immunology and pathogenesis Flashcards
what causes periodontal disease
bacterial pathogens and the host immune response
t/f. acute inflammation causes vascular permeability
true. it then results in redness, edema, and increased GCF flow
bacterial species that invade periodontal soft tissue
P gingivalis and Aa
effects of bacterial metabolic waste products
ammonia, indole compounds, FA, hydrogen sulfide
damaging bacterial enzymes
leukotoxins (Aa) and gingipains (proteases from Pg)
immunostimulatory molecules
LPS (G-), lipoteichoic acid (G+), gingipains, formylpeptides (stim. leukocyte chemotaxis)
what does LPS do
complement activation, pmn activation, macrophage activation, B-cell mitogen activity, pyrogenicity, stim bone resorption, stim prostaglandin synthesis, induction of TNF-alpha
host defense of gingivitis
acute inflammation (also seen in an abscess)
host defense of periodontitis
chronic inflammation (also seen in Tb)
after Tx, there is typically an increase or decrease in protease levels?
decrease
what do proteinase inhibitors do and what are 2 examples
inhibit degradation of matrix proteins
alpha-2 macroglobulin, alpha-1 antitrypsin
what do MMPs do
degrade ECM (ex. PMN collagenase)
are there higher or lower concentrations of MMPs in inflamed gingiva
higher
what do IL-1beta and TNF-alpha do
proinflammatory cytokines that stimulate bone resorption and inhibit bone formation
what does IL-8 do
chemotactic activity
PGE2
prostaglandin that induces vasodilaiton and cytokine and MMP production
t/f. pmns are only in GCF in disease states
false. health and disease
primary and secondary granules found in periodontitis lesions
elastase - primary, lactoferrin - secondary
osteoclast activating cytokines
IL-1beta, 6, 11, 17, PGE2, TNF-alpha
RANKL:OPG ratio
RANKL (osteroclast activationg) higher and OPG (ostoblast activating) lower in periodontitis
innate immunity defense in periodontitis
biofilm, gingival crevice, mechanical barrier
acquired immunity
acute and chronic inflammatory process
how does GCF provide innate immunity
carries antibodies, lactoferrin, lysozyme
4 steps the innate immune sys takes to provide a defense mechanism
oral mucosa makes antimicrobial peptides
oral epithelium produce pro inflammatory cytokines (IL-1B and TNF-alpha, IL-8)
GCF flows to the site of injury
phagocytic function of PMNs and macrophages
what do TLRs do for immuntiy
recognize MAMPs and signal cells to make cytokines, chemokines, antimicrobial peptides, NO and eicosanoids
responds to ox LDL
in chronic periodontitis, describe the relative amount of plasma cells to Blymphocytes to T lymphocytes
plasma cells > B lymphocytes > T lymphocytes
Th1 cytokines involved in chronic periodontitis
IL-2, IFN gamma, TNF alpha
Th2 cytokines involved in chronic periodontits
IL-4, 5, 6, 10, 13
t/f. in chronic periodontitis, IgG2
true. IgG2 is predominant in aggressive periodontitis annd recognizes LPS
t/f. Th2>Th1 in chronic periodontitis
true. plasma cells are the most predominant and active secretory cells in advanced periodontitis
an advanced periodontitis lesion is characteristic of what stage in periodontitis
4
what happens in advanced periodontits
plasma cells dominat the ct, PMNs dominate the JE, apical migration of the JE = attachment loss