aetiology and pathogenesis

Question 1

gingival crevicular fluid

Answer 1

more released during disease than in health

contains AMPs , cytokines, chemokines, lactoferrin , IgG

Question 2

why does poor OH contribute to gingivitis and periodontitis risk

Answer 2

poor OH = plaque accuulation = sustained inflammatory response

Question 3

polymicrobial dysbiosis

Answer 3

community of microbes working together to actively disrupt normal homeostatic balance for their own benefit

Question 4

virulence factors of P gingivalis

Answer 4

asaccharolytic - gets energy from breakdown of proteins which the immune response provides
gingipains - proteases that degrade host protiens and they can then be used as an energy source
atypical LPS (endotoxin) - blocks host signalling through TLR 4 receptors
inflammophillic - adapted to thrive in inflammatory conditions

Question 5

hallmarks of periodontitis

Answer 5

increased pocket depth
attachment loss
degradation of alveolar bone

Question 6

process of gingivtis

Answer 6

begins when host detects an accumulation of plaque via TLRs
increased activation of TLRs = increased production of pro inflammatory mediators e.g cytokines , chemokines , AMPs
these trigger clinical signs of inflammation e.g redness, swelling , bleeding , vasodilation and cell migration

Question 7

what are the functions of the immune cells that migrate to the area of gingivitis

Answer 7

neutrophils - main contributor , degradative enzymes e.g MMPs
monocytes - differentiate to macrophages and phagocytose
lymphocytes - t cells coordinate response , B cells release antibodies into GCF

Question 8

what is the triad of cytokines involved in bone formation and resorption

Answer 8

RANKL - produced by activated T and B cells , stimulates osteoclasts to resorb bone
RANK - receptor for RANKL on osteoclasts
OPG - RANKL inhibitor

Question 9

in periodontitis what is the ratio of RANKL to OPG

Answer 9

RANKL in excess therefore more bone resorption than formation

Question 10

process of periodontitis

Answer 10

activation of TLRs on gingiva = secretion of cytos, chemos and AMPS causing vasodilation and immune cell migration
activated lymphocytes express RANKL/ OPG which disrupts the balance causing bone resorption
pro inflammatory cytokines inhibit bone formation
elevated and disregulated MMP production = connective tissue destruction