Periodontal Immunology Flashcards
what is gingivitis?
- inflammation localised to the gingival tissues
- acute inflammation
- normal physiological response to infection or injury
what is periodontitis?
- inflammation of the gingival tissues and supporting periodontal structures (periodontal ligament and alveolar bone)
- chronic inflammation
- pathological inflammatory response associated with tissue destruction
is gingivitis or periodontitis reversible?
gingivitis = YES periodontitis = NO
what is the function of gingival crevicular fluid?
predominant immune defence of sublingual portion of teeth and it contains:
- cytokines
- chemokines
- IgG
- AMPs
- lactoferrin
how does the oral mucosa play a part in immunological defence?
acts as a physical and functional barrier
how does the oral mucosa act as a functional barrier?
can detect & respond to microbial challenge through activation of TLRs, this leads to activation of inflammatory pathways
can periodontitis occur in the absence of bacteria?
NO
- bacteria is the trigger for inflammation
explain the meaning of polymicrobial dysbiosis in relation to periodontitis?
periodontitis is associated with a COMMUNITY of microorganisms that work together to actively disrupt the normal homeostatic balance of the oral cavity (for their own benefit)
what are some virulence factors of P. gingivalis?
- asaccharolytic
- gingipains
- atypical LPS
- inflammophilic
- drives dysbiosis
what is the meaning of asaccharolytic?
a organism gets nutrients from breakdown of proteins and peptides (not carbs)
what is the aetiology of periodontitis associated with?
- accumulated plaque bacteria
- presence of periodontal pathogens
- polymicrobial dysbiosis
in SUSCEPTIBLE HOSTS***
what are the hallmark clinical signs of periodontitis?
- increase in pocket depth
- attachment loss
- degradation of alveolar bone
what events occur that cause alveolar bone resorption?
- bacterial products bind TLRs on epithelium which stimulates secretion of cytokines, chemokines and AMPs
- vasodilation occurs and selective recruitment of leukocytes (neutrophils, monocytes and lymphocytes)
- bacterial products activate neutrophils, further release of pro-inflammatory mediators
- activated lymphocytes express RANKL & the RANKL/OPG balance is disrupted
- RANKL binds RANK on osteoclast precursors which activates osteoclastogenesis leading to alveolar bone resorption
what is the role of adaptive immunity in periodontal destruction?
- T and B lymphocytes present in early lesion
- unable to regulate dysbiotic biofilm
- inflammation induces alveolar bone loss and loss of attatchment
