Periodontology Flashcards
what are the features of healthy gingivae?
pink, firm, stippled, knife edge margin, no bleeding
how do the gingivae maintain health?
JE, shedding of epithelial cells, collagen fibres maintain form and attachment to tooth, GCF, antibodies, phagocytosis by neutrophils and macrophages, complement activity
what is gingivitis?
reversible inflammation of the gingivae
what are the clinical signs of gingivitis?
redness starting at papillae and progressing along gingival margin
loss of stippling
smooth and glossy surface
swelling
rolling of the gingival margin
loss of triangular shape of interdental papillae
bleeding on probing
what are the histological features of plaque induced gingivitis?
increased GCF
increased vasodilation and capillary permeability
collagen breakdown
more inflammatory cells
what is periodontitis?
irreversible inflammation of the gingiva and loss of attachment and bone
what are the clinical signs of periodontitis?
some/all signs of gingivitis true pocketing on probing recession suppuration mobility drifting furcations radiographic evidence of bone loss
what is the prevalence of chronic periodontitis?
47% of US population over 30 have periodontitis
8.5% mild, 30% moderate, 8.5% severe
what is the prevalence of aggressive periodontitis?
ethnic variation
periodontal disease is…
polymicrobial
describe the specific plaque hypothesis
specific microorganisms are responsible for the development of periodontal disease
eg Aa linked to LAP and Pg linked to generalised aggressive periodontitis but both found at non diseased sites
describe the non specific plaque hypothesis
disease results from sheer mass of pathogens
describe the environmental disease hypothesis
pathogenic species are required in sufficient numbers in the biofilm, species are co dependent
describe the microbial complexes of varying virulence
clusters of bacteria in discrete micro environments
how can host factors contribute to periodontal tissue destruction?
inflammatory and immunological responses —> modulation of host response e.g. drugs, diabetes, smoking —> modulated by subject specific risk factors e.g. PMNL function
how can parasite factors contribute to periodontal tissue destruction?
bacterial load and composition —> virulence factors, toxins, cell signalling molecules —> modulated by site based risk factors e.g. plaque retention factors
what is the role of the host immune response in the pathogenesis of periodontal disease?
in health PMNL are predominant defence cell, innate immunity functions at low level, no tissue damage
increased plaque –> increased endotoxin –> complement activation, increased inflammatory response, epitheliotoxin, gingival tissue damage
T lymphocytes kill bacterial cells
B lymphocytes produce antibodies and activate complement
untreated disease in susceptible patients exceeds the threshold where tissue damage occurs
active periodontal lesions full of plasma cells causes collateral damage due to enzymes and free radicals
what type of inherited genetic disease/predisposition is chronic periodontitis?
complex
what percentage of variance for gingivitis, probing depth and clinical attachment loss is due to genetic variation?
38-82%
which polymorphism is linked to chronic periodontitis?
IL-1 polymorphism
what type of inheritance risk is associated with aggressive periodontitis?
familial pattern of inheritance, autosomal dominant, x - linked
what genetic alterations are involved with complex diseases such as chronic periodontitis?
normal variants
present in everyone
subtly alter the gene and protein
what are the effects of smoking on the periodontium?
3-6 times more periodontal disease than non-smokers
more sites with deeper pockets
more clinical attachment and bone loss
more furcations
more likely to suffer from necrotising ulcerative periodontitis
accumulate more calculus
less likely to respond to therapy
what are the effects of nicotine on the periodontium?
vasoconstriction, prolonged thermal and chemical irritation of oral mucosa causing smokers keratosis, speckled leukoplakia
changes oral microflora resulting in predisposition to candiosis
increased staining
etc (see handout)