periodontal disease Flashcards
(22 cards)
Periodontium
Tissue supporting and anchoring the tooth: Gingiva, gingival attachment, cementum, periodontal ligament, alveolar bone.
Tooth supporting structures of periodontium
Cementum, periodontal ligament, alveolar bone
What is necessary to initial periodontal disease?
Bacterial plaque.
Direct effect of periodontal disease
Invasion of bacteria, exotoxin release, and proteases
Indirect effect of periodontal disease
Immune and host response that leads to tissue destruction
Types of periodontitis
Chronic, aggressive, and systemic disease periodontitis.
Chronic periodontitis
Most common, from plaque/calculus formation. tissue destruction proportional to amount of plaque.
Aggressive periodontitis
Not consistent with plaque/calculus, rapid, gram neg. actinobacillus actinomycetemcomitans. Abnormality PMN and hypersensitive macrophages. Increases prostaglandins and IL-1B…..two forms
Localized aggressive periodontitis
strong antibody response. Associated with actinobacillus actinomycetemcomitas. Abnormal neutrophil and rapid destruction around 1st molars/incisors
generalized aggressive periodontitis
poor antibody response. Genetic factor. Rapid bone/attachment loss.
Are all bacterial plaque equally pathogenic?
No, specific bacteria responsible for destructive periodontitis
Actinobacillus actinomycetemcomitans
Localized aggressive periodontitis…is gram negative.
Virulent factors of periodontal disease
Proteases, hemagglutinin (bind host cell receptor), LPS, Fimbriae, polysaccharide capsule
Hemagglutinins and protease
Used by P. gingivalis to lyse RBC to extract nutrients. Protease also degrade serum antibodies, complement, and cytokines.
Leukotoxin
Secreted by Actinobacillus actinomycetemcomitans to destroy PMN and monocytes.
Host innate response to oral infections
Secrete IL-1B and TNF-a and prostaglandins (PGE2). LPS bind to CD14 and TLR-4
PGE2 (prostaglandins)
Found in GCF. Responsible for bone re-absorption/induction/destruction in P. gingivalis
NSAIDS and dexamethasone
Decrease/complete inhibit of loss of alveolar bone.
Early periodontal lesions
Cell immune response. T cells and macrophages. Th1-cell with IL-12, and INF-y. Cytokines lead to macrophage activation.
Established and late lesions
B cells and plasma cells. Progression controlled by Th2-cell derived cytokines with antibody production and disease progression. Increased overproduction of cytokines IL-1 and inflammation. Chronic inflammation
Localized aggressive periodontitis characteristics
Elevated levels of IgG2
T-helper 1 antibody periodontitis
early Aggressive periodontitis