Exam 2 Combined

- a membrane-bound glycoprotein involved in maintenance of alveolar bone - ALP in GCF are higher in diseased than healthy sites

Alkaline phosphatase

1. MMP-2 - gelatinase A 2. MMP-3 - stromelysin-1 3. MMP-8 - collagenase 2 4. MMP-9 - gelatinase B 5. MMP-13 - collagenase 3

MMP involved in initial destruction of periodontal ECM

- A group of disorders in which autoantibodies towards components of the basement membrane result in detachment of the epithelium from the CT - Deposits of C3, IgG and other Ig.s - 3 types: • Bullous • Benign mucous membrane • Cicatricial (scar formation) - Female predominance > 50 years age - Nicholsky sign (rubbing of the gingiva creates bulla formation) - Treatment: plaque removal with daily use of chlorhexidine and/or topical corticosteroid

Pemphigoid

- Ulcerated (may resemble purulence) - Gingival margin (75% of all cases) - When occurring during pregnancy, the influence of female sex hormones on biological behavior of gingival tissues should be considered - Reddish or bluish, sometimes lobulated, sessile or pedunculated. Bleeding is common - Highly vascular with chronic inflammatory cells

Pyogenic granuloma

- presence of severe periodontitis was associated with a 6X higher risk of worsening glycemic control over 2 year period - treatment with a combination of SRP and oral tetracycline reduced pocket depth and Pg - poor perio are more likely to have elevated HbA1c levels

Studies associating periodontitis and diabetes

- most likely genetic polymorphism - AD - familial aggregation: including transmission among family members

aggressive periodontitis genetic predisposition

- a wasting - a decrease in size of tissue

atrophy

- probing depth + recession

attachment level equals

- expected intermittent multidirectional forces - would occur when a tooth/implant is in normal function (everyday loading)

functional force

- Candididosis - Other mycoses (i.e. histoplasmosis, aspergillosis)

fungal infections causing gingivitis

- bacterial plaque

gingivitis primary etiologic factors

1. gingival disease 2. periodontitis

periodontal disease types

1. Sensory feedback through receptors localized within PDL (viscoelasticity) and within bone (elasticity)... - Necessary for fine tuning of jaw and limb motor control 2. Detection thresholds of 20 µm of thickness in between antagonist teeth and 1-2 g upon tooth loading 3. After placement, detection thresholds of 50-100 µm of thickness and 50-100 g upon tooth loading 4. Teeth - can feel easily and early if the thing we bite is hard or soft - with an implant it takes longer and cannot detect that difference as well/as fast as with teeth

"Tactile Sensibility" and "Thickness Discrimination" between natural teeth and implants

- gingival inflammation, presenting as gingivitis, is not always due to accumulation of plaque

"desquamative gingivitis"

- less than 20 is slight - 20-50 is moderate - 50 is severe

% of bone loss considered slight, moderate, and severe

- <30 years of age but patients may be older - generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors

1999 AAP classification: generalized aggressive periodontitis

- cicumpubertal onset - localized CAL in first molar/incisors (at least 1 first molar must be affected) - no more than 2 teeth are affected other than first molars and incisors

1999 AAP classification: localized aggressive periodontitis

1. extent - localized <30% - generalized >30% 2. severity - slight -- 1-2 mm CAL - moderate -- 3-4 mm CAL - severe -- >5 mm CAL

2 chronic periodontitis classifications?

1. sensitivity 2. specificity

2 factors for the validity of a diagnostic test

1. necrotizing periodontitis 2. periodontitis as a direct manifestation of systemic diseases 3. periodontitis

3 types of periodontitis

1. gingival abscess 2. periodontal abscess 3. periodontitis-related abscess 4. non-periodontitis-related abscess

4 abscesses in the periodontium

1. functional dentition 2. painless function 3. stability of periodontal apparatus 4. psychological and social well being

4 cardinal characteristics of periodontal health

1. pristine periodontal health with a structurally sound and uninflamed periodontium 2. well-maintained clinical periodontal health with a structurally and clinically sound (intact) periodontium 3. periodontal stability, with a reduced periodontium 4. periodontal disease remission/control with a reduced periodontium

4 levels of periodontal health

1. pristine health, structurally sound and uninflamed periodontium - doesn't really exist 2. well-maintained clinical health, structurally and clinically sound periodontium 3. perio disease stability, reduced periodontium (may have underwent crown lengthening...) 4. perio disease remission/control, with a reduced periodontium

4 types of periodontal health

- bacterial zone - neutrophil rich zone - necrotic zone - spirochetal infiltration zone

4 zones found within the necrotic periodontal tissue

1. facultative anaerobe 2. nonmotile 3. virulence factors: - lekotoxins kill PMNs and macrophages - LPS activates cells to produce PGs, IL-1beta, TNF-alpha - Collagenases degrade collagen fibers 4. immunosuppressive factors - lymphocyte suppressing factors - chemotactic suppressing factors 5. translocate across the JE 6. invade the CT

A.A. in aggressive periodontitis

- Occlusal trauma has no role in the severity and pattern of inflammatory periodontal disease progression - In trauma from occlusion, crushing of tooth against bone causes injury to the periodontal ligament at sites of pressure and tension

Advancing Plaque Front Theory (Waerhaug)

_ CEJ is not at the same angle/line as bone level loss - potential to regenerate is okay

Angular (vertical bone loss)

No, but they correlate with clinical attachment level.

Are radiographs diagnostic of periodontal disease

released during tissue destruction - periogard periontal tissue monitors is a chair-sde test kid - marked elevation of AST levels in GCF from sites with sever gingival inflammation - inability to discriminate between sites with severe inflammation with or without attachment loss

Aspartate amino-transferase

- progressive disease in which large to medium sized muscular and large elastic arteries become occluded with fibro-lipid lesions called atheromas - coronary thrombosis and acute MI are common complications - three effects are: increased BP, emboli, decreased quality of blood due to turbulence

Atherosclerosis

- lysosomal enzyme degrades proteoglycans and ground substance - elevated in GCF from sites with severe periodontal disease - high sensitivity and specificity when related to occurrence of clinical attachment loss - good predictor for future periodontal breakdown

Beta-glucuronidase

(CEJ-Crest-2mm) / (CEJ-Apex-2mm)

Bone Loss % equaiton

- conventional radiographs are specific but lack sensitivity - dental CBCT detects periodontal defects in 'in vivo' settings

CBCT

- Often reddish and ulcerated reactive lesion - Fibrous proliferation in which bone or cementum-like hard tissue is formed - Highly cell-rich areas below ulcerated sites - Although usually smaller than 1.5 cm in diameter, can reach a larger size and rarely cause separation of adjacent teeth and resorption of alveolar crest

Calcifying fibroblastic granuloma

- C. albicans, C. glabrata, C. krusei, C. tropicalis, C. parapsilosis and C. guillermondil

Candida species isolated from the mouth

1. Most clinical characteristic of gingival candidal infections is redness of the attached gingiva, often associated with granular surface 2. Different types of oral mucosal manifestations: - Pseudomembraneous (whitish patches that can be wiped off) - Erythematous (red, associated with pain) - Plaque type (whitish plaque that cannot be removed; need to differentiate from oral leukoplakia) - Nodular (slightly elevated nodules of white or reddish color)

Candidosis Clinical characteristics

1. Diagnosis: - A culture on Nickersons medium at room temp - Microscopic examination of a smear of the material scraped from the lesion and stained 2. Treatment: - The use of antimycotic/antifungal agents (i.e. Nystatin given as a mouthrinse or systemically)

Candidosis Treatment and Diagnosis

- Oral carriage of C. albicans in healthy adults is high (it is considered as part of normal commensal organism of oral cavity but also an opportunistic pathogen) - Reduced host defense (immunosuppressed individuals, infant, and adult who has been on antibiotic therapy for some time) - C. albicans is frequently isolated from the subgingival flora of patients with severe periodontitis - Cancer patients receiving high dose radiation or chemotherapy - Patients who are using several different antibiotics over a period of several weeks or months - Diabetic patients - Women who develop vaginal candidiasis - Pregnancy and the use of contraceptives

Candidosis found?

- Painless or slightly sensitive - Red and white lesions - Lesions can be scraped or separated from mucosa

Candidosis lesions

- signs and symptoms that are confined to the gingiva - the presence of dental plaque to initiate and/or exacerbate the severity of the lesion - there are clinical signs of inflammation

Characteristics Common to All Gingival Diseases

1. plaque present at gingival margin 2. disease begins at the gingival margin (inflammation confined to the free and attached gingiva and do not extend beyond MGJ) 3. reversible with plaque removal 4. change in color 5. change in gingival contour 6. sulcular temperature change 7. increased gingival exudate 8. bleeding upon provocation 9. absence of attachment loss 10. absence of bone loss

Characteristics of plaque-induced gingivitis

- whole genomic digoxigenin-labeled DNA - up to 40 oral bacterial species in a single test - not been generalized for diagnostic purpose

Checkerboard DNA-DNA hybridization

- AR - rapid periodontal destruction around primary and permanent teeth which occurs before puberty

Chediak Higachi syndrome periodontal manifestation

- absence of BOP, erythema, edema - no patient symptoms and attachment/bone loss - physiological bone levels range from 1.0 to 3.0 mm apical to the CEJ

Clinical features of gingival health on an intact periodontium

1. sign of inflammation - redness & swelling - plaque index, gingival index 2. periodontal probing - PD, BOP, CAL 3. tooth mobility 4. furcation involvement 5. radiographs - bone changes - amount of bone loss

Clinical manifestation of periodontitis

- occlusal trauma may be a co-destructive factor that alters the severity and pattern of inflammatory periodontal disease - Periodontal disease (PD) may find a pathway into the PDL

Co-destruction Theory (Glickman)

- paper strips placed within the crevice for 30 seconds - fluid volume can be quantified by Periotron - captured samples may not represent the entire periodontium - selection of the teeth and sites is often difficult

Collecting GCF sites

- color - texture/edema - bleeding - exudate - plaque

Common clinical changes from health to gingivitis

- Theory: spread of bacteria from the oral cavity causes many chronic diseases

Concept of focal infection as a cause of systemic disease?

- Severe malocclusion - Non-ideal but tolerated occlusion - Severe wear - Patient in pain - If no suitable end point

Contraindications to occlusal therapy by selective grinding

- hand-foot-and-mouth disease - A common contagious vesicular viral disease affecting skin and oral mucosa including gingiva - Primarily seen in children - Mainly caused by coxsackie viruses A6, A10, A16

Coxsackie virus

- chronic granulomatous infiltrates of the wall of the GI tract (mucosal folding/defective neutrophil functions)

Crohn's disease

- doesn't take into account other morphologic factors like root number and shape - favorable is 1:2 - unfavorable is 2:1

Crown to root ration

- measure the total contents of GCF - used to characterized GCF from healthy, gingivitis, and periodontitis sites - vibrations of peptide groups: C=O stretching (amide I band) and N-H bending (amide II band) - IR spectroscopy of GCF is reagent free, requiring only small sample volumes, requiring minimal training for operator - high sensitivity and specificity

Diagnosis of Periodontitis based on IR spectra of GCF

1. Etiology... Bacteria (NPDs) - Herpes simplex virus (PHS) 2. Symptoms - Ulceration and necrotic tissue, yellowish white plaque (NPDs) - Multiple vesicles which burst leaving small round fibrin covered ulcers (PHS) 3. Duration... - 1-2 days if treated (NPDs) - 1-2 weeks (PHS) 4. Contagious - No (NPDs) - Yes (PHS)

Differential diagnosis of necrotizing plaque diseases (NPDs) and primary herpetic gingivostomatitis (PHS)

- Occlusal trauma does not initiate periodontitis - Consistently weak evidence that occlusal trauma alters the progression of periodontitis - Lack of evidence that periodontal occlusal trauma leads to gingival recession

Does occlusal trauma initiate periodontitis and why?

