periodontal pathogenesis Flashcards
describe the pathogenesis of human periodontitis
microbes release LPS’s & Ag’s which causes the body to launch immuno inflammatory response( antibodies, cytokines, prostanoids MMPs) this affects connective tissue and bone metabolism which causes the clinical signs of the disease and progression.
what do environmental risk ( smoking)factors affect?
host immunoinflammatory response and connective tissue and bone metabolism
Whats the non-specific plaque hypothesis?
its the high number of bacteria that cause the problems
whats the specific plaque hypothesis?
its the quality of bacteria that causes problems
whats the ecological plaque hypothesis?
environment shifts from aerobic to anerobic
What are some bacterial virulence factors associated with plaque?
exotoxins and endotoxins
Innate immunity factors in defense
1st line of defense, present at birth, not enhanced by prior exposure, lacks memory, fast but lacks specificity
examples of innate immunity
saliva, GCF, epithelium, commensal microflora
explain why innate immunity can cause damage?
its not specific,
Epitheliums role
barrier( tight jxns), high turnover rate,
Salivas role
prevents bacterial attachment, contains IgA, IgM, IgG
charecteristics of adaptive immunity
specific, memory, diverse, recognition of self cells, humoral( antibodies), cell mediated( immune cells)
inflammatory mediators purpose is…
to initiate, perpetuate, and terminate an inflammatory response.
what are the pro-inflammatory cytokines?
interleukins, chemokines, interferins
Interleukin 1-
major mediator of periodontitis
Which cells does IL1 target?
T-cells, epithelial cells ,endothelial cells, fibroblasts
IL1 induces what?
proinflammatory proteins, hematopoesis, differentiation of Th17 cells
IL 2-5 are all what?
lymphocyte signaling cytokines
IL2 is produced by what?
CD4, CD8, and activated T lymphocytes
what does IL4 do?
regulated immunoglobilin production, suppresses activated macrophages and causes their apoptosis
TNF-a is produced by what and does what?
macrophages, works like IL1 and mediates inflammatory response and connective tissue destruction
what are the 2 key mediators of chronic inflammatory diseases?
TNFa, IL-1
what does IL6 do?
causes fusion of monocytes to form osteoclasts
what does IL8 do?
induces directional migration of PMNs, monocytes, Tcells to accumulat at inflammation sites
what does IL10 do?
suppresses immune and inflammatory response,
what does transforming growth factor B do?
its a chemoattractant for monocytes and suppreses their activation
prostaglandins are ________ derivatives?
arachidonic, important inflammation mediators
matrix metalloproteinases do what?
tissue remodeling and degradation of ECM. Their regulated by hormones, growth factors and cytokines
Bone loss in response to inflammation depends on ….
concentration of inflammatory mediators in gingival tissues.
what are the proinflammatory cytokines that lead to bone resorption?
IL1, 6, 11, 17, TNFα, Oncostatin M, Leukemia inhibitory factor, Bradykinin, Kallidin and Chemokines
what are antiinflammatory cytokines that inhibit bone resorption?
IL4, 10, 12, 13, 18, IFN-β, IFN-γ
whats RANKL
receptor activator of nuclear factor kappa B ligand, its expressed by osteoblasts, fibroblasts, tcells, bcells
RANK
the receptor for RANKL and is on osteoclasts
OPG
osteoprotegerin, expressed by osteoblasts, it binds to RANKL to prevent it from activating osteoclasts
RANKL, RANK, OPG and bone resorption
elevated RANKL / =OPG or =RANKL / lowerOPG
RANKL, RANK, OPG and bone formation
lowered RANKL / =OPG or =RANKL / elevated OPG
