunctive therapy, e.g., IND 2. To assess treatment outcome - Diagnosis affects Prognosis - Teeth with different pulpal PA status have different treatment outcome

What are the Classification of Apical Diseases?

*Classification of Apical Diseases* 1. Normal apical tissue 2. Symptomatic apical periodontitis (SAP) 3. Asymptomatic apical periodontitis (AAP) *4. Chronic apical abscess (CAA)* *5. Acute apical abscess (AAA)* 6. Condensing osteitis

What are the Diagnosis and Treatments for Endo?

*Diagnosis and Treatment* 1. Treatment of vital pulp - Pulpectomy 2. Treatment of necrotic pulp - Root canal treatment of a necrotic pulp will disrupt the microbial ecosystem by removing bacteria, bacterial byproducts, and substrate from the root canal system 3. Emergency Treatment of Necrotic Pulp - Severe infections require multifaceted approach: a) Debridement of pulp space b) Drainage from canal or soft tissue - Need to drain the pus to resolve the swelling - Can do "Incision to drain of the tooth" = I&D or drain from the soft tissue c) Pharmacotherapeutics *Goals of Endodontic Treatmemt* - The core concept of endodontic treatment is therefore directed at: 1. Thorough chemo-mechanical debridement 2. Biomechanical preparation 3. Quality obturation of the root canal system

Lecture 1 - Kang - Endodontic Armamentarium

*Endodontic Armamentarium* 1. Endodontic Instruments and Usage 2. File Types - Stainless Steel - Nicket Titanium 3. Intracanal Medication 4. Smear Layer 5. Temporization

What are the Different Endodontic Instrument Types?

*Endodontic Instrument Types* *1. Hand operated - 1884 to present* - *Files & reamers* - Cleaning/Shaping; Getting access to canals - *Barbed broaches* - Pulp tissue debridement - *Hedstrom files* - Cleaning/shaping; Retreatments; *Aggressive* Instrumentation; Removal of Gutta Percha *2. Engine driven - 1889 to present * - *Constant clockwise* rotary motion - *Nickel Titanium* (NiTi) rotary files & *Gates Glidden* drills - *Reciprocating (90°) files*: WaveOne and Twisted Files - Extra: only the number of confluent roots per unit length of the file is the difference between files and reamers -> file has dense confluences - Barbed broaches can flick off and cause problems - Gate Glidden has flame shaped ends and size are referred by the number of stripes in the shaft ("Number 3 Gates")

What are the Assessment of Endodontic Treatment Outcome?

*Endodontic Treatment Outcome* *Engstrom 1964: Correlation of Positive Cultures with Prognosis of Endodontic Treamtent* - If you reduce bacteria alone within the root canal system, then you will have better prognosis - Success is linked to reduction of bacteria *Sjogren 1997: Influence of infection at the time of root filling on the outcome of endodontic treatment of teeth with apical periodontitis* - Endodontic therapy can fail!

What is the Endodontic Treatment Proper?

*Endodontic Treatment Proper* 1. Endodontic access 2. Working length determination 3. Root canal disinfection 4. Intracanal medication 5. Placement of the root filling 6. Restoration 7. Observation and follow up

What are the Characteristics of the Fabricius Study?

*Fabricius 1982: Etiology of Endodontic Infection* - Influence of Combination of Oral Bacteria on Periapical Tissues of Monkeys 1. Monkey teeth are similar to human teeth - Inoculated monkey teeth to create pulp exposures and induced pulpal necrosis - Analyzed types of bacteria 2. Endodontic infections are *NOT* normal infections, they are mixed infections - Different types of bacteria cause infection and are present in different proportions 3. Took bacteria in equal proportions and inoculated in regular health teeth - After 6 months and sampled necrotic pulp - Found bacteria no longer present in equal proportion but were present in proportion observed initially in necrotic pulp they were removed from - Suggest some bacteria are more dominant than others *Bacteria Found* 1. Streptococcus millieri 2. Streptococcus faecalis 3. Peptostreptococcus anaerobius 4. Actinomyces bovis 5. Propionebacterium acne 6. Bacteroides oralis 7. Fusobacterium necrophorus *8. Fusobacterium nucleatum* - virulent bacteria of endodontic infection

What are the Characteristics of File Design and Cross Sectional Shape?