- May be caused by accumulation of melanin, deposits of drug or drug metabolites, synthesis of pigments under the influence of a drug, or deposition of iron following damage to the vessels - Antimalarial drugs (Quanine derivatives such as quinolone, hydroxyquinolone, amodiaquine) - Longterm use of minocycline

Drug-induced pigmentation (DIP) (antimalarials; minocycline)

- Porcelain fracture - Implant to abutment (screw loosening or fracture) - can fracture that little piece of screw - may have to remove the whole thing if the screw breaks even if bone integration is fine - Implant fixture fracture - this is the part that is sitting in the bone, this is not fun (hopefully figure out the problem before it gets to this)

Early signs of heavy loading on implants

- AD - aggressive periodontitis in both permanent and primary dentitions - fragility of gingiva - excessive hemorrhage

Ehlers-Danlos syndrome periodontal manifestation

- proteolytic enzyme found in lysosomal granules of neutrophil - Periocheck is a chair-side test kit - positive correlation of elastase in GCF with clinical attachment loss

Elastase

- Fibrous epulis: irritation fibroma/focal fibrous hyperplasia - Calcifying fibroblastic granuloma (ossifying fibroid epulis, peripheral ossifying fibroma) - Pyogenic granuloma (vascular epulis) (telangiectatic granuloma, pregnancy granuloma, pregnancy tumor, vascular epulis) - Peripheral (or central) giant cell granuloma (giant cell epulis, peripheral giant cell reparative granuloma)

Epulide Types

- Acute, sometimes recurrent, vesiculobullous disease affecting both mucous membranes and skin - Oral involvement is uncommon - Swollen lips often with extensive crust formation of the vermilion border - Bullae that rupture and leave extensive ulcers - Characteristic skin lesions (iris appearance + bullae) - Extensive necrosis: Stevens-Johnson syndrome (oral, ocular, genital, skin) - May occur at any age but mostly young individuals

Erythema Multiforme

- Appears to be a cytotoxic immune reaction towards keratinocytes precipitating by a wide range of factors including herpes simplex virus and various drugs - Histopathology is not specific - Treatment: plaque control, local/systemic corticosteroids

Erythema multiforme of palatal mucosa

- The red counterpart of leukoplakia in the sense that is a red lesion, which cannot be diagnoses as any other disease - Erythroplakia usually has a higher premalignant potential - The lesions are uncommon and seldom affect the gingiva

Erythoplakia

- associated with the activity of matrix metalloproteinases - produced by inflammatory, epithelial, and CT cells

Extracellular destruction enzymes

- A local fibrous hyperplasia causes by irritation - Sessile, well-circumscribed smooth-surfaced nodules - Cell-pool, hyperplastic collagenous tissue - May show hyperkeratinization - The size varies from small to large tumorlike processes with a diameter of several centimeters

Fibrous Epulis

- Immediate loading (at the time of placement) - Early loading (before conventional healing time) - Late loading (following 3 or 6 months based on location) (conventional way) - Main thing to look at is primary stability to decide

Functional loading of the implant phases

- pathological resorption of bone within a furcation - shows up as a radiolucency - lower molar it is called a furcation radiolucency - upper molar it is called a furcation arrow

Furcation bone loss

1. over 1166 proteins present, 65 indicative of periodontitis - host-derived enzymes and their inhibitors - byproducts of tissue breakdown - inflammatory mediators and host-response modifiers

GCF proteins

1. provides supplemental information 2. biological features of the disease - history-based analysis of the rate of periodontitis progression - assessment of the risk for further progression - analysis of possible poor outcomes of treatment - assessment of risk that the disease or its treatment may negatively affect the general health of the patient

Grading of periodontitis

1. Crohn's disease - gastro-intestinal diseases 2. Sarcoidosis 3. Persistent enlargement of the soft tissues in the oral cavity as well as the facial region can occur concomitant with various systemic conditions 4. No consensus on whether orofacial granulomatosis is a distinct clinical disorder, or an initial presentation of Crohn's disease or sarcoidosis, or an allergic reaction

Granulomatous inflammatory conditions - orofacial granulomatosis

- a vertical defect in the presence of adjacent roots - half of a septum remains on one tooth - one-walled defect

Hemiseptal defect

1. chicken pox or shingles affecting V nerve 2. Virocella-zoster virus causes varicella (chicken pox) mainly in children (in later life = shingles) 3. Small ulcers usually on the tongue, palatal and gingiva 4. Latent in the dorsal root ganglion 5. Unilateral lesions 6. 2nd and 3rd branch of the trigeminal ganglion 7. Skin lesions may be associated with intraoral lesions, or intraoral lesions may occur alone 8. Initial symptoms are pain and paresthesis

Herpes (varicella) zoster virus

1. Diagnosis: - Usually obvious due to unilateral occurrence of lesions associated with severe pain 2. Treatment - Soft diet, rest, atraumatic removal of plaque, and diluted chlorhexidine rinses - This may be supplemented with antiviral drug therapy

Herpes (varicella) zoster virus diagnosis and treatment

1. Lifethreatening in immunocompromised patients 2. If sampling is needed, aspiration from vesicle is the best way! 3. Blood samples to determine increase antibody titer against virus (works better for primary infection) 4. Histopathology is not specific 5. Treatment: - Careful plaque removal to limit bacterial superinfection of ulcerations - Systemic uptake of an antiviral medication such as acyclovir

Herpes virus infection overview and treatment

- Granulomatous disease caused by Histoplasma capsulatum - Acute and chronic pulmonary histoplasmosis and a disseminated form... immunocompromised patients - Any area of the oral mucosa (mainly tongue) - Nodular or papillary and later may become ulcerative tyope of lesions with pain - Diagnosis: clinical view and histopathology, systemic manifestations - Treatment: systemic antifungal therapy

Histoplasmosis

- CEJ at same angle/line as bone level loss - good to regenerate

Horizontal bone loss

1. intracellular destruction enzymes 2. extracellular destruction enzymes

Host-derived enzyme types

1. More than 100 types of HPV 2. Following types are detected in oral lesions (total 25): 1- 7, 10, 11, 13, 16, 18, 31-33, 35, 40, 45, 52, 55, 57, 58, 59, 69, 72, 73 3. Benign lesions associated with HPV infection: • Squamlous cell papilloma • Condyloma acuminatum • Verruca vulgaris • Focal epithelial hyperplasia 4. Oral benign HPV lesions are mostly asymptomatic and, may persist or regress spontaneously

Human papilloma virus (HPV)

1. Type I reactions (immediate type) - mediated by IgE 2. Type IV reactions (delayed type) - mediated by T-cells - 12-48 hours following contact with allergen

Hypersensitivity Reaction

- Dental restorative materials (type IV, contact allergy) [mercury, nickel, gold, zinc, chromium palladium, acrylics and others] - Oral hygiene products, chewing gum and food (generally flavor additives or preservatives) - A diffuse fiery red edematous gingivitis sometimes with ulcerations or whitening

Hypersensitivity reaction allergies to?

- vibrating covalent bonds of organic molecules absorb a characteristic wavelength of IR light - wavelength of light absorbed depends on the nature of the covalent bond, the type of vibration, and the environment of the bond - the spectrum of absorbed light can be used to establish a molecular fingerprint of a tissue or fluid

IR spectroscopy

- increasing mobility of adjacent teeth - if there is a reduced periodontium this is often missed - if you load a single implant or 2-3 together the opposing or adjacent teeth start becoming more mobile

Implant in excessive occlusion - effect on tooth mobility

- malocclusion is often observed following functional loading of the dental implant - implant cannot move but the teeth can

Implant in excessive occlusion - eruption of adjacent teeth

1. Cytokines - TNF-alpha - IL-1alpha - IL- 1beta - IL-6 - IL-8 - PGE2 2. traditional immunoassays analyze only a single cytokine at a time 3. bio-plex cytokine assay: multiplex bead-based assays designed to quantitate multiple cytokines

Inflammatory mediators from GCF

- tooth resorption beginning within the pulp

Internal resorption

- Intracoronal splints (require tooth preparation) - Occlusal adjustment by selective grinding - Orthodontics - Orthognathic surgery

Irreversible method of occlusal therapy

- no! - you can have health once you recover from disease but your risk for disease is very high - heath is defined as site based and case based - healthy patients can have inflamed sites

Is health just the absence of disease?

No.

Is using the integrity of crestal lamina dura a good indicator for the need of periodontal treatment

- Acute and chronic leukemia based on clinical behavior, and lymphocytic/lymphoblastic or myeloid depending on their histogenetic origin - Oral lesions occur in both but more common in acute form - The signs and symptoms are varied - Bacterial, viral, and fungal infections including candidosis and herpes simplex infection may also be present

Leukemia

- acute leukemia consists of cervical lymphadenopathy, petechiae, and mucosal ulcers - swollen, glazed, and spongy gingival tissue - gingival bleeding as initial signs of acute and chronic leukemia due to thrombocytopenia and clotting factor deficiencies - gingival enlargement due to leukemic cells and the infiltration of gingivae

Leukemia and gingivitis

- Lesions occur most frequently on the buccal mucosa, mandibular gingiva, tongue, and floor of the mouth - It manifests clinically as homogenous and nonhomogenous subtypes - The size of the lesions and clinical features are determinants of the prognosis. Thus, larger lesions and non-homogenous types of lesions imply a greater risk of malignant transformation than homogenous leukoplakia

Leukoplakia manifestation

- Oral involvement alone is common - Prevalence = 0.1-4%; any age but rare in children - A premalignant potential(0.5-2%) - Characteristic skin lesions (Wickham striae) - Various clinical appearances (popular, reticular, plaque-like, atrophic, ulcerative, bullous) - Any area of the oral mucosa - Patchy inflammation at marginal gingiva - Reticulated hyperkeratotic lesions - Popular, reticular, plaque-like forms... generally asymptomatic - Atrophic, ulcerative, bullous forms... generally symptomatic - Subepithelial, band-like accumulation of lymphocytes and macrophages characteristic of a type IV hypersensitivity reaction - Fibrin in the basement membrane - Deposits of IgM, C3, C4, and C5 - Inflammatory reaction toward an undifferentiated antigen in basal epithelial layer/basement membrane zone

Lichen planus

1. lack of sensitivity and reproducibility 2. probe depth depends on: - gingival inflammation, insertion force, placement and angulation, size, probing technique, probe calibration, presence of subgingival calculus, overhanging restorations

Limitations of Probe penetration

1. limited sensitivity in small bone change - changes in bone may be identified by eye one after 30-50% of bone mineral has been lost 2. no value in evaluating disease activity or progression

Limitations of Radiographic Examination

1. Degeneration of basal cells and increased width of basement membrane 2. Deposits of various immunoglobins, C3 and fibrin along the basement membrane - Discoid forms (mild chronic which affects skin and mucous membrane) - Systemic forms of the disease (can be fatal)

Lupus Erythematosus Histology

- Autoimmune CT disorders in which autoantibodies form to various cellular constituents - Central atrophic area with small white dots surrounded by irradiating fine white striae with a periphery of telangiectasia (vascular lesion formed by dilation of a group of small blood vessels - Lesions can be ulcerated and cannot be differentiated from leukoplakia or atrophic oral lichen planus - Together with characteristic skin lesions (butterfly) - Atrophic gingival discoid lupus erythematosus

Lupus erythematosus

- General term given to tumors of the lymphoid system - Most common hematologic malignancy - May originate from B and T-lymphocyte cell lines - Two forms: Hodgkin and non-Hodgkin lymphoma - Oral manifestations of Hodgkin lymphoma are rare

Lymphoma

- bony exostosis on the lingual aspect of the mandible - normally in the premolar-molar region - commonly bilateral

Mandibular Tori

- secreted by fibroblasts and macrophages - responsible for remodeling and degradation of ECM components - regulated by tissue inhibitors of MMPs - high levels in GCF are at greater risk for progression to periodontitis - GCF MMP level reduces in response to treatment

Matrix Metalloproteinases

- may be seen as far forward as the distal of the 1st premolar and as posterior as the mesial of the 1st molar

Mental foramen radiographic location

- gold standard method - assess for antibiotic susceptibility of microbes - only grow live bacteria: strict sampling and transport conditions are essential - putative pathogens are fastidious and difficult to culture - low sensitivity: detection limits for selective/nonselective media average 10^4 to 10^5 bacteria - sophisticated equipment and experienced personnel required; time-consuming and expensive

Microbiologic Testing - Bacterial Culturing

- alternative to culture method - dark-field or phase-contrast microscopy - morphology and motility of bacteria in a plaque sample - most of the main putative perio pathogens are non motile and difficult to identify

Microbiologic Testing - Direct Microscopy

- Pg, Tf, Aa possess a common trypsin-like enzyme that hydrolyzes a substrate BANA - chairside kit was available in the 90s - inability to distinguish between different bacteria - may be positive at clinically healthy site - negative result doesn't rule out the presence of other important periodontal pathogens

Microbiologic Testing - Enzymatic Methods

1. use AB that targets specific bacterial Ag - direct and indirect immunofluorescent microscopic assay - able to id pathogens using a plaque smear - used mainly to detect Aa and Pg - comparable to bacterial culture - does not require viable bacterial cells

Microbiologic Testing - Immunodiagnostic Methods

1. cytofluorography (flow cytometry) - complexity and cost prevents use 2. Enzyme-linked immunosorbent assay (ELISA) - used to detect serum antibodies to perio pathogens - membrane immunoassay: chairside use to detect Aa, Pg, and Pi 3. Latex agglutination - based on binding of protein to latex - latex beads are coated with species-specific antibody - currently these are only for research

Microbiologic Testing - Imunodiagnostic method types

1. analysis of DNA, RNA, and structure or function of protein from target microorganisms 2. Types - nucleic acid probes - checkerboard DNA-DNA hybridization - PCR - Real-time PCR

Microbiologic Testing - Molecular Biology Techniques

1. Expensive and well training personnel required - bacterial culturing - direct microscopy - immunodiagnostic methods - enzymatic methods - molecular biology techniques

Microbiologic tests of periodontal diseaes

- supragingival plaque composition - subgingival biofilm composition

Microbiological determinants of periodontal health

- an intra-bony resorptive lesion involving one or more surfaces of supporting bone

Moat-like defect

1. trauma from occlusion without periodontitis 2. trauma from occlusion with periodontitis: but no co-destruction 3. trauma from occlusion with periodontitis: co-destruction occurs

Models for role of occlusal trauma on the periodontium

- Poxvirus family - Contagious disease with infrequent oral manifestations - Infants with immature immune systems (mainly skin lesions) - In adults, lesions in genital areas and often sexually transmitted

Molluscum contagiosum virus

plaque-induced gingivitis

Most common form of periodontal disease

0: calculus is absent 1: supragingival calculus but no subgingival calculus is present 2: supragingival and subgingival or subgingival calculus only is present

NIDR calculus index measures

- measure of oxygen saturation of the tissues - wavelength region (500-600 nm) dominated by absorption from oxygenated and deoxygenated hemoglobin - tissue oxygenation at periodontitis sites significantly decreases as compared to gingivitis and healthy control sites

NIR spectroscopy

- involvement of palatal mucosa --> necrotizing stomatitis - involvement of regional lymph nodes - typically related to severely compromised immune system (HIV infection, malnutrition) - may develop into life-threatening situation - fever and malaise - poor hygiene - moderate elevation of temperature can be observed - white membrane of desquamated cells, bacteria, saliva proteins - membrane can be easily removed

Necrotizing Ulcerative Periodontitis

- bacterial origin - Necrotizing gingivitis (only gingival tissues with absence of attachment loss) - Necrotizing periodontitis - Necrotizing stomatitis (ulceration extending >1 cm from the gingival margin, including beyond the MGJ) - A constant and variable part of the microflora in NPD lesions have been described - There are both constant and variable flora

Necrotizing periodontal diseases (NPDs)

- height of the crest lies at a level about 2 mm below the level of the CEJs of adjacent teeth - normal crest follows the CEJ

Normal Height of Alveolar Crest?

- space between tooth root and alveolar bone containing the PDL - appears as a PDL space of 0.4 - 1.5 mm on radiograph - tends to be wider at the apex and alveolar crest and narrow in the mid-root areas

Normal PDL space

- synthesized and labeled DNA (20-30 nucleotides) - genomic DNA probe (whole strand DNA); significantly decrease in sensitivity and specificity due to cross-reactivity to non-target microorganisms - 16S rRNA - oligonucleotide probes (high sensitivity and specificity)

Nucleic Acid probes

- Periodontal occlusal trauma - Post-orthodontics - Prior to extensive restorations - Certain types of TMD - Certain wear patterns

Occlusal therapy by selective grinding indications

- secondary - traumatic occlusion by itself won't cause periodontal loss - may be a primary etiological factor for peri-implant disease

Occlusal trauma is a ______ etiological factor for perio disease

1. Some of the changes may represent adaptation 2. Some may be due to extension of inflammatory periodontal disease without occlusal trauma as a factor 3. Widened PDL Space (left) and/or thickened radicular lamina dura 4. Trabecular bone - Hypofunction - Hyperfunction 5. Angular bone loss & furcations - Controversial - May purely be due to tooth and bony anatomy and the progression of inflammatory periodontal disease

Occlusal trauma: radiographic signs

- PDL attachment apparatus - allows them to adapt to heavy forces, there is physiologic movement - teeth do better than implants with heavy occlusion or forces - Can "adapt" to heavy forces - Tooth mobility as a physiologic/pathological phenomena - Bone, PDL, and cementum

Occlusion on natural teeth

1. An uncertain background 2. Examples: lesions in contact with dental restorations, lesions associated with various types of medications (NSAIDs, diuretics, beta-blockers, etc.), a group of systemic diseases (liver disease) 3. Treatment: - Take biopsy (handling is different than regular biopsy) - Take sample for culture if questioning candida infection (about 38% of OLP cases have secondary infection) - A traumatic dental plaque control - Topical corticosteroids to control pain, discomfort

Oral lichenoid lesion

- buccal and lingual wall - two wall defect - a cup/bowl shaped defect in the interalveolar bone - show up on PA but not as well on BW

Osseous Crater

- high sensitivity and specificity for the identification of target pathogens - PCR lower detection limit (25-100 cells) - unable to quantify pathogens accurately in clinical samples

PCR

- facial gingiva surface is divided in 3 scoring units: P-M-A - gingival units affected with gingivitis are counted - presence of inflammation is counted as 1 - absence of inflammation is counted as 0 - severity component can be considered - score computed for tooth subject population

Papillary-marginal-attachment index

- AR - rapid periodontal destruction around primary and permanent teeth which occurs before puberty

Papillon-Lefevre syndrome periodontal manifestation

- Autoantibody reactions against hesmidesmosome and lamina lucida components - Complement-mediated cell destructive processes may be involved in the pathogenesis

Pemphigoid histology

- a localized collection of pus within the tissues of the periodontium - 3rd most common emergency condition in clinic (8-14%) - rapid destruction with a negative effect on the prognosis of the affected tooth - associated with tooth loss - severe systemic consequences

Periodontal Abscesses

1. bacteria - similar to those in periodontitis - P. gingivalis (50-100%) 2. risk factors - pre-existing periodontal pocket - non-periodontitis patients

Periodontal Abscesses etiology & risk factors

- diverse family of complex and distinct pathological entities found within the periodontium that are the result of a variety of etiologies

Periodontal disease

- Almost entirely on the basis of its clinical manifestation

Periodontal disease is currently diagnosed by?

- free from inflammatory periodontal disease - allows an individual to function normally and avoid consequences due to current/past disease - site based and case based - 4 types

Periodontal health

1. before disease commences but can be restored to an anatomically reduced periodontium as well

Periodontal heath can exist ____ but can be restored _____ as well

1. Tooth extraction >>> sensory amputation - You basically remove all the sensation from there 2. Myelinated fiber content of the inferior nerve reduced by 20% (in that area after tooth extraction) 3. Presence and potential function of sensory nerve fibers in the bone and peri-implant environment - Sensory is different around the implant so patient will hit harder on it before they feel anything 4. Gradual increase in free nerve endings close to implant-bone interface during healing 5. Existing mechanoreceptors in the periosteum

Periodontal tactile perception and peri-implant Osseoperception

- Individuals with poor oral hygiene have an increased risk of developing chronic respiratory disorders - Patients with a history of COPD have significantly more periodontal attachment loss than subjects without COPD - Reviews failed to detect conclusive evidence for an association between periodontal disease and COPD

Periodontitis and risk of COPD

1. Respiratory pathogens can colonize dental plaque and serve as source of subsequent infection, resulting in hospital-acquired pneumonia - 50% of healthy subjects aspirate oropharyngeal contents during normal sleep - It is plausible that plaque can serve as a reservoir for bacteria that cause hospital-acquired pneumonia 2. An association between periodontitis and hospital-acquired pneumonia is emerging, but further study is needed 3. Oral hygiene is likely to become an important consideration for hospitalized patients at risk for pneumonia

Periodontitis and risk of bacterial pneumonia

- Anywhere on the gingival mucosa (mostly marginal gingiva) - Most common reactive lesions of the oral cavity (30% of all reactive lesions) - Pedunculated (has a stalk), sessile (broad base), red or purple, commonly ulcerated - Focal collection of multi-nucleated osteoclast-like giant cells with a richly cellular and vascular stroma separated by collagenous septa - Probably originated from periodontal ligament

Peripheral (or central) giant cell granuloma

1. inflammatory response of the gingival tissues resulting from bacterial plaque accumulation located at and below the gingival margin 2. loss of symbiosis between biofilm and host immunoinflammatory response, and development of an incipient dysbiosis 3. various systemic factors, including endocrinopathies, hematologic conditions, diet, and drugs can modify response

Plaque-Induced Gingivitis

- Uncommon inflammatory condition - Usually anterior maxillary gingiva - Uncertain etiology - Diffuse gingivitis and chelitis due to contact allergy to flavor additive in dentifrice

Plasma cell gingivitis

- if the maxillary sinus is close to or has invaginated among the roots of the maxillary teeth, there may be difficulties with surgical treatment of the perio problems

Position of the maxillary sinus and surgical treatment?

