IntroToPerio - Final 01

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  1. Most common one of the four types of oral candidiasis
    Pseudomembranous, aka thrush
  2. Gingival diseases of fungal origin
    • Common in immunocompromised patients caused by disease (HIV etc) or medication (steroids etc).
    • Seen in patients where normal flora is disrupted (opportunistic).
    • Most common oral fungal infection is Candidiasis.
    • a. Common under prosthetic devices.
    • b. White patches on gingiva, tongue, or oral mucous membranes. Can be easily wipe off.
    • c. Diagnosis of candida infection can be made by culture, smear or biopsy.
    • Histoplasmosis.
    • Treat w/ common anti-fungi drugs.
  3. Herpetic gingivostomatitis
    • HSV-1
    • children
    • vesicle formation,
    • fever,
    • gingival inflammation
    • Acute onset (severe or not, depending on the patient and dose of virus exposed to)
    • vesicles are contagious
    • Latency in ganglia
  4. Herpetic gingivostomatitis - oral symptoms
    • Generalized “soreness” of the oral cavity
    • Ruptured vesicles are the focal sites of pain
    • Eating, drinking, oral hygiene affected
  5. Secondary Herpetic gingivostomatitis
    • Stimuli: sunlight, trauma, fever, stress
    • Herpes labialis
    • palate, gingiva , mucosa
    • pain away from the site of stimuli 2 to 4 days later
  6. HIV-related periodontal disease
    • Oral Signs & Symptoms
    • Candidiasis
    • Lymphadenopathy
    • Viral Lesions
  7. Oral Hairy Leukoplakia (HL)
    • White lesions
    • Primarily found on lateral border of tongue.
    • Surface of lesion can be smooth or corrugated & doesn't rub off
    • Most likely a viral induced lesion
  8. HIV-related periodontal diseases - Viral Lesions
    • Oral Papillomas
    • Condyloma acuminatum
    • Focal eipthelial hyperplasia
  9. HIV-related neoplastic lesions
    • Kaposi Sarcoma
    • Malignant lesion arising from lymphatic or vascular endothelium
  10. HIV associated gingivitis (HIV-G) or Linear Gingival Erythema (LGE)
    • Persistent & easily bleeding.
    • Lesions can be localized or generalized.
    • May be limited to marginal tissues.
    • Can also extend into attached gingiva and into alveolar mucosa.
    • Oral candida identified with LGE.
    • Some LGE lesions may undergo spontaneous remission.
  11. HIV associated periodontitis (HIV-P) - Treatment
    • Mechanical debridement.
    • Chemotherapeutic agents.
    • Home care instructions.
    • Routine maintenance care.
  12. Oral lesions strongly associated with HIV-infection
    • Candidiasis
    • HL
    • Kaposi’s sarcoma
    • Non-Hodgkin’s Lymphoma
    • Periodontal Diseases - LGE, NUP, NUG
  13. Muco-cutaneous disorders: desquamative gingivitis
    • Tissue peeling off
    • Lichen Planus - T cells involved
    • BMMP - Benign mucus membrane pemphigoid; targets B cells
    • Pemphigus Vulgaris
  14. Most common additive in toothpaste is ________ flavoring and can cause ________.
    • cinnamon
    • desquamative gingivitis
  15. must do immunofluorescence biopsy on intact tissue to diagnose or differentiate between
    Lichen planus and BMMP
  16. desquamative gingivitis - Treatment:
    • Eliminate etiology
    • Steroids
    • 1. Topical
    • 2. Intra-lesional
    • 3. Systemic
    • Appropriate referral to medical specialist
  17. Prognosis is established after __________ and before __________.
    • the diagnosis is made
    • the treatment plan is established
  18. Essential Elements of Prognosis
    • 1. Definition of the intended outcome
    • 2. Timing of the projection
    • 3. Consideration of individual teeth versus the overall dentition
  19. Timing (length) of the Projection:
    • short term < 5 years
    • long term > 5 years
  20. ________ is the most important single factor in prognosis.
    Osseous Defect Morphology
  21. Neutrophil Dysfunction
    • Severe aggressive periodontal breakdown is associated
    • with:
    • Chediak-Higashi syndrome
    • Chronic granulomatous disease
    • Chronic neutropenias
    • Papillon-Lefevre syndrome
    • Down syndrome
  22. Major Negatives for Prosthetics
    • Furcation involvement
    • >50% Attachment loss
    • Poor crown/root ratio
    • Poor root form
    • Root proximity
  23. Drug-Induced Gingival Enlargement
    • Rare in edentulous mouths
    • Genetic predisposition
    • Acanthosis of epithelium, elongated rete pegs
  24. Anticonvulsants
    • Phenytoin (Dilantin)
    • 50% of patients
    • Occurrence and severity not related to dosage
    • More often in young patients
    • Stimulates proliferation of fibroblasts and epithelium
    • Induces a decrease in collagen degradation
    • Pathogenesis not known
  25. Immunosuppressants
    • Cyclosporine
    • More vascularized than phenytoin enlargement
    • 30% of patients
    • Presence of plasma cells and abundant amorphous ground substance
    • May be hypersensitivity response to drug
    • Increased enlargement in patients taking both cyclosporine + Ca channel blocker
  26. Calcium Channel Blockers
    • Nifedipine , Diltiazem ,Verapamil, Felodipine, Nitrodipine
    • similar to anticonvulsants and immunosuppressants
    • Pathogenesis unknown
  27. Idiopathic Gingival Enlargement
    • Pink, firm, almost leathery gingiva
    • Characteristic minutely pebbled surface
    • relatively avascular connective tissue, dense collagen, numerous fibroblasts, thickened, acanthotic epithelium
    • Etiology: unknown
    • Some hereditary basis
  28. False Gingival Enlargement -
    Underlying osseous lesions: Exostoses, Paget’s disease, Fibrous dysplasia, Cherubism, Central giant cell granuloma, Ameloblastoma, Osteoma, Osteosarcoma
  29. “Stillman’s clefts”:
    a specific type of gingival recession, narrow, triangular-shaped gingival recession
  30. “McCall festoons”:
    a rolled, thickened band of gingiva usually adjacent to the cuspids when recession approaches the mucogingival junction.
  31. Miller Class I
    • Marginal tissue recession that does not extend to the mucogingival junction
    • There is no periodontal loss (bone or soft tissue) in the interdental area
    • 100% root coverage can be anticipated
  32. Miller Class II
    • Marginal tissue recession to or beyond MGJ
    • No periodontal loss (bone or soft tissue) in the interdental area
    • 100% root coverage can be anticipated
  33. Miller Class III
    • Marginal tissue recession to or beyond MGJ
    • presence of interdental tissue loss or malpositioning of the teeth
    • Partial root coverage can be anticipated
  34. Miller Class IV
    • Marginal tissue recession to or beyond MGJ
    • Severe Interdental Tissue loss and/or malpositioning of teeth
    • root coverage cannot be anticipated
  35. Necrotizing Diseases
    • Necrotizing diseases of the periodontium:
    • - Necrotizing ulcerative gingivitis (NUG) - NECROSIS AND SLOUGHING OF GINGIVA; painful, metallic taste, "pasty" saliva
    • - Necrotizing ulcerative periodontitis (NUP)
    • Necrotizing stomatitis
    • Trench mouth
    • Vincent’s infection/Vincent’s Angina - affects oropharynx and throat
  36. Microbiology of NUG
    • Fusiform bacilli and spirochetes
    • Treponema microdentium
    • Prevotella intermedia
    • Fusobacterium
    • Heterogeneous flora
    • Mere presence insufficient to cause the disease
  37. Listgarten’s Four Zones of NUG:
    • Bacterial zone: the most superficial, varied bacteria, few spirochetes
    • Neutrophil-rich zone : PMNs, bacteria, various types spirochetes
    • Necrotic zone: dead tissue, fibrin, numerous spirochetes
    • Spirochetal infiltration zone: well preserved tissue infiltrated with spirochetes of intermediate and large size, no other microorganisms (~300μm)
  38. Diagnosis of NUG
    • clinical findings of gingival pain, punched out interdental papillae, and bleeding
    • bacterial smear not necessary
  39. Allergic Reactions in the Gingiva
    • Uncommon
    • Associated with several restorative materials (Hg, Ni, acrylic, etc.), toothpastes, mouthwashes, chewing gum, and foods
    • Typically, delayed hypersensitivity reactions
    • Diagnosis may prove difficult
    • Histology: dense infiltrate of eosinophilic cells
  40. Chronic Periodontitis Increases with age:
    age-associated not age-related disease
  41. Chronic Periodontitis Progression models
    • continuous model: slow and continuous, constantly progressive rate of destruction
    • random or episodic-burst model: short bursts of destruction followed by periods of no destruction; random with respect to the tooth sites affected and the chronology of the disease process
    • asynchronous, multiple-burst model: defined periods of bursts of activity (periodontal destruction around affected teeth) interspersed with periods of inactivity or remission; chronology of bursts asynchronous for individual teeth or groups of teeth
Card Set
IntroToPerio - Final 01
IntroToPerio - Final 01
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