Pathogenesis of Periodontal Disease Flashcards
What is the main factor in transitioning from clinical health to gingivitis?
Do all patients progress to periodontitis?
Is there a cure for periodontitis?
- largely due to the presence of sufficient amounts of plaque, the amount of plaque and length of time present (differs between patients of different susceptibilities)
No, some patients are genetically resistant to periodontitis whereas others with FH of periodontitis increases susceptibility.
No, periodontitis cannot be cured, it can only be stabilised. If conditions allow, disease will restart e.g. smoking, plaque/poor OH
What are the theories of periodontal progression?
Socransky proposed 3 different models to describe the possible patterns and rate of progression of periodontitis:
- continuous rate theory
- random burst theory
- asynchronous multiple burst theory
Briefly describe the continuous rate theory:
- sites are active or inactive
- at active sites, the rate of progression continues at a constant rate over time, unless treatment is carried out
- different active sites may be progressing at different rates
Briefly describe the random burst theory:
What is the difference to asynchronous multiple burst theory?
- sites can be active or inactive
- at active sites there are random bursts of periodontal destruction followed by periods of no activity with possible periods of repair
- different sites are active at different times, progress at different rates and are active for different periods of time
Asynchronous is similar to random burst theory, but multiple active sites breakdown within a short defined period of time
What is RAL?
What is GAL?
How does susceptibility affter these terms?
RAL - rapid attachment loss: extensive LOA detected in a short period of time (detectable by manual probes e.g. CP12)
GAL - gradual attachment loss: small LOA over time in lots of mini-bursts or slow continuous LOA (only detectable by very sensitive electronic probes e.g. Florida probe)
High susceptibility patients progress in bursts of RAL
Low susceptibility patients progress more slowly with GAL
GAL and RAL may occur in the same patient at different sites in the mouth
What risk factors are there for periodontitis?
Primary aetiological factor for periodontitis is dental plaque bacteria
Risk factors:
- high genetic susceptibility
- smoking
- uncontrolled diabetes
- immunