Chapter 4: Periodontal Disease Flashcards
Gingivitis
-‐ Puberty gingivitis: increased susceptibility to gingivitis from 9-‐14y
-‐ Marginal gingivitis: confined to free gingival margins
-‐ Papillary gingivitis: confined to interdental papilla
-‐ Chronic hyperplastic gingivitis: enlargement from edema or fibrosis
Necrotizing ulcerative gingivitis
-‐ Decreased neutrophilic chemotaxis and phagocytic response
-‐ Caused by Fusobacterium nucleatum, Prevotella intermedia, Porphyromonas gingivalis, Treponema spp, and Selenomomas spp.
-‐ Associated with mononucleosis.
-‐ Tx: penicillin and metronidazole
-‐ Necrotizing ulcerative periodontitis: loss of attachment
-‐ Necrotizing ulcerative mucositis/stomatitis: spread to soft tissue
-‐ NOMA (cancrum oris): spreads to skin
-‐ NUG, NUP, NUS and NOMA: spectrum of necrotizing gingivostomatitis?
Granulomatous gingivitis
-‐ Unexplained granulomatous inflammation in gingiva.
-‐ Must r/o foreign-‐body, fungal, bacteria, chron’s, sarcoidosis and wegener’s
-‐ Clinically, resembles LP (but is a single lesion and there is no migration)
-‐ Histology: 80% lichenoid or mixed inflammation; 20% granulomatous.
Drug-‐related gingival hyperplasia
-‐ Cyclosporine, phenytoin and nifedipine. Drugs affect calcium remodeling (reduce calcium influx)
-‐ Also: erythromycin, verapamil
-‐ Prevalence: P-‐50%, C,N-‐25% (after 1-‐3m of use). Age of patients P-‐<25, N-‐older, C-‐broad range
-‐ Pts with GVHD on cyclosporine can show ST growth similar to PG
Localized juvenile spongiotic gingival hyperplasia
-‐ Distinct subtype of gingival hyperplasia
-‐ Nearly all lesions on anterior gingiva, with 81% affecting maxillary gingiva
-‐ Papillary, often pedunculated, red and easily bleeding gingival overgrowth in young patients.
-‐ Histo: subtle papillary epithelial hyperplasia with prominent intercellular edema and neutrophilic exocytosis of the hyperplastic surface squamous epithelium.
Gingival fibromatosis
-‐ Idiopathic or familial
-‐ Familial GF: other findings include hypertrichosis, periodontitis, epilepsy, mental retardation, deafness, hypothyroidism, GH deficiency
-‐ Familial GF: isolated or part of syndrome (Zimmermann-‐Laband, Murray-‐Puretic-‐Drescher, Rutherfurd, Cowden, Cross, Ramon, Jones and prune belly)
-‐ GINGF (HGF) 1, 2, 3 mutations located in chromosome 2 and 5. SOS1 locus in GINGF
-‐ Ramon syndrome: mental + growth retardation, fibrous dysplasia, cherubism and GF
-‐ Jones: gingival fibromatosis + sensorineural hearing loss
Periodontitis
-‐ Chronic periodontitis risk: 50% genetics, 20% tobacco, 20% specific bacteria
-‐ Risk factors periodontal abcess: closure of pockent entrance, furcation involvement, enamel pearls, dens-‐invaginatus and diabetes
-‐ Risk factors pericoronitis: stress, tonsillitis and pharyngitis. Can give rise to localized NUG-‐like necrosis
Aggressive periodontitis
-‐ Neutrophil dysfunction (deficiency in immune response) not associated with systemic disease and without systemic manifestations.
-‐ Localized (more common) or generalized.
-‐ Localized: 11-‐13y; strong serum Ab response; affects 1st molars and incisors, and max 2 other teeth; little plaque; AA predominant pathogen
-‐ Generalized: >30y; poor serum Ab response; 1st molars and incisors + 3 teeth; heavy plaque; more complex pathogens
Papillon-‐Lefevre syndrome
-‐ Severe perio disease (teeth floating in air) and diffuse transgradient palmoplantar keratosis.
-‐ Related to AA
-‐ Cathepsin C gene mutation (chromosome 11). Co-‐sanguinity in 33% of cases
-‐ Due to defect in neutrophil chemotactic and impaired B/T cell activity
-‐ Haim-‐Munk: palmoplantar keratosis, periodontal disease (less severe), skin infections (more severe), skeletal abnormalities. Also cathepsin C gene mutation
-‐ Unna-‐Thost syndrome, Meleda disease: skin changes only, no oral findings
-‐ Focal palmoplantar and oral mucosa hyperkeratosis syndrome: no perio disease