*File Design and Cross Sectional Shape* - Hedstrom files have cutting edge - K-files (smal)) have square shape and square symbol with 10/15 - Flex R files are triangular = more flexible due to less bulk of material (size 20 to 50, 60, 70) and has rounded handle - Know K files are small ones with 10/15 while other files are bigger - Make sure to use K files before moving onto Flex R files

What is the History of Endodontic Instruments?

*History of Endodontic Instruments* - *1746* - Pierre Fauchard used watch makers reamers to shape the canals. - *1875* - Thin steel wires similar to barbed broaches - 1930 - C.J. Grove made first standardized instruments - *1955* - J.I. Ingle proposed need for stainless standard instruments - *1961* - J.I. Ingle standardized instruments and obturation materials - *1965* - AAE adopted the standard instruments - *1976* - ADA Council on Dental Materials approved "Specification No. 28."

What are the Characteristics of Hyperplastic Pulpitis?

*Hyperplastic Pulpitis* 1. "Pulp Polyp." 2. Gross coronal defects - Complete coronal exposure and hyperplastic pulp 3. Prevalent in young patients. - Often those who are very active 4. Symptom: Usually none 5. Tissue insensitive to touch and highly vascularized. - When you do RC, have to remove all tissue and will bleed a lot 6. Tx: RCT. Histology: - Embryologically the pulp arises from the dental papilla which is ectomesenchyme from neural crest cells, should not have any epithelium - However, pulp polyp outer portion looks like it has stratified squamous epithelium and explains why there is no sensation or hypersensitivity to cold stimuli

Why are Pulpal Diseases Progressive?

*Pulpal Diseases Are Progressive* 1. Pulpal inflammation is non-compliant 2. Pulp is like cranium. - Inflamed cranium pushes against dura *Pulp is highly vascularized tissue

What are the Characteristics of Instrument Sizing and Taper?

*Instrument Sizing and Taper* 1. Lathe ground or micro-machined - Hedstrom, most NiTi, & K-files 2. Ground to shape and then twisted - Ground in square, triangular, and rhomboid - Twisted counterclockwise to produce helical cutting edges - Files have more twist/mm than reamers 3. Lengths - 21, 25, and 31 mm (most done with 25 mm tho) *How to Calculate* *1. Taper - "Degree of change in diameter with respect to change in length."* - "Fatness" - "Conical shape of file" - Taper of file is critical for taper of the canal. 2. Taper = Δ Diameter / Δ Length *Questions* 1. *#30 Flex-R file has D0 = 0.30mm, D16 = 0.62mm, what is the Taper of the File?* -> (0.62-0.30)/16 = 0.32/16 = *0.02 (or 2%)* 2. *What is the diameter of 30 size file at D16 with 0.02 taper?* - Taper x Δ Length = Δ Diameter - 0.02 x 16 mm = (x-0.30) - 0.32 + 0.30 = x - x = 0.62 mm -> *D16 = 0.62 mm* Extra: Most of our standarized file has flute length of 16 mm (thus have D0 and D16) *Files are numbered by D0* - File #10 - 0.10mm at D0 - File #15 - 0.15mm at D0 - File #20 - 0.20mm at D0 - File #25 - 0.25mm at D0 - File #30 - 0.30mm at D0 - File #35 - 0.35mm at D0 - File #40 - 0.40mm at D0 - File #45 - 0.45mm at D0

What are the Characteristics of Intracanal Irrigants Medicaments?

*Intracanal Irrigants Medicaments* *1. NaOCl (6%) - AKA BLEACH* - Most COMMON irrigant - Kills bacteria - Tissue dissolution (by 20mins pulp dissolves) - Multiple tissue reactions - Extremely toxic to tissues NaOCl "accident" (NaOCl pushed out beyond the apex due to irrigant pushed into canal via positive pressure, need to irrigant with saline in canal and prescribe ABX) *2. NaOCl (6%): Technique for intracanal irrigation* - Loaded in 3 ml (3 cc) syringe with safety tip (opening that prevents positive pressure when delivering) - Never engage the needle into the canal (avoid positive pressure) - Always move the needle around in the chamber when injecting *3. Chlorhexidine (2% or 0.12%):* - 2% = irrigant, 0.12% for mouth rinse - Ex: Periogard mouth rinse, as effective as 2% irrigant so we use this - Kills bacteria - No tissue dissolution ability (can forcefully flush canal with some sort of solution) - Safe irrigant, especially if NaOCl is contraindicated. *4. RC Prep (15% EDTA)* - Canal lubricant - To be applied on files - Used to remove smear layer AFTER we do instrumentation *5. EDTA solution (17%):* - Some antimicrobial effects - Remove smear layer

What are the Characteristics of Irreversible Pulpitis (IP)?

*Irreversible Pulpitis (IP)* 1. "Unrepairable pulpal injury." 2. cc: Spontaneous sharp. HS to cold/hot. Maybe asymptomatic. - Pain may radiate to ear 3. Will progress to pulpal necrosis if untreated. - Open tooth and break through pulp horn to see blood oozing out = hyperemic pulp (increased blood flow to this part) 4. Diagnostic feature: Coronal breakdown. Lingering cold and hot sensitivity. - Histology hows microabscess next to furcation of caries - Won't see radiolucency unless its necrotic due to bone loss 5. Radiographically, widened PDL 6. Treatment: RCT *Example* 1. Patient C/O sharp radiating pain on LLQ 2. Pain is mostly with cold and hot 3. "Pain wakes me up at night" 4. "I cannot drink coffee" - 19 is vital so there is coronal breakdown causing lingering hypersensitivity - 18 is non-vital, no response to cold - 19 should be treated first because thats patietn's chief complaint *Example* 1. Patient C/O constaint pain on LLQ 2. Pain started last week after biting on hard food 3. Pain exacerbates with cold and hot -> Symptomatic Irreversible Puplitis - Treat now instead of later

Pictures of Convention RCTs Working

*It Works!* 1. Conventional RCTs are highly successful: - >95% success.

What are the Characteristics of the Kakehashi Study?

*Kakehashi 1965: Etiology of Endodontic Infection* - Bacteria are the etiologic agent of Pulpal Infection and Periradicular Lesion Formation 1. 2 Group of rats: Germ-free vs Normal - Deliberate pulp exposure - Sacrificed mice after end of 2 weeks 2. Results - Germ-free mice retained normal pulpal function - Normal mice developed pulp necrosis which resulted in full destruction and abscess formation 3. Conclusion - Bacteria are the cause of pulpal disease, necrosis, and periapical lesions

What did Kakehashi's Study of Lab Mice Show?

*Kakehashi: Effects of Surgical Exposure of dental pulps in germ-free and conventional lab rats* 1. Classic study to demonstrate: - Microorganisms cause root canal infections after pulp exposure 2. Experimental animals (rats) were kept in normal vs germ-free environment after pulp exposure to maxillary first molars - After 7 days, there was severe tissue destruction in normal rates - At 8 days, normal rat shows colonies of micro-org stained - At 14 days, normal rat shows complete pulpal necrosis in both roots with apical bascess formations - At 14 days, germ-free mice showed dentin bridge repair - At 41 days, normal rat shows two colonies of microorganisms in soft tissues beyond apical foramen 3. Histology of degree of pulp necrosis and inflammation in two different animal groups

Where are the Locations of Microorganisms in Endodontic Infections?

*Locations of Microorganisms in Endodontic Infections* 1. Extraradicular - Resorption of lacunae - Periapical soft tissue lesions - Peridontal plaque on the root surface 2. Intraradicular - In necrotic pulp tissue (the major site) - In dentinal tubules

What are the Characteristics of Microbiologic Analysis of Teeth with Failed Endodontic Treatment?

*Microbiologic Analysis of Teeth with Failed Endodontic Treatment* 1. Nair 2005 2. Sundqvist 1998 - The *microbiologic flora* in root canalas after failed endodontic treatment differs markedly from flora of untreated teeth - The most commonly recovered were bacteria of species *Enterococcus faecalis (most commonly implicated species in FAILED endo treatment)* - Strain is resistant to a lot of chemicals and is able to cause stable biofilms - Microorganisms recovered as single species from root canals after removal of the root filling material = Enterococcus faecalis, Streptococcus sp., Actinomyces israeii, Bacteriodes gracilis, Candida albicans 3. Molander 1998 4. Waltimo 1997 5. Sjogren 1996

For RFE209 Winter Quarter, What are the Tooth Requirements?

*Minimal Teeth Required* - 2 Maxillary Anterior - 1 Maxillary Premolar - 1 Maxillary Molar - 1 Mandibular Molar *Tooth Requirements* 1. Intact crown or small restoration 2. Small decay must be removed and restored with IRM 3. Complete root formation - Closed Apex 4. Visible pulp and canal space 5. Root curvature less than 30 degrees 6. Molars - First molars, separate roots, no thirds 7. For Max Molars, it should fit in the tooth mounting socket! 8. Length - Should be between 21 - 24 mm (edge to apex)

What are the Characteristics of the Sundqvist 1992 Study?

*Sundqvist 1992: Ecology of Root Canal Flora* 1. Associations between prevalent bacterial species in root canal infections 2. Possible nutritional relationships between bacteria in root canal - Endodontic treatment = disrupt bacterial relationships

What are the Characteristics of the Nair Studies?

*Nair 1990: Fungi as a potential agent in the pathogenesis and maintenance of human apical periodontitis* - Fungi can be implicated in failed endo treatment as well 1. Mixed Microbial Flora at the Apical Foramen - In longstanding lesions, lesions will get bigger, and the larger the lesions, the greater the number of bacterial strains present - Biofilm will grow = harder to eradicate *Nair 2005: Biofilms in Root Canal Systems* 1. Organization of microbial flora as biofilms in inaccessible areas of root canal system 2. Treatment measures are needed to disrupt the biofilms and reduce intraradicular microbila load for the most favorable long-term prognosis - Want to begin treatment as early as possible *Stojicic 2013: Effect of Source of Biofilm, Level of Biofilm Maturation, and Type of Disinfecting Agent on Susceptibility of Biofilm Bacteria to Antibacterial Agents* - Conclusion: 1. The change of biofilm bacteria from sensitive to resistant against disinfecting agents occur between 2 and 3 weeks of biofilm maturation 2. The results emphasize the importance of knowing the maturation timeline of each biofilm model used to test the effectiveness of endodontic disinfecting agents against biofilm bacteria *Results of PCR DGGE of Dr. Wenyuan Shi* - Pseudomonas sp. - Fusobacterium nucleatum - Beta proteobacterium - E. faecalis

What are the Characteristics of Niti Files?

*Niti Files* *1. Nickel Titanium..* - 50/50 alloy - Developed by US Navy - 1960 - Highly corrosion resistant - Super elastic (shape memory) - You cannot bend it (if you do see it bent, it is almost separated already) - Higher fracture resistance than stainless steel - Made by micro machine, but some twisted files - Has latch type handles that go into our electric motors

What are the Characteristics of Normal Apical Tissue?

*Normal Apical Tissue* 1. Symptom: no chewing pain 2. Periapical Endo tests: *non- painful response* to percussion or palpation. - Notes: Perc & palp (-). - NOT talking about cold test, periapical test = tap mirror on tooth - Palpation - = no response 3. Radiographic findings: PDL and lamina dura should be intact. 4. Tx: depends on Pulpal Dx - If pulpal necrosis -> need RCT Note: - Cold test + = normal response to cold - Cold test - = tooth doesn't respond to cold

What are the Characteristics of Partial Necrosis?

*Partial Necrosis* 1. Non-standard diagnosis term 2. Cold test might be negative, but some bleeding, inflamed pulp was found after access 3. Usually found in *multiple rooted teeth* - Common in molars 4. Progressive nature of endodontic disease Pic: - Tooth is necrotic but part of pulp is still normal, so will cause bleeding when you open it up - Pulp does NOT die all at once, it is progressive

What are the Characteristics of Periapical Radiolucency of Non-Endodontic Origin?