1. through oral mucosal epithelium, virus penetrates a neural ending and travels to the trigeminal ganglion 2. Symptoms: - Painful severe gingivitis with redness - Ulcerations with serofibrinous exudate - Edema accompanied by stomatitis 3. Characteristics - Incubation period is one week - Formation of vesicles, which rupture, coalesce and leave fibrin-coated ulcers - Healing within 10-14 days

Primary herpetic gingivostomatitis

- excessive force - normal periodontium

Primary occlusal trauma

- assess bone loss - condition of alveolar crest - pattern of bone loss - bone loss in furcation area - width of PDL space - trabecular pattern and gradient - vessels in interdental bone - local factors: calculus, defective restoration - pathologic considerations: caries, root resorption

Radiographic Assessment of Periodontal Conditions

- thickened radicular lamina dura - widened PDL space

Radiographic signs of occlusal trauma

- real time PCR: good correlation between the fluorescent signal measured and the number of bacterial cells being used - expensive and sophisticated technology in real time PCR

Real-time PCR

1. Herpes labialis (more than once per year) 2. Vermilion border and/or the skin adjacent to it 3. 20-40% of individuals with primary infection 4. Trauma, UV light exposure, fever, menstruation 5. Diagnosis - Generally considered an aphtous ulceration - Ulcers in attached gingiva and hard palate

Recurrent herpetic infections

- Herpes virus can stay latent in trigeminal ganglion for years - Found in gingivitis, Necrotizing Periodontal Diseases (NPDs) and periodontitis - Mostly seen in adults and mostly mistaken for aphthous ulcerations - More primary viral infections occur at older ages in industrialized society

Recurrent intraoral herpes simplex lesions

- Night guard (bite plane) - Extracoronal splints - Muscle relaxants (medications) - Muscle exercises

Reversible method of occlusal therapy

if the roots are less than 2.5 mm apart you may have loss that happens quickly - periodontal bone loss will affect the entire interproximal area

Root proximity and bone loss

1. type and concentration of specific periodontal pathogens - apply DNA PCR - id specific periodontal pathogens 2. genetic susceptibility to periodontitis in individuals - test genetic variations: over expression of IL-1alpha and IL-1beta - determine risk factors but not if destruction will occur

Salivary Diagnostic tests can determine what?

- Melanocytic pigmentation of the oral mucosa due to cigarette smoking - Mostly observed on the mandibular anterior facial gingiva

Smoker's melanosis

- severity of disease at presentation - complexity of disease management

Staging of periodontitis based on

- revealed significant association between poor oral health and MI - reported periodontitis is associated with a small increase in risk for coronary heart disease in men - small association between tooth loss and coronary heart disease - periodontitis can influence atheroma formation - A.a, P.g. T. forsythia, T. denticola and atherosclerosis relationship - there was a 2-fold increase in the risk of CHD in subjects with periodontitis vs healthy subjects

Studies with evidence for associating periodontal disease and atherosclerosis

- If TFO with increasing mobility and inflammatory infiltrate (periodontitis) occur at the same site - The two lesions merge - Downgrowth (apical migration) of pocket epithelium - Enhanced (accelerated) attachment loss = co-destruction

Summary: TFO, increased tooth mobility & periodontitis → co-destruction

1. also known as biological width 2. histological dimensions of the dento-gingival junction in heath: - .69 mm sulcus depth - .97 mm epithelial attachment - 1.07 mm CT attachment 3. minimum of 3 mm coronal to alveolar crest for healing and health

Supracrestal attached tissues

- If TFO and inflammatory periodontitis are separate (independent) processes - No enhanced attachment loss

TFO & periodontitis - no co-destruction

- ECM of periodontium composed of collagen, proteoglycan (versican, decorin, biglycan, syndecan) and non-collagen proteins - elevated levels of hydroxyproline (collagen breakdown), glycosaminoglycans (matrix degradation) and osteocalcin and Type I collagen (alveolar bone destruction) can be found in GCF from sites with periodontitis

Tissue breakdown products from collagen destruction

periodontal examination and radiographs

Traditional diagnostic procedures

1. tooth adapts, no influence on the course of periodontal disease - No attachment loss • Previous attachment loss (reduced but healthy periodontium)

Trauma From Occlusion with no inflammation

- injury to the periodontium - injury to teeth - an injury to the attachment apparatus as a result of excessive occlusal forces

Trauma from occlusion may include

1. Reduced periodontium: periodontitis and trauma from occlusion - Supracrestal periodontitis lesion - Supracrestal periodontitis with occlusal trauma lesion: independent processes - Supracrestal periodontitis lesion with adaptation to occlusal trauma - Supracrestal periodontitis after occlusal therapy (not valid): must control periodontitis first

Trauma from occlusion with periodontitis: but no co-destruction

1. Reduced periodontium: periodontitis and trauma from occlusion (TFO) - Subcrestal (infrabony pocket) with inflammatory infiltrate (periodontitis) - Subcrestal periodontitis with TFO: conditions are established for co-destruction 2. Periodontitis and trauma from occlusion - Then periodontitis merges with increased tooth mobility (occlusal trauma): co-destruction occurs - Subcrestal periodontitis after occlusal therapy (not valid): must control periodontitis first

Trauma from occlusion with periodontitis: co-destruction occurs

1. Injury results in acute (not plaque associated) inflammation 2. PDL collagen destruction 3. Cementum resorption 4. Bone loss 5. No attachment loss 6. Adaptation may occur: tooth may become mobile, but no further injury 7. Development of occlusal trauma with jiggling forces (heavy forces on a normal periodontium) - Injury to PDL and cementum 8. Adaptation and with occlusal therapy - Adaptation: mobility, widened PDL space - With occlusal therapy: signs of occlusal trauma may diminish 9. Reduced periodontium without periodontitis (secondary occlusal trauma) - Reduced, but healthy periodontium - Reduced healthy periodontium with TFO: no further attachment loss - Reduced periodontium: adaptation and with occlusal therapy - Adaptation: mobility, widened PDL space - With occlusal therapy: signs of occlusal trauma may diminish

Trauma from occlusion without periodontitis

- there was a perio problem and at some point the tooth became necrotic and then there was an endo problem - pulpal and periodontal pathologies initiate independently and coalesce

True combined lesion

- use a probe with a hollow tapered tip that is filled with water for coupling of the ultrasonic beam into the tissues - non-invasive

Ultrasonic Periodontal probing

- 5%

Using digital subtraction, what percentage of change is needed to be visible

- appear as radiolucent lines bordered by thin radiopaque lines

Vessels within Inderdental bone on radiograph

gene polymorphism

What molecular marker is a risk marker for periodontitis

- caries

What's wrong here?

- defective restoration -- may accumulate plaque leading to gingival inflammation....

What's wrong here?

- radiographic calculus -- make it difficult to clean with a toothbrush

What's wrong here?

Periapical radiolucency

What's wrong here?

- abundant fluid and easy to collect and store - highly enriched content of disease biomarkers such as Sjogren's and oral cancers

Why use saliva for diagnosing perio disease

1. reproducibility - ability to produce the same result every time the test was repeated in the same patient 2. validity - ability of a test to discriminate between people with and without disease

accuracy of periodontal tests affected by what 2 factors?

1. necrotizing periodontal diseases 2. periodontal abscesses 3. endo-perio lesion 4. pulp necrosis 5. pericoronitits 6. herpetic gingivostomasis

acute lesions in the periodontium

1. complement components - opsonization - lysis - chemotaxis 2. protease inhibitors - alpha2-macroglobulin 3. C-reactive protein - opsonization 4. fibrinogen - coagulation factor - chemotaxis 5. plasminogen - degrades blood clots

acute phase reaction cascade: important proteins

- macrophages - fibroblasts - endothelial and other cells

acute phase reaction cascade: local reaction

- TNF-alpha - IL-1 - IL-6 - IFN-gamma

acute phase reaction cascade: mediators

- fever and leukocytosis - complement activation - C3a, C5a - serum glucocorticoids increased - altered synthesis of acute phase protein

acute phase reaction cascade: secondary systemic reaction

- infection - necrosis - surgery - neoplasia - radiation

acute phase reaction cascade: triggering factors

- mechanism by which periodontitis could potentially influence systemic diseases - triggering factors → local reactions→ mediators→ secondary systemic reaction

acute-phase reaction cascade

- lack of deep pockets - merging of papillary and marginal involvement - characteristic foetor - central necrosis results in crater formation - involvement of periodontal ligament and alveolar bone (NUG --> NUP)

advanced lesion of necrotizing periodontal disease

- spirochetes (treponema) - fusiform bacteria - P. intermedia - Selenomonas

aggressive causative agents of necrotizing periodontal diseases

multifactorial - develops as a result of complex interactions between specific host genes and the environment - inheritance of AgP susceptibility is insufficient for the development of the disease -- also need exposure to virulent pathogens - host inability to effectively deal with bacterial aggression and to avoid inflammatory tissue damage results in initiation of the disease process - interactions between disease process, environment, and genetic controls all contribute to determining the clinical manifestation of the disease

aggressive periodontitis is considered to be a ____ disease

- localized - generalized

aggressive periodontitis may be identified as either?

- refer to periodontist - full mouth scaling and root planing - Amoxicillin + Metronidazole - possible periodontal surgery - supportive therapy: after resolution of the infection, patient should be placed on a tailored maintenance care program

aggressive periodontitis treatment principles

- implants should be parallel to each other - distal implants will tilt distally about 20 degrees - cantilever will be short so the distal implant isn't traumatized much - middle implants will be parallel to each other

all-on-4 technique

- Pigmentation of the oral mucosa due to amalgam - Well-defined bluish, blackish, or greyish discoloration - Radiographic imaging may demonstrate amalgam debris

amalgam tattoo

- pathogens translocate from the mouth to the placenta - weaken placenta and the mom can have a preterm birth - severe periodontitis were 4x more likely to deliver preterm infants

association between periodontitis and adverse pregnancy outcomes

1. preterm low birth weight: < 2.5 kg - preterm birth: <37 weeks - intrauterine growth restriction - combination 2. preterm birth often result in longterm disabilities - GU tract infection is a known risk factor for preterm low birth rate

association between periodontitis and adverse pregnancy outcomes

- periodontitis results in translocation of bacteria and endotoxin into the systemic circulation - inflamed periodontal tissues produce significant quantities of inflammatory mediators including IL-1beta, IL-6, TNF-alpha, and PGE2 - cytokines may have systemic effects

association between periodontitis and preterm birth and low birth weight

- Pemphigus vulgaris - Pemphigoid - Lichen planus - Lupus erythematosus

autoimmune disease causing gingivitis

• Neisseria gonorrhoeae (gonorrhea) • Treponema pallidum (syphilis) • Streptococcal gingivitis (strains or streptococcus) • Mycobacterium tuberculosis (TB) or other organisms

bacteria involved in a gingival lesion of specific bacterial origin

- Necrotizing periodontal diseases (NPDs): - Neisseria gonorrhoeae (gonorrhea) - Treponema pallidum (syphilis) - Mycobacterium tuberculosis (tuberculosis) - Streptococcal gingivitis (strains of streptococcus)

bacterial infections causing gingivitis

- change in gene transcription from non-inflamed to inflamed gingival units - host-bacterial interactions - host cell chemotaxis - phagocytosis and degranulation - novel cellular/molecular pathway signaling - T-lymphocyte response - angiogenesis - epithelial immune response

biologic changes as modifiers for gingivitis

- effect of periodontal bacteria on platelets - invasion of endothelial cells and macrophages by periodontal bacteria - endocrine-like effects of pro-inflammatory mediators - systemic pro-inflammatory mediators are up-regulated for endocrine-like effects in vascular tissues - studies show chemotaxis and fibrinogen are elevated in periodontally diseased subjects - S. sanguis and P. ging may induce thrombo-embolic events mediated by collagen platelet aggregation associated proteins made by bacteria - gingipains from p.ging up-regulate expression of angiopoeitin 2 and down-regulate angiopoeitin 1 in heart cells, promoting atherosclerosis

biological rationale: pathways relating atherosclerosis and periodontitis

- bleeding tendency is assessed upon probing a periodontal pocket using standardized pressure - periodontal probe is inserted into bottom of pocket - bleeding is observed 15 seconds following retraction of probe - presence of bleeding is scored as 1 - absence of bleeding is scored as 0 - not to be confused with bleeding as scored in GI - valid indicator for periodontal stability - poor indicator for periodontal breakdown

bleeding on probing

- Implant doesn't do well with lateral forces - Implant becomes loose over time, patient can fracture the implant from the screw - hard to retrieve it - Longer and wider dental implants are better to tolerate challenges (if you can) - Surrounded with thick bone support - Forces parallel to long axis of the implant are ideal because we cannot control lateral forces

bruxism and implants

- a large blister or skin vesicle filled with fluid

bulla

- simplified oral hygiene index - periodontal disease index - probe method - calculus surface index - marginal line calculus index - NIDR calculus index

calculus indices

- examiner's reluctance to rate at either the positive or negative extreme, so all scores cluster in the middle

central tendency error

1. healthy gingiva is firm and resilient 2. with inflammation: - increase in ECF and exudate - degeneration of CT and epithelium - engorged CT and thinning of epithelium 3. soft, swollen, friable 4. in severe gingival disease: sloughing with grayish flake-like debris (necrosis)

changes in consistency of the gingiva from health to gingivitis

1. signs and symptoms limited to the gingiva 2. reversibility of the disease by removing the etiology 3. the presence of high dental plaque 4. systemic modifying factors which can alter the severity of inflammation 5. stable (non-changing) attachment levels on a periodontium which may or may not experience a loss of attachment or alveolar bone

characteristics common to all dental-plaque induced inflammatory gingival conditions

1. Etching - surface etching by various chemical products with toxic properties - Examples: chlorhexidine-induced mucosal desquamation, acetylsalicylic acid burn, cocaine burn - Incorrect use of caustics by the dentist 2. Chlorhexidine 3. Acetylsalicyclic acid 4. Cocaine 5. Hydrogen peroxide 6. Dentifrice detergents 7. Paraformaldehyde or calcium hydroxide

chemical (toxic) insults to gingiva

- fibrosis and epithelial proliferaiton

chronic inflammation can induce?

- most prevalent in adults - destruction is consistent with local factors - subgingival calculus a frequent finding - variable microbial pattern - slow to moderate progression with periods of rapid progression - can be associated with local predisposing factors - may be modified by and/or associated with systemic diseases - can be modified by environmental factors

chronic periodontitis

- pocket formation - loss of attachment - bleeding/suppuration - bone loss - tooth mobility and drafting

chronic periodontitis clinical manifestations

adult periodontitis

chronic periodontitis formally known as

- A.A - P. gingivalis - B. Forsythus - P. intermedius - E. corrodens - P. micros - C. rectus - F. nucleatum - T. denticola

chronic periodontitis microbes

- changes in gingival morphology - BOP - increased probing depth - attachment loss - gingival recession - alveolar bone loss: vertical or horizontal - furcation involvement - increased tooth mobility - drifting of teeth - tooth loss

clinical features of chronic periodontitis

- pain (spontaneous or mastication) - percussion sensitivity - mobility - radiographic signs - other clinical signs -- no swelling -- no increased probing depths

clinical periodontal-endodontic interrelationships

• Fiery red edematous painful ulcerations • Asymptomatic chancres • Mucous patches • Atypical non-ulcerated, highly inflamed gingivitis

clinical presentation involved in a gingival lesion of specific bacterial origin

- ulceration of necrosis of interproximal papillae - pain - bleeding - bone destruction - other: halitosis, adenopathy, fever

clinical presentation of necrotizing periodontal disease

- enlarged gingival contours due to edema or fibrosis - color transition to a red or bluish-red hue - elevated sulcular temperature - bleeding upon stimulation - increased gingival exudate

clinical signs of inflammation

normal: coral pink + pigmented - tissue's vascularity and overlying epithelial layers inflamed: red - increased vascularization and decreased epithelial keratinization severely inflamed: red + cyanotic - vascular proliferation and reduction in keratinization + venous stasis -- changes start at interdental papillae and gingival margin and spread to the attached gingiva

color changes in the gingiva from health to gingivitis

- systemically healthy - rapid attachment loss and bone destruction - familial aggregation

common features of aggressive periodontitis

• Treponema species • Selenomonas species • Fusobacterium species • Prevotella intermedia

constant bacterial flora in an infection

- gingivitis on an intact periodontium - gingivitis on a reduced periodontium in a non-periodontitis patient (recession/crown lengthen) - gingival inflammation on a reduced periodontium in a successfully treated periodontitis patient

dental plaque biofilm induced gingivitis

- Biopsy - Microbiologic examination

diagnosis involved in a gingival lesion of specific bacterial origin

1. probing depth 2. gingival recession 3. CAL = probing depth + gingival recession 4. BOP (expressed as % of total sites available) 5. furcation involvement 6. mobility 7. fremitus: mobility of a tooth in occlusion 8. bone defects: - horizontal vs vertical - 1 wall, 2 wall, 3 wall bony defects

diagnosis of chronic periodontitis

- implant diameter is more critical than the length in reducing the bone stress - If you need to go short, you should go fat - Create more surface - Going wider is more important than going longer - important because we are very limited in vertical height in some areas (maxilla posterior, maxillary sinuses coming down after extractions) (on the mandible we have the mandibular nerve, the bone could be resorbed already)

diameter and length of implant importance

1. distinguish between a periodontal abscess and: - periapical (endodontic) abscess - vertical root fracture - endo-perio abscess - other: -- osteomyelitis -- periodontal cyst -- tumors: SCC, myxoma

differential diagnosis of a periodontal abscess

1. biopsy to differentiate from other diseases like: - primary herpetic gingivostomatitis - oral mucosal diseases: vesicular bullous disease

differential diagnosis of necrotizing periodontal disease

- no

does gingivitis always progress to periodontitis?

- no, not directly

does plaque induced gingivitis cause tooth loss?

generalized

does smoking affect localized or generalized aggressive periodontitis more?

- A.A - P. ging - E. corrodens - T forsythus - F. nucleatum - Campylobacter rectus

dominant microorganisms in aggressive periodontitis

- necrotic lesion of the papilla initially then progressing to gingival margin - punched-out appearance - spontaneous bleeding - pain

early clinical signs of necrotizing periodontal disease

1. both diseases are more likely to occur in persons who are: - older - male - of lower socioeconomic or educational status - smokers - hypertensive - under psychological stress - diabetic 2. observations suggest two diseases may share similar risk factors or common pathways

early observations relating atherosclerosis and periodontitis

- after you load the implant, there is another phase of adaptation - wound healing never stops around implants

effect of functional implant loading

- perio patients treated with SRP experienced significant reduction in serum CRP and IL-6 - patients with a favorable clinical response to SRP were 4X more likely to exhibit decreased CRP than patients with poor clinical reponse - other studies haven't shown biomarkers consistently reduced perio therapy

effect of periodontal therapy on cardiovascular disease biomarkers

- very few studies have been conducted - recent large multi-center pilot study was not conclusive because the subjects treated periodontal therapy did not have a sustained improvement of their periodontal health - lack of strong evidence that treatment of periodontitis reduces risk of atherosclerotic vascular disease

effect of periodontal therapy on prevention of cardiovascular events

- patients who have favorable clinical response to non-surgical periodontal therapy exhibited a concomitant improvement in endothelial function -

effect of periodontall therapy on endothelial function

- puberty-associated gingivitis - menstrual cycle-associated gingivitis - pregnancy-associated gingivitis - pregnancy-associated pyogenic gingivitis - diabetes mellitus-associated gingivitis

endocrinotropic gingival diseases

complications include perforations, vertical fractures - 75% will fracture - taking away the pulp makes the tooth brittle, adding a restoration and bite is off leads to fracture

endodontic therapy: effects on the periodontium

- >47% of US population has periodontitis -- ~65 million people - 8.7% mild periodontitis - 30% moderate periodontitis - 8.5% severe periodontitis

epidemiology statistics of chronic periodontitis

- bacterial plaque in a susceptible host

etiology of aggressive periodontitis

- forces that well exceed those of teeth/implant in function - examples would be cantilevered implants

excessive forces

1. localized - <30% of sites 2. generalized > 30% of sites

extent of chronic periodontitis

- resorption of tooth structure beginning on the external surface

external resorption

- Usually seen in young patients - Unusual tissue damage in areas that can be easily reached by fingers and instruments

factitous injurt

- probing force - probe angulation - tissue condition

factor affecting probe readings

- Limited physical trauma from brushing may result in gingival hyperkeratosis, a white leukoplakia-like lesion

frictional keratosis

- increases bone to implant contact - 100% bone-implant surface contact isn't possible - it is super important to control the loading - maximum successful implants have up to 60% contact, the rest is emptiness

functional loading increases?

1. Candidosis (most common mouth mycosis) 2. Other mycoses (i.e. histoplasmosis, aspergillosis, blastomycosis, coccidioidomycosis, paracoccidioidomycosis, cyrptococcosis, geotricosis, mucormycosis) 3. Oral mycoses can cause acute, chronic, and mucocutaneous lesions 4. Most common fungal infections that may affect oral cavity: - Candidosis - Histoplasmosis

fungal infections causing gingivitis

- usually affects persons under 30 but patients may be older - poor serum antibody response to infecting agents - pronounced episodic nature of destruction of attachment and bone - generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors

generalized aggressive periodontitis

- more than 30% of the sites with clinical signs of gingival inflammation

generalized gingival enlargement

more than 30% of the sites with clinical signs of gingival inflammation

generalized gingivitis

- hereditary gingival fibromatosis

genetic disorders causing gingivitis

1. with increasing inflammation: - dilation and engorgement of capillaries - thinning or ulceration of the sulcular epithelium 2. chronic or recurrent bleeding, provoked by trauma 3. spontaneous bleeding occurs in acute/severe gingival disease and may be related to systemic health problems

gingival bleeding and gingivitis

1. leukemia-associated gingivitis - gingival lesions are primarily found in acute leukemia - reductions in dental plaque can limit the severity of lesion

gingival disease associated with blood dyscrasias

1. ascorbic acid-deficiency gingivitis - malnourished individuals have a compromised host defense system which may make individuals susceptible to infectious diseases - the precise role of nutrition in periodontal diseases remains to elucidated - human studies have failed to show a relationship between nutrition and periodontal diseases

gingival disease modified by nutrition

- drug influenced gingival enlargements - oral contraceptive associated gingivitis

gingival diseases modified by medications

- endocrine system (endocrinotropic) - blood dyscrasias - medications - nutrition

gingival diseases modified by systemic factors associated with?

- chronic inflammatory response characteristic with exudative and proliferative features - clinically deep red lesions with soft, friable, smooth, shiny surface and bleeding tendency - relatively firm, resilient and pink lesions with greater fibrotic component, abundant fibroblasts and collagen fibers

gingival enlargement

1. < 10% of sites with BOP 2. no probing depths of 4 mm or greater that BOP 3. optimal improvement in other clinical parameters and lack of progressive periodontal destruction

gingival health on a reduced periodontium in a stable patient: BOP and inflammation

1. isolated and delayed BOP in one or two sites 2. inflammation in one or two sites

gingival health on an intact periodontium: BOP and inflammation

- gingival health is < 10% bleeding sites with probing depths < 3 mm

gingival health: number of allowable bleeding sites?

1. severity of inflammation is assessed in 4 distinct areas: - distofacial papilla - facial margin - mesiofacial papilla - lingual gingival margin 2. scores: - 0-3 - bleeding is considered - presence of bleeding automatically leads to a score > 2 3. score for tooth, subject, population 4. useful for the calculation of prevalence and severity in population and individual 5. frequently used index in clinical trials

gingival index

0: healthy gingiva 1: mild inflammation - slight change in color - slight edema - no BOP 2: moderate inflammation - redness - edema - glazing - BOP 3: severe inflammation - marked redness - edema - ulceration - spontaneous bleeding (eat, chew, blood on pillow)

gingival index criteria 0-3

- Infective gingivitis and stomatitis - The lesions may be due to bacteria - The lesions may or may not be accompanied by lesions elsewhere in the body - associated with periodontal attachment loss - may progress to Noma or cancrum oris

gingival lesions of specific bacterial origin

1. Factors that may cause oral pigmentation: - Drugs - Heavy metals - Genetics - Endocrine disturbances (Addison's disease) - Syndromes (Albright syndrome, Peutz-Jegher syndrome) - Postinflammatory reactions 2. Physiological pigmentation is usually symmetric, occurring on the gingival, buccal mucosa, hard palate, lips, tongue

gingival pigmentation / melanoplakia

- Gingival pigmentation - Gingival pigmentation/melanoplakia - Smoker's melanosis - Drug-induced pigmentation (antimalarials; minocycline) - Amalgam tattoo

gingival pigmentation causing gingivitis

1. prevalence and severity of gingivitis are increased in general, unrelated to the amount of dental plaque present - deeper probing depths - increased BOP - increased bleeding during toothbrushing - elevated flow of gingival crevicular fluid 2. pregnancy may also be associated with the formation of pregnancy-associated pyogenic granuloma 3. changes appear during 2nd trimester 4. exaggerated localized host response modulated by levels of endogenous hormones

gingivitis and pregnancy

- peri-mucositis - inflammation limited to mucosa

gingivitis around implants

1. early studies - all gingivitis led to periodontitis 2. late studies - gingivitis and CP separate entities 3. gingivitis can be stable for years 4. bacterial plaque induces gingivitis but host response determines is CP will develop 5. now gingivitis and CP are different aspects of the same disease

gingivitis as a risk factor for chronic periodontitis

1. local factors - calculus - marginal deficiencies in restorations and rough surfaces - malocclusion - tooth/root anomalies

gingivitis secondary etiologic factors

- eliminate etiology - eliminate or reduce risk factors - prevent recurrence

goals of treatment of chronic periodontitis

- Crohn's disease - Sarcoidosis

granulomatous inflammatory conditions causing gingivitis

- examiner's general impression of target distorts his/her perception of the target on specific dimensions

halo effect

1. Diffuse gingival enlargement 2. Disease entity or a part of a syndrome 3. Example: hypertrichosis, mental retardation, epilepsy, hearing loss, growth retardation, abnormalities of extremities) 4. May interfere with or prevent tooth eruption 5. Possible mechanism (s): - TGF-β1 favor the accumulation of ECM - May be located on chromosome 2 in human - defect in the Son of Sevenless-1 gene on chromosome 2p21-p22

hereditary gingival fibromatosis

- Acantholysis (due to destruction of desmosomes) Pericellular epithelial deposits of IgG and C3 - Circulating antibodies against interepithelial adhesion molecules (antibodies against desmoglein-3)

histology of a pemphigus vulgaris

- necrosis of epithelium and superficial layers of the CT - hyperemic CT with engorged capillaries and dense infiltrations of PMNs

histopathology of necrotizing periodontal disease

1. local predisposing factors - periodontal pockets - dental restorations - root anatomy - tooth position and crowding 2. systemic modifying factors - host immune function - systemic health - genetics

host determinants of periodontal health

1. immunocompromised individuals - HIV with CD4 < 200 - detectable viral load 2. malnutrition 3. pre-existing gingivitis, poor oral hygiene, history of NPD 4. psychological stress, lack of sleep 5. smoking and alcohol consumption

host factors causing necrotizing periodontal disease

- intense recruitment of PMNs - B-cells and plasma cells dominate mononuclear infiltrate - plasma cells produce mostly IgG and IgA - Ig levels in sulcus fluid are higher than in peripheral blood - Ab levels against Aa are extremely high but GAP patients have low titers - IgG2 seems to play a special role - increased response to B-cell mitogens

host response to bacterial pathogen in aggressive periodontitis

- gingivitis is common in children with poorly controlled type I diabetes - in adults, most of it is known is on the association between type I diabetes and clinical attachment loss instead of gingivitis

hyperglycemia and gingivitis

- contact allergy - plasma cell gingivitis - erythema multiforme

hypersensitivity reactions causing gingivitis

- diseases like Sjogren's syndrome, anxiety, poorly controlled diabetes may cause xerostomia

hyposalivation and gingivitis

- Periodontitis (inflammation) must be present for attachment loss to occur - Occlusal trauma in the absence of periodontitis may be reversible and may result in adaptation (a mobile but otherwise healthy tooth) - No repair can occur unless inflammatory periodontal disease is first resolved - Occlusal trauma superimposed on an existing periodontitis may under certain conditions accelerate attachment loss - Occlusal therapy in conjunction with periodontal treatment is indicated when occlusal trauma is present - Occlusal therapy should not be done until inflammatory PD is first controlled during initial periodontal therapy (helps decrease inflammation and tooth mobility) - Occlusal therapy is especially indicated prior to periodontal regenerative therapy - Occlusal adjustment is not justified in the absence of periodontal disease as a periodontal disease preventive measure

if a tooth wiggles, is it bad?

1. stable periodontitis patients - remain at higher risk for recurrent disease 2. non-periodontitis patients - no increased risk for disease

in a healthy gingiva, reduced periodontium may be seen in what two scenarios?

- only a few sites are affected with mild signs of gingival inflammation - can be considered "gingival health" having high risk of developing "gingivitis"

incipient gingivitis

- used by ramfjord in 1957 to study disease progression - tooth numbers 3,9,12,19,25,28 - advantages: -- representative of changes in entire mouth -- less time

index teeth (ramfjord teeth)

- as the apex narrows, the immune cells wall out from it to protect the periodontium

infection at the root of the tooth

1. hypersensitivity reactions 2. autoimmune diseases 3. granulomatous inflammatory conditions

inflammatory and immune conditions causing gingivitis

- removal of both sub and supragingival plaque - adequate oral hygiene - remove local and systemic risk factors

initial periodontal therapy of chronic periodontitis

1. possible marker of active perio destruction 2. released from dead PMN/neutrophils from periodontium - aspartate amino-transferase - alkaline phosphatase - beta-glucuronidase - elastase

intracellular host destruction enzymes

- want to reduce lateral forces to obtain a proper occlusal scheme - lateral loads induce higher bone strains and implant stress than vertical loads

lateral forces and implants

- examiner's tendency to be lenient or severe

leniency / severity error

- color - consistency - contour - BOP

leo and silness gingival index parameters of gingival condition

- Definition: a white lesion of the oral mucosa that cannot be characterized as any other definable lesion - A clinical diagnosis arrived at by exclusion in that all other potential causes of a white lesion have been ruled out or addressed - Lesions are generally asymptomatic and cannot be rubbed off - Approximately 20% of leukoplakic lesions demonstrate some degree of dysplasia or carcinoma upon biopsy and most oral cancers are preceded by a long-standing area of leukoplakia. Thus, leukoplakia can be considered a premalignant condition - The prevalence of malignant transformation in leukoplakia ranges from 0.13% to 34%

leukoplakia

- poor reliability and reproducibility - limited practical value

limitation of CAL

- Primary stability of the implant - Implant design - Restorative design - Presence/absence of risk factors

loading time depends on

1. circumpubertal onset 2. robust serum antibody response to infecting agents 3. localized first molar/incisor presentation - interproximal attachment loss on at least 2 permanent teeth - one of which is a molar - involving no more than 2 teeth other than first molars and incisors

localized aggressive periodontitis

- smoking - age - diabetes - educational and socioeconomic status

major confounding factors relating atherosclerosis and periodontitis

- Squamous cell carcinoma - leukemia - lymphoma

malignant neoplasms of periodontal soft tissue

- nutritional deficiencies and their effect on periodontal tissues - depletion of plasma ascorbic acid (vit C) - lack of vitamins A, B2, and B12 complex

malnutrition and gingivitis

1. anticonvulsants (phenytoin and sodium valproate) 2. immunosuppressant (cyclosporin A) 3. calcium channel blocking agents (nifedipine, verapamil, diltiazem, amlodipine, felodipine)

medications associated with gingivitis

- modest inflammatory changes that may be observable during ovulation - increase in gingival crevicular fluid flow by at least 20% during ovulation in over 75% of women tested - a modest change in women with pre-existing periodontal conditions - most women with menstrual cycle-associated gingival inflammation will present clinically non-detectable conditions

menstrual cycle and gingivitis

- The majority are intraosseous - Soft tissue metastasis from lung cancer - Most of the metastasis cases are carcinoma and not sarcoma

metastasis to the gingiva

- gingival papilla

mild gingival enlargement

- minor change in color and little change in the texture of the tissue

mild inflammation

- gingival papilla and marginal gingiva

moderate gingival enlargement

- glazing, redness, edema, enlargement and bleeding upon probing

moderate inflammation

any agent or condition that alters the way in which an individual responds to subgingival plaque accumulation

modifying factors

1. clinical features - papilla necrosis - bleeding - pain - linear erythema 2. host immune response impairments - stress - nutrition - smoking - poor oral hygiene

necrotizing gingivitis: clinical features + host immune response

1. necrotizing ulcerative gingivitis - limited to gingival tissues 2. necrotizing ulcerative periodontitis - lesion confined to periodontal tissues

necrotizing periodontal disease

- poor oral hygiene - swelling of regional lymph nodes may occur -- normally submandibular lymph nodes -- cervical lymph nodes may also be involved - fever and malaise aren't consistent characteristics - increased salivation

necrotizing periodontal disease findings

- <14% of WWII danish military staff - 6.7% of college students during the first 2 years in 1960's - very rare in developed countries - continues to be relevant in developing countries - HIV-seropositive US population ~1%

necrotizing periodontal disease prevalence

1. necrotizing gingivitis 2. necrotizing periodontitis 3. necrotizing stomatitis

necrotizing periodontal diseases

= necrotizing gingivitis + attachment loss - with more frequent extraoral signs in chronically immunocompromised patients

necrotizing periodontitis

- bone denudation extended through the alveolar mucosa

necrotizing stomatitis

1. Premalignant - Leuoplakia - Erythroplakia 2. Malignant - Squamous cell carcinoma - Leukemia - Lymphoma

neoplasms causing gingivitis

1. hereditary 2. specific infections 3. inflammatory and immune 4. reactive 5. neoplasms 6. endocrine, nutritional and metabolic 7. gingival pigmentation

non plaque induced gingivitis

- elastin - fibronectin - laminin - osteocalcin - osteopontin - bone sialoprotien - osteonectin - tenascin

non-collagen proteins broken down during collagen destruction

1. foreign body impaction - oral hygiene devices - food particles 2. harmful habits 3. orthodontic factors 4. gingival enlargement 5. root morphology alterations - iatrogenic (endodontic perforation) - external root resorption - cemental tears

non-periodontitis-related abscess: 5 types

1. Progressive tooth mobility 2. Teeth moving teeth - Fremitus - Functional mobility 3. Pathologic migration 4. Infrabony pockets (controversial) - Periodontal pocket is apical to the crest of the bone 5. Buttressing (thickened) bone (controversial)

occlusal trauma: clinical signs

1. Direct bone-implant surface mechanical binding (osseointegration) - like an ankylosed tooth - no attachment apparatus 2. Continuous bone remodeling at bone-implant surface interface - Can turn into bone resorption - microfractures and switch from remodeling to resorption 3. Implant mobility as a pathologic phenomena - If the fixture starts moving you cannot reverse it 4. Osseointegration: direct contact between living bone and the implant surface - Mechanical binding between the screw and the bone - Need living bone for it to integrate

occlusion on dental implants

- early studies reported an association with increased gingival inflammation and gingival enlargements - current contraceptive concentrations are way lower than the original dose - current formulations of contraceptives do not induce clinical changes in gingiva

oral contraceptives and gingivitis

- hyposalivation - prominent subgingival restoration margins

oral factors affecting gingivitis

- prominent subgingival restoration margins - hyposalivation

oral factors enhancing plaque accumulation for plaque-induced gingivitis

1. bone formation and remodeling 2. conventional healing time comes from trabeculation, maxilla has more trabeculation/soft bone - mandible takes 3 months and has more cortical bone - maxilla takes 6 months and primary stability is weaker

osseointegration and implant loading: healing at the interface

- stability of the implant at the time of placement (mechanical interlocking mechanism between a screw and bone surface) (screws are root shaped for better stability) - cortical bone density gives initial stability - implant fixture design

osseointegration and implant loading: primary stability

1. probing depth reduction after therapy - gingival recession - gain of clinical attachment - pocket shrinkage 2. sites with initially shallow pockets tend to lose CAL 3. greater risk for additional attachment loss if presenting multiple sites with residual probing depth > 6 mm after active treatment -- you cannot maintain 6 mm pockets

outcomes of initial therapy of chronic periodontitis

- prevalent in adults, may be seen in kids - tissue destruction commensurate with oral hygiene and plaque levels and local/systemic factors - specific subgingival species are implicated in disease -- individual species vary among individuals - subgingival calculus is invariably present at disease sites - rate of progression is slow to moderate -- rapid bursts of destruction can occur - host factors determine pathogenesis and progression - untreated diseased sites more likely to sustain further breakdown

overall characteristics of chronic periodontitis

a small, inflammatory, congested spot on the skin; a pimple

papula

- plaque accumulation - calculus formation - gingival inflammation - periodontal destruction - periodontal treatment needs

parameters commonly used in clinical periodontology

- Formation of intraepithelial bullae in skin and mucous membranes - Strong genetic background (Jewish and Mediterranean) - Painful desquamative lesions, erosions, or ulcerations - Chronic course with recurrent bulla formation - Typically in middle age or elderly - Involvement of oral cavity in about 54% of cases

pemphigus vulgaris

- pain/gingival tenderness - swelling - suppuration which may be spontaneous or occur after pressure - deep periodontal pocket - increase tooth mobility - radiographs showing widened PDL, bone loss - fever, malaise, lymphadenopathy

periodontal abscess diagnosis

1. acute lesion management - debridement - drainage - irrigation and antiseptics - remove foreign body, if present - OHI - antibiotics - review after 24-48 hours - 1 week later the definitive treatment should be carried out 2. definitive treatment - prophylaxis - SRP - surgery, if necessary

periodontal abscess therapy

- root surface defects - bacteria on surface and in the periodontium - no inflammatory changes in pulp - mineralization present - access to pulp -- accessory canals, apical foramen, dentinal tubules - studies failed to confirm direct relationship between progression of periodontitis and pulp changes

periodontal disease: effects on the pulp

1. autosomal inherited trisomia of chromosome 21 2. frontal prominence / mesial epicanthus 3. periodontium - severe inflammation - accelerated attachment loss - PMN chemotaxis and killing defects

periodontal manifestation in down syndrome

1. early detection - PSR includes evaluation of all sites - highly sensitive technique for detecting deviations from periodontal health 2. speed - once learned, PSR takes only a few minutes to conduct for each patient 3. simplicity 4. cost effective 5. recording ease - six numerical scores, one for each sextant of the mouth 6. risk management - proper, consistent, and documented use of PSR shows that the dentist is evaluating a patient's periodontal status

periodontal screening and recoding benefits

- furcation involvement - mobility - mucogingival problem - recession extending to colored band

periodontal screening and recoding code *

- designed to detect periodontal diseases - not intended to replace a comprehensive periodontal examination - not indicated for recalls - for use with adults only - limited utility in screening children and adolescents

periodontal screening and recoding limitations

- colored band completely visible - no BOP - no calculus or defective margin - treatment: prophylaxis and preventive care

periodontal screening and recording code 0

- colored band completely visible - BOP present - no calculus or defective margin - treatment: OHI and subgingival plaque removal

periodontal screening and recording code 1

- colored band completely visible - supra or subgingival calculus detected - defective margins seen - treatment: -- subgingival instrumentation to remove plaque and calculus -- correction of defective margins -- OHI

periodontal screening and recording code 2

- colored band partially visible - BOP present - no calculus, defective margins - plaque may be present

periodontal screening and recording code 3

1. comprehensive periodontal examination and charting of the affected sextant - identify probe depths - mobility - recession, mucogingival defects - furcation involvements 2. when 2+ sextants score code 3 - a comprehensive full mouth periodontal examination and charting is required - includes radiographs 3. patient is counseled regarding appropriate treatment plan

periodontal screening and recording code 3 treatment

- colored band not visible - BOP present - calculus - plaque may be present - PD > 5.5 mm - Treatment: -- comprehensive periodontal assessment -- patient is counseled regarding appropriate treatment plan

periodontal screening and recording code 4

- early detection - easy to use - cost effective - identify individuals in need of more extensive evaluation - indicated for all new patients and recall visits more than a year - educate and motivate patients - not a monitoring tool in periodontal disease

periodontal screening and recording uses

1. periodontal instrumentation - root exposure (recession) - cementum (and dentin) removal - dentinal tubule exposure 2. pulp vitality unaffected 3. dentin hypersensitivity - sharp pain, rapid onset - temperature, sweet, acid, touch, airflow - peak at 1st week, then subside - may become chronic - few teeth in few patients become highly sensitive

periodontal therapy effect on pulp

1. anatomical connection between pulp and PDL 2. apical foramen - main pathway between the pulp and the periodontium 3. accessory canals - frequency increases towards apex - more common towards the apex - molars tend to have accessory canals on the distal root, in furcation areas, that go in multiple directions 4. dentinal tubules - in cervical area - caused by loss of cementum

periodontal-endodontic interrelationships

- atherosclerotic vascular disease - adverse pregnancy outcomes - diabetic complications - respiratory infection

periodontitis and systemic disease examples

1. associated with hematologic disorders - acquired neutropenia - leukemias 2. associated with genetic disorders - familial and cyclic neutropenia - down syndrome - leukocyte adhesion deficiency syndrome - papillon-lefevre - chediak-higachi - histiocytosis syndromes - glycogen storage disease - infantile genetic agranulocytosis - cohen syndrome - ehlers-danlos syndrom - hypophosphatasia

periodontitis as a manifestation of systemic diseases

1. sources of risk - 48% of americans older than 30 have periodontitis - periodontal pockets provide a significant SA exposed to gram-negative biofilm - infected and inflamed tissues 2. as a result, there is systemic exposure to - bacteria and bacterial products - inflammatory cytokines

periodontitis as a risk factor for systemic disease: source of risk and results

- gingivitis

periodontitis starts with?

1. exacerbation of chronic lesion - untreated patients - recurrent infection 2. post-therapy abscess - following SRP (calculus) - following surgical therapy (calculus, foreign bodies) 3. post-antibiotic abscess - super-infection

periodontitis-related abscess: 3 types

- prevalence in 13-20 years old is <1% - 0.2% in whites and 2.6% in blacks aged 5-17 - increase in extent and severity with time

permanent dentition epidemiology of aggressive periodontitis

a patch on the skin or on a mucous surface

plaque

- association between plaque and pneumonia is stronger than for plaque and exacerbation of COPD

plaque and pneumonia / COPD

- assesses the amount of plaque at the gingival margin, examining the same anatomical units as the GI - plaque scores range from 0 - 3 - a probe is used to distinguish between scores 0 and 1 - visible plaque is scored a 2 or a 3 - the plaque index is computed for a tooth, subject, or population

plaque index

0. no plaque 1. plaque detected by running probe margins 2. visible plaque 3. abundant plaque

plaque index scoring criteria: 0-3

1. androgens, estrogens, progestins 2. plaque bacteria in conjunction with elevated steroid hormone levels are necessary to produce a gingival inflammation - pubery - pregnancy - oral contraceptives

plaque-induced gingivitis exacerbated by sex steroid hormones

- reduced periodontium following active periodontal treatment and the resolution of inflammation from periodontitis is a common finding - plaque-induced gingivitis on a reduced periodontium is characterized by the return of bacterially induced inflammation to the gingival margin on a reduced periodontium with no evidence of progressive attachment loss

plaque-induced gingivitis on a reduced periodontium

- have more periodontal attachment loss

poorly controlled diabetics have?

