Periodontitis: aetiology and pathogenesis Flashcards
(50 cards)
What are the risk factors for periodontitis?
- behavioural
- environmental
- genetic
- epigeneitc
What is the inflammation like in clinical health, gingivitis and periodontisis
clinical health- acute resolution of inflammation
gingivitis - chronic resolution of inflammation
periodontisis - chronic non-resolving inflammation
What is the role of plaque in periodontal disease
plaque is NECESSARY but NOT SUFFICIENT for periodontal disease
plaque will cause gingivitis but not always periodontal disease
What is the pathogenesis of gingivitis
Microbial challenge (plaque)
- local plaque retention factors e.g. calculus, restoration margins, crowding, mouth breathing
- systemic modifying factors e.g. sex hormones, medication
Clinical disease (gingivitis)
What does gingival health look like
- knife edge, scalloped gingival margin
- stippling (about 30%)
- pink
- oral epithelial cells shed continuously
- flow of GCF (antibodies inside)
- cellular immune response is small and regulated
- intact barrier provided by the junctional epithelium
What does gingivitis look like
- red margins, inflamed, no stippling
- increase plaque and change in its composition
- increased GCF, increased immune cells
- proliferation and ulceration of epithelium (bleeds)
- predominance of plasma cells
(all increases as gingivitis becomes more established)
What happens to gingivitis when you remove the microbial challenge
return to health
What does periodontitis look like
- bone loss (irreversible)
- apical migration of the junctional epithelium
- plasma cells >50%
How can we tell the difference between gingivitis and periodontitis
by using a BPE probe
Why can smokers gingiva be misleading
they have paler gingiva and look healthy but can have deep pockets
Does gingivitis always progress to periodontitis
not always
Once periodontitis is initiated, how does attachment loss progress
episodic rather than continuous
Do all regions of the mouth progress to periodontitis at the same rate
no, can be very different within the same mouth
How quickly does attachment loss happen
generally very slow (0.05-0.1mm per year) but this is highly variable
What is a big factor as to how fast patients are to periodontitis
their microbiome/ immune response
what is a biofilm
one or more communities of microorganisms, embedded in a glycocalyx, attached to a solid surface
What are the properties of biofilms?
- provide protection for colonising species from competing organisms and environment (host defences, antibiotics etc)
- facilitate uptake of nutrients and removal of metabolic products
- development of appropriate physiochemical environment e.g. pH, O2 concentration
- communication between bacteria
What is bacterial virulence
- ability to colonise and compete in an ecological niche
- ability to evade the host defences
How can we work out whether specific bacteria cause periodontal disease
- presence in elevated numbers at diseased sites
- reduced numbers following periodontal therapy
- presence of an elevated specific immune response
- production of virulence factors
- evidence from animal models
Is there any proved causative microorganisms in periodontal disease
no, none satisfy koch’s postulates
- complexes are more likely
what is a key stone pathogen
will change to make the whole community bad
What are the 3 microorganisms at the ‘top’ of the periodontal disease pyramid
- P. gingivalis
- B. forsythus
- T. denticola
Periodontitis is a synergistic infection what does this mean
plaque ecology is important
there are other host and environmental factors which modify the disease
What mechanisms does the host immune response have against periodontal disease
- saliva
- epithelium (physical barrier, shedding of cells, production of inflammatory mediators)
- GCF
- inflammatory and immune responses