*Periapical Radiolucency of Non-Endodontic Origin* 1. Commonly found: Periapical Cemental Dysplasia (in woman) 2. Benign lesion occurs *near PDL*, usually at mandibular incisions. 3. Asymptomatic, harmless. 4. Early stage: periapical radiolucency. 5. Late stage: form calcification in the radiolucent area. Mixed lesion. 6. Differential Dx: Pulp vitality. 7. Tx: RCT not required. Monitor. - Radiopacy not necessary for all 3 of these teeth (vital test on all these teeth are normal) - Typical found in incisors of women, commonly middle-aged - Monitor and you ll eventually see it become a mixed lesion (dynamic lesion) - Pulp is normally functional, don't need RCT

What are the Periradicular Diagnostic Tools?

*Periradicular Diagnostic Tools* - *Radiographics* critical for diagnosis to know periapical radiolucency - Sometimes patient has pain in response to percussion

What are the Pet Peeves of Endodontic Files?

*Pet Peeves of Endodontic Files: Torsional Limit* *1. Torsional Limit: Amount of force applied before file separation.* - Smaller files (<20) withstand higher force than larger files. - Machined files deform more readily than twisted files - File separation is one of the main complications of endodontic treatments. *2. How to avoid file separation:* - Inspect each instrument before use - Unwinding occurs during clockwise rotation; roll-up occurs during counterclockwise rotation. - Inspect the tip for brittleness and corrosion *3. During rotation, if you feel "stuck"......* - Stop and pull out the file and inspect for unwinding/roll-up - File separation occurs more readily in counterclockwise direction than clockwise direction Extra: Maybe <3% of the time instrument can separate in the canal, but as long as we can clean the root canal its not a problem - File may be stuck in dentin and if we turn it past torsional limit, it will unwind

What are the Characteristics of the Placement of Root Filling?

*Placement of Root Filling* - Healing of Periapical Lesion

What are the Polymicrobial Endodontic Infection Species?

*Polymicrobial Endodontic Infection* - Recent Taxonomic Changes for Previous Bacteroides Species 1. Porphyromonas, black-pigmented - *Porphyromonas gingivalis* - *Porphyromonas endodontalis* 2. Prevotella, black-pigmented - Prevotell melanogenica - Prevotella denticolla - Prevotella intermedia - *Prevotella nigrescent (Biggest culprit, most prevalence bacteria in severe root canal infections)* 3. Prevotella, non-pigmented - *Prevotella buccae* *Infections dominated by gram-negative anaerobes*

What are the Portals of Entry to the Pulp?

*Portals of Entry to the Pulp* 1. Pulp exposure due to - Crack, caries, trauma 2. Dentinal tubules exposed due to - Caries, fracture - Marginal leakage around fillings - Cavity or crown preparation - Root planing, root resorption 3. From periodontal pockets via - Exposed dentinal tubules - Exposed accessory canals - Blood vessels in case of trauma 4. Transient bacteremia by anachoresis (microrganisms transported in blood/lymph to area of tissue damage) with - Oral bacteria - Other bacteria

What are the Characteristics of the Progression of Pulpal Inflammation?

*Progression of Pulpal Inflammation* 1. Single-Rooted Tooth - We don't know the exact point at which the pulp becomes necrotic - If only part of the pulp is necrotic, patient can still respond to our stimuli and this can be challenging in terms of diagnostic - Irreversible pulpitis = some vital tissue is still responsive to stimuli - Necrotic pulp = pulp NOT responsive to any stimuli (no remaining vital tissue) - Once bacteria populate root canal space -> periapical immune response occurs - 2nd line of pulpal immune defense is set up in periapical region 2. Multi-Rooted Tooth

What are the Pulpal Diagnostic Tools?

*Pulpal Diagnostic Tools* - Subjective symptoms tell you about the patient's experience - Vitality of tooth based on pulp health - When you tap on tooth using back end of mirror, you should observe how patient responds to percussion -> gives info about absence or presence of periapical inflammation - *Vitality/Thermal Response is the uttermost important for pulpal diagnosis*

What are the Characteristics of Pulpal Necrosis?