1. halo effect 2. leniency/severity error 3. central tendency error

potential problems of examiner bias

- probability of not having the disease when the test is negative

predictive value negative

- probability of disease in a subject with a positive test result

predictive value positive

- any agent or condition that contributes to the accumulation of dental plaque

predisposing factors

- Systemic diseases like ulcerative colitis, blood dyscrasias and nutritional deficiency states - Abnormalities of white blood cell function - Patients suffering from AIDS

predisposing factors involved in a gingival lesion of specific bacterial origin

leukoplakia erythroplakia

premalignant neoplasms

- highest in men, mexican americans, adults with less than a high school education, adults below 100% federal poverty levels, and current smokers

prevalence of chronic periodontitis

- Non-contributory medical history (No significant systemic conditions) - Rapid Attachment Loss and Bone Loss - Familial aggregation

primary characteristics of aggressive periodontitis

- few studies in 5 to 11 year olds - prevalence reported between 0.9% and 4.5%

primary dentition epidemiology of aggressive periodontitis

managing gingivitis

primary preventive strategy for periodontitis

- extracting teeth didn't necessarily cure disease - people with good oral health and no infection still developed systemic diseases - people with no teeth still developed systemic diseases

problems with focal infection theory

- prominent subgingival restoration margins promote gingivitis by increasing the local accumulation of bacterial plaque

prominent subgingival restoration margins and gingivitis

- increase in gingival inflammation in circumpubertal age and in both genders without a concomitant increase in plaque levels

puberty and gingivitis

- deep caries - trauma (accident) - restorative procedures - infectious and non-infectious agents

pulpal disease risks to pulp vitality

- periodontal treatment of CP is effective (<.1 mm tooth loss/year) - non-compliant patients had double the rate of tooth loss (0.2 teeth/year) - untreated patients lost about 0.6 teeth/year

rationale for periodontal therapy of chronic periodontitis

1. Epulides - Fibrous epulis - Calcifying fibroblastic granuloma - Pyogenic granuloma (vascular epulis) - Peripheral giant cell granuloma (or central)

reactive processes causing gingivitis

- Mixed natural teeth and implants makes it harder to control forces - Lateral forces are not good for implants which becomes more of an issue when you have several implants side by side - Single tooth restoration - cannot modify occlusion too much - Multiple unit fixed type restoration (splinted versus individual crowns) - Full mouth fixed type implant supported restoration - need a certain # of implants to distribute loads (max 5-6 and mandible at least 5) - Full mouth removable type implant supported restoration - can start with 2 overdentures and move to 4 depending on needs - these #'s come from needing to distribute occlusal load - Don't like cantilevers on implants- can't take lateral forces very well

restorative design of dental implants

mesh; in the form of a network

reticular

- lesion/bone loss occurs at tip of the implant (not at collar) - believed to be due to trauma only because generally it is aseptic (no bacteria in that area) - at the apical portion of the implant

retrograde peri-implantitis

- return of inflammation to sites treated for periodontitis is common - recurrent inflammation may be confined to the gingival tissues and may not cause further attachment loss

return of inflammation and periodontitis

- non-modifiable factors -- age -- gender

risk determinants in chronic periodontitis

- putative risk factors that have been identified in cross sectional studies but not confirmed longitudinally -- HIV/AIDS -- osteoporosis -- infrequent dental visits

risk indicators in chronic periodontitis

- characteristic associated with elevated risk for disease but may not be part of the causal chain -- furcation involvement -- calculus -- history of attachment loss

risk markers for chronic periodontitis

- in older adolescents and adults, periodontal probing is a more appropriate screen examination that use of radiographs - marginal bone loss, in the presence of clinical attachment loss, increased probing depth are all specific indicators of periodontitis - for completed erupted dentition, 2-3 mm from CEJ to bone crest is considered normal

screening permanent dentition for aggressive periodontitis

- distance of 2 mm between CEJ and alveolar crest, in the absence of local factors (like proximal caries, fillings, crowns, open contacts) argues for a suspected diagnosis of aggressive periodontitis

screening primary dentition for aggressive periodontitis

- lack of consistency between bacterial deposits and severity of breakdown

secondary characteristics of aggressive periodontitis

- generally but not universally present - microbial deposits are inconsistent with the amount of periodontal destruction - elevated A.A. and P. gingivalis - phagocyte abnormalities - hyper-responsive macrophage phenotype (elevated levels of PGE2 and IL1beta) - progression may be self-arresting

secondary features of aggressive periodontitis

- Normal (or excessive forces) - Applied to a weakened periodontium

secondary occlusal trauma

- probability that a test result will be positive when the test is administered to people who actually have the disease in question

sensitivity

- gingival papilla, gingival margin and attached gingiva

severe gingival enlargement

- overt redness and edema with a tendency toward bleeding when touched rather than probed

severe inflammation

1. slight - 1-2 mm attachment loss 2. moderate - 3-4 mm attachment loss 3. severe - 5 mm or more of attachment loss

severity of chronic periodontitis

health: scalloped with gingiva filling interdental spaces (papilla) inflammation: - knife edge gingival adaptation or loose gingival margins - in some cases, clefts (Stillman's) or festoons (McCall's) may develop

shape of gingival margin in health and gingivitis

- introduced in 1967 - association of plaque and pregnancy gingivitis - measures abundance of plaque - no disclosing - index teeth - look at 4 parameters of gingival condition

silness and loe plaque index

- direct exposure of inhaled cigarette smoke to periodontal tissues causes vasoconstriction of periodontal microvasculature and gingival fibrosis - smokers have fewer clinical signs and symptoms of gingival inflammation

smoking and gingivitis

- saliva - GCF - most commonly used - blood serum - blood cells - urine

sources of sample for host response

- probability that a test will be negative when administered to people who are free of the disease in question

specificity

- About 20% of intraoral carcinomas have gingival representation - Mandible, premolar and molar regions - Common in edentulous areas, mobility of adjacent teeth - Invasion of the underlying alveolar bone in about 50% of cases - Nodular lesions, often with ulceration and surrounding leukoplakia - May mimic other oral lesions affecting periodontium (reactive or inflammatory) - Regional lymph-node metastasis is common - Squamous carcinoma of the soft palate and mucosa posterior to the tuberosity appearing as a speckled leukoplakia - Early squamous carcinoma - white path on the lateral border of the tongue

squamous cell carcinoma

1. initial periodontitis - up to 2 mm attachment loss 2. moderate periodontitis - 3-4 mm attachment loss 3. severe periodontitis with potential for additional tooth loss - 5 mm or more, may lose teeth 4. severe periodontitis with potential for loss of the dentition - basically just need a full mouth extraction

stages of periodontitis

constant forces applied as in orthodontic movement

static force

- Primary herpetic gingivostomatitis - Recurrent intraoral herpes simplex lesions - Recurrent herpetic infections

strains of herpes simplex viruses causing gingivitis

- accurately diagnose disease - predict affects of a systemic status of the patient on the course of the disease - confirm the prediction with assessment of therapy

successful management of periodontal disease depends on the ability of a clinician to?

heath: dull surface with stippling (possibly) inflammation: - loss of stippling smooth and shiny if exudative change occurs - firm and nodular if fibrotic changes occur

surface texture changes in gingiva in heath and gingivitis

- mostly painless -- localized dull pain -- gingival tenderness, 'itching' gums - loose teeth - food impaction - drifted teeth/increased spacing - root sensitivity - bleeding gums

symptoms of chronic periodontitis

- hyperglycemia - leukemia - smoking - malnutrition

systemic conditions and gingivitis

1. sex steroid hormones - puberty - menstrual cycle - pregnancy - oral contraceptives 2. hyperglycemia 3. leukemia 4. smoking 5. malnutrition

systemic conditions that are modifying factors for plaque-induced gingivitis

1. acute therapy - debridement - oral rinse (0.12% CHX) - antibiotics: metronidazole (250 mg TID) 2. further mechanical therapy - treat preexisting condition 3. surgical therapy - eliminate defect 4. predisposing factor elimination

therapy for necrotizing periodontal disease

- Burns of mucosa - Minor burns from hot beverages - Mostly seen on palatal and labial mucosa - Painful, erythematous lesions -mVesicles may develop

thermal insult to injury

- 27% of adults - 31% of african americans - 26% of hispanics - 25% of whites - 16% of middle school students use at least one form of tobacco - 28% of high school students use one form of tobacco

tobacco smoking in ohio statistics

- Varies from superficial gingival laceration to major loss of tissue resulting in gingival recession

toothbrushing-induced gingival ulceration

1. Physical/mechanical insults - Frictional keratosis - Toothbrushing-induced gingival ulceration - Factitous injury (self-harm) 2. Chemical (toxic) insults - Etching - Chlorhexidine - Acetylsalicyclic acid - Cocaine - Hydrogen peroxide - Dentifrice detergents - Paraformaldehyde or calcium hydroxide 3. Thermal insults - Burns of mucosa

traumatic lesions causing gingivitis

- index is biased toward the gingival third of the tooth surface - facial and lingual surfaces are examined - plaque is made visible using a disclosing agent and scored using a 0 - 5 scoring system - scores are computed for subject and population - most frequently used plaque index in clinical trials

turesky modification of quigley-hein plaque index

0: no plaque 1: spots of plaque at cervical margin 2: thin, continuous band of plaque,<1 mm wide, at cervical margin 3: plaque band > 1 mm but < 1/3 of crown height 4: plaque covering > 1/3 but < 2/3 of crown height 5: plaque covering > 2/3 of crown height

turesky modification of quigley-hein plaque index scoring criteria: 0-3

1. dental plaque biofilm induced gingivitis 2. non dental plaque induced gingival disease

two types of gingivitis

- insulin dependent - destruction of pancreatic beta cells - hypo-production of insulin - usually occurs before age 30

type 1 diabetes

- non-insulin dependent - target tissues don't respond to insulin - usually occurs later in life

type 2 diabetes

- affected with an ulcer - open sore or lesion of the skin or mucosa accompanied by sloughing of inflamed necrotic tissue

ulcerative

• Neisseria gonorrhoeae (gonorrhea) • Treponema pallidum (syphilis) • Mycobacterium tuberculosis (tuberculosis) • Streptococcal gingivitis (strains of streptococcus)

variable bacterial flora in an infection

- Coxsackie virus (hand-foot-and-mouth disease) - Herpes simplex ½ (primary and recurrent) - Varicella zoster virus (chicken pox or shingles affecting V nerve) - Molluscum contagiosum virus - Human papilloma virus (squamous cell papilloma, condyloma acuminatum, verruca vulgaris, and focal epithelial hyperplasia)

viral infections causing gingivitis

- coxsackie virus - herpes simplex viruses type 1 and 2 - herpes (varicella) zoster virus - molluscum contagiosum virus - human papilloma virus

viral infections causing gingivitis

1. vitamin deficiencies - vit C (scurvy

vitamin deficiencies causing gingivitis

- determines the quantity of supragingival calculus - lingual surfaces of lower anteriors (#22-27) - quantity is determined in mm of calculus along the 2 diagonal and the central lines drawn over the lingual surface of each tooth - index, expressed in mm, is computed for tooth, subject, population - most frequently used calculus index in longitudinal studies

volpe-manhold index

1. consistency of association - studies with similar results 2. strength of association 3. correct time sequence - potential factor must precede the occurrence of the disease 4. specificity of associations - if a given factor is related to other diseases, its association with the disease is less likely to be interpreted as casual 5. degree of exposure 6. biological plausibility 7. support from experimental evidence

what defines a risk factor