Pathogenesis Of Periodontal Disease Flashcards
What hypothesis is mainly used now
Specific plaque hypothesis
**red complex
P gingivalis
Tannerella forsythia
Treponema denticola
What are the main receptors in recognition of perio pathogens and what do they respon to?
TLR 2 and TLR 4
Respond to LPS stimulation
Which interleukin is in high concentration in dental plaque
IL8. Concentration gradient down deeper into the connective tissue. Neutrophils migrate up the gradient where they are most likely to encounter bacteria
Which cytokines are significantly increased in perio disease
IL-1 and TNFa significantly increased in diseased perio sites. Graves and Cochran 2003
IL-1 positive correlates to increased probing depth and clinical attachment loss delima et al 2002
Perio therapy reduces il1b and tnfa al shammari et al 2021
Wha does il1 do
Stimulate osteoclast proliferation, differentiation, and activation. Stimulate osteoclastic bone resorption.
Potent inflammatory molecule
Describe the rank/rank ligand pathway
Osteoclast precursor has rank receptor. Osteoclast has rank ligand. Rank meet rankl, osteoclast precursor become mature active osteoclast. Tnfa and IL1 promote rank/rankl pathway hence cause more bone resorption
What drug can be used to reduce osteoclast formation via rankl path way
Osteoprotegerin which is decoy for rankl. Binds to rank receptor and blocks pathway
How do pro inflammatory cytokines regulate bone resorption
Induce synthesis of rankl
What are mmps and how are they involved in perio disease
Increased levels of MMP 1,3,8 in periodontal disease
Mmps are proteolytic or collagenolytic. They degrade extracellular matrix molecules eg collagen, elastin, and cause periodontal destruction
What is the etiology of periodontitis
Bacteria in a susceptible host (due to presence of risk factors
At which stage does gingivitis progress to periodontitis
Page and schroeder 1976
Established (14-21 days)
Key histological feature at established state of gingivitis. Is bone loss present?
Established stage = periodontitis. Proliferation, apical migration, lateral extension of JE. No appreciable bone loss
When does established tip over to advanced periodontitis
When there is change in microbes or host response
At advanced stage see increased probing depth, sappuration persistent established lesion, significant bone loss
Why dont all gingivitis progress to periodontitis
Intact barrier provided by junctional epithelium
Regular shedding of epithelial cells into oral cavity
Outward flow of GCF that might wash away unattached micro organisms and noxious products
Antibodies in GCF
Phagocytes eg macrophages