*Pulpal Necrosis* 1. "Loss of vitality." 2. cc: Usually none. If symptomatic, it is coming from periradicular tissues (acute abscess). Then main issue is with pressure/chewing. - Usually no pain because no vital tissue but may still have discomfort - May have dull ache 3. Mostly necrotic pulp tissue. 4. May be partially necrotic in multi- rooted teeth. - Still have to treat whole tooth - Necrotic changes happen *coronal to apical* direction 5. Radiographically, may be associated with PARL (Periapical radiolucency) - Not all pulp necrosis have PARL 6. Tx: RCT with intracanal medication. *Even if patient doesnt respond to cold, there may be vital tissue left -> May be hyerpsensitive when you put endo file in and cause injury*

What are the Pulpal and Periapical Irritants?

*Pulpal and Periapical Irritants* 1. Bacteria (dental caries and biofilm) are the primary cause of pulp and periapical diseases. - Control = see inflammatory cells - Germ-free = no lesion formation 2. Bacterial invasion is often deeper than radiograph shows. 3. Direct pulp exposure to caries is not required to have pulpal infection and irritation. 4. Dentin is permeable to micro-organisms through dentinal tubules (0.6 - 2.5 um).

What are the Reaction of the Pulp to Bacteria?

*Reaction of the Pulp to Bacteria* 1. Studies shown that if you have superficial caries in enamel along, there are inflammatory processes that will occur in the dental pulp - Not all pulp succumbs to this infection 2. If caries goes untreated, then it will progress into dentin and inflammation of the pulp will get deeper inside the canal 3. If goes untreated, there will be a massive infection of dentinal tubules and lesions from infection will become confluent (no longer just cavity/pulpal inflammation) - Gradual progressing destruction of the pulp

What are the Characteristics of Reversible Pulpitis?

*Reversible Pulpitis* 1. "Reactive inflammatory process." - It is a clinical term 2. cc: Pain with pressure & temperature following an incident. - Often heightened response to cold temperature stimuli 3. Radiographically normal - Do NOT expect to see periapical radiolucency 4. Ex: Incipient caries, acute trauma, restorative procedure 5. Inflammation is self-limiting with time and after removal of insult. 6. RCT is not indicated. Recommend monitor for 2 weeks. *Example* 1. CC: Pain on LLQ 2. Pain started two months ago - Periradicular area of 19 is normal, can find PDL outline = no radiolucency at root - 19 has some inflammation because it responds to cold differently from adjacent teeth

What are the Objectives of Root Canal Obturation?

*Root Canal Obturation: Objectives* 1. Filling the root canal space with "Gutta Percha" and "Root Canal Sealer." 2. Goal - Prevent leakage between RC and Tissue Fluid

What are the Characteristics of Rotary Electric Motor: X-Smart?

*Rotary Electric Motor: X-Smart* - Motor Setting: *1. Speed* - Generally spin NiTi files at 300rpm, some can go up to 500 rpm tho *2. Torque* - Rely on torque limit for safety issues because we don't get tactile feedback like we do with hand files *3. Auto-Reverse* - If stop limit greater than torque limit, it will pull out

What are the Factors Influencing Treatment Outcome?

*Strindberg 1956 - Dependent of result of pulp therapy on certain factors: 6 yr followup of 344 patients* *Strindberg Criteria* 1. Size of Apical Lesions 2. Length of Instrumentation 3. Effect of Obturation Length on Success *Treatment will have Good Results If:* 1. There is no apical lesion 2. Instrument to working length of root canal 3. Obturate within 2 mm from the apex *Treatment will have Poor Results If:* 1. Retreat with apical lesion >5 mm 2. Instrumentation SHORT of apex 3. Obturation beyond root canal length *Dental Factors* 1. Presence of Pulpal and Periradicular Disease: - Diagnosis - Prognosis "coupling" - Presence, size, and shape of PARL 2. Tooth consideration - Complex root canal anatomy: Isthmuses, lateral canals, dentinal tubules, and oval canals. - Oval canals present challenge to clinicians.

What are the Summary Slides for Dr. Khang?

*Summary* 1. Pulpal and periradicular diseases are progressive. 2. Pulpal and periradicular diseases are progressive. Endodontic treatment outcome largely depends on two things: - Pre-Operative condition: Diagnosis - Prognosis Coupling - Persistence of root canal infection - Linked with therapeutic intervention. 3. Outcome also depends on technical mastery of endodontic therapies.

What are the Characteristics of the Sundqvist Study?

*Sundqvist 1976: Bacteriological Studies of Necrotic Dental Pulps - Sweden Human Study* *1. Bacteriological Investigation of the non-vital (necrotic) pulp* - Studied teeth that sustained traumatic injury but remained intact - teeth did NOT have caries, exposed dentin or pulp - Some time after injury teeth underwent pulpal necrosis - Injury caused disruption of blood supply results in necrosis of dental pulp = *sterile necrosis* 2. Sterile Necrosis - No blood supply, no infection yet - Can't last for a long time because bacteria in our body circulate and through different mechanisms bacteria will eventually enter the pulp - Once blood supply severed, metabolic activties cannot be pertained (no oxygen/immune cells) and anaerobic bacteria will thrive 3. Teeth were never exposed to bacteria in oral cavity - Therefore, most virulent anaerobic bacteria survived and will ultimately form an abscess *4. Teeth with intact crowns & periapical osteitis were studied* *5. All teeth (except one), with periapical osteitis (apical periodontitis) harbored bacteria* *6. No bacteria were isolated from teeth without periapical osteitis* - Need bacteria to develop periapical lesion *7. Most samples contained more than one strain of bacteria (mixed flora)* *8. Predominance of obligate anaerobic bacteria:* - *Fusobacterium, Bacteroides*, Eubacterium, Peptococcus, Peptostreptococcus and Camphylobacter *Relationship Between Periapical Lesions and Presence of Bacteria* 1. There is a periapical lesion if there is bacteria present - If no bacteria, then there is no periapical lesion 2. Larger the lesion = more strains of bacteria present

Patient Case 2

- There is crack on the root = radiographic finding and requires extraction

What is of Symptomatic Apical Periodontitis (SAP)?

*Symptomatic Apical Periodontitis (SAP)* - Most common diagnosis we may encounter 1. Symptom: chewing pain/pain to pressure 2. Periapical Endo tests: *painful* response to percussion or palpation or biting test. - Tongue pressed against tooth can cause pain - Just need response to one of them 3. Radiographic findings: *PDL could be intact/widened/presence of PARL* - Radiographic finding not significant, rely on sympatoms/complaints 4. Dx: *Symptomatic* (patient complaint, or clinical exam) 5. Tx : RCT; occlusal reduction - Done to relieve pain when chewing - Pulp Dx? Always linked with pulpal disease (Irreversible pulpitis or Pulp necrosis) Picture: - See large decay near cervical #29 - Pulpal diagnosis is pulp necrosis

What are the Characteristics of Temporization?

*Temporization* *1. Intermediate Restorative Material (IRM)* - Zinc Oxide Eugenol (ZOE) - based. - Excellent short-term sealing (3 weeks) - Must be placed in dry field - otherwise no retention *2. Cavit* - Not used due to leakage *3. Fuji IX* - Gloss ionomer resin - Excellent sealing/build-up material (long-term) *4. Absolutely CRITICAL!!!* - Leakage will cause root canal failure - Inter-appointment temporization: Failure leads to flare-up - Must remain intact until final restoration *5. Procedure:* - Clean the pulp chamber - Dry the field - Add clean cotton pellet (or else harder to remove temporary when do core buildup) - Apply IRM or Fuji IX; 5 mm in thickness - Must be out of occlusion

What are the Characteristics of Thermomechanical Irritation to Pulp?

*Thermomechanical Irritation to Pulp* 1. Pulp hemorrhage associated with crown prep: "Blushing" - Blushing = bleeding inside pulp space due to excessive heat during preparation 2. Temp. change of 5.5°C causes pulpal necrosis in 15% teeth

What are the Characteristics of Tooth and Dental Dam Disinfection?

*Tooth and Dental Dam Disinfection* 1. 30% H2O2 2. 5% Iodine tincture or 0.5% CHX tincture (Moller 1966) 3. 6% Sodium Hypochlorite (Fouad 2003) *Lin: The Effect of Rubber Dam Usage on Survival Rate of Teeth Receiving Initial Root Canal Treatment: Nationwide Population Based Study* - p<0.05 - Study shown that outcome of endodontic treatment is significantly better if tooth is treated with a rubber dam *Van Nieuwenhuysen 1994: Retreatment or radiographic monitoring in endodontics* 1. Endodontic treatment was performed 2. Rubber Dam isolation was used in 51.1% of cases 3. Use of rubber dam had statistically significant influence on the successful outcome of endodontic re-treatment, P<0.05 4. This was in addition to the size of the preoperative periapical lesion, obturation technique and level of root filling

What are the Steps of Endodontic Access in Tooth and Dental Dam Disinfection?

*Tooth and Dental Dam Disinfection* 1. Endodontic Access 2. Root Canal Irrigants/Disinfectants - NaOCl: 8% - 0.5% (primary disinfectant, use 4% at school) - CHX (chlorhexidine): 0.12% - 2% - IKI (iodine potassium iodide): 2% - 5% 3. Removal of Smear Layer - Microfilm - Smear layer created in process of chemomechanical debridement of root canal spear (layer of microcrystalline and organic praticle debris found spread on root canal walls after root canal instrumentation) - Want to expose dentinal tubules to irritants a) Citric Acid b) EDTA 17% c) MTAD *Torabinejad 2003: Removal of the Smear Layer* A. Smear layer on surface of root canal irrigated with distilled water B. Root canal irrigated with 5.25% NaOCl and 17% EDTA

What are the Periapical Responses to Endodontic Infection?

*Wang & Stashenko 1994: Periapical Responses to Endodontic Infection* 1. A periapical immune response occurs when the infection process overwhelms pulpal defenses and destroys the pulp tissue - The second line of local immune defense is then set up in the periapical region 2. The accumulation of inflammatory cells and destruction of bone in the periapical region result in *periapical lesion*

What are the Possibly Treatments when Pulpally Diseased?

*When Pulpally Diseased* 1. Conventional Root Canal Therapy - <10% of cases for root canal fail, can do retreatment 2. Root Canal Retreatments 3. Endodontic Surgery (Apicoectomy) - Make incision around gum line, reflect tissue, treat the root end surgically 4. Extraction & Implant

Practice Case 1

- Can track sinus tract to tooth apex (can assume tooth is necrotic) - Apical diagnosis = Chronic apical abscess - Pulp diagnosis = Necrotic

Endo Cassette and Files Diagram

- K files = square symbol on handle (10/15 numbers, color coded too) - D11T = spreader to fill canal with obturation gutta percha - Glick = plubber and beaver tail burnisher used for temporization of pulp chamber using IRM and finishing the pulp

What are the Characteristics of Pulpal & Periradicular Inflammation?

- Localized Irritants like localized caries cause release of inflammatory mediators that eventually goes through vasodilation, increase pulpal pressure, and ischemia - See inflammation and necrosis at *coronal pulp* and gets worse *apically* (almost always, remember for clinical reasons)

Patient Case 3B

- Most common combination of pulp and Apical Dx requiring RCT

File Design and Cross Sectional Shape Diagram

- Roydent Company

What 3 types of Irritants can cause Pulpal Disease?

1. Microbial 2. Chemical 3. Micromechanical

What are the Characteristics of Endodontic Infections?

1. Often associated with acute emergencies - Patient often present with varying degrees of pain, facial swelling - Often patients are asymptomatic - We treat patients and the teeth, we do NOT treat radiographs 2. Abscesses = soft tissue - Often an acute exacerbation of chronic or pre-existing - Radiolucent area = radiographic sign of osteolysis (breakdown of bone at apex of tooth in response to infection) 3. Endodontic infection ALWAYS start with caries - Start superficially in enamel and eventually extends into dentin through dentinal tubules, progressing towards apex of tooth ultimately causing necrosis of pulp tissue 4. *Bacteria, fungus, and viruses* can be implicated in the diseased process

Chemical Irritation at Periapex Pics

1. Root canal pushed back the apex - Inflammatory cells surround foreign material although material is inert 2. Root canal overfill may cause chronic inflammation and post-op symptom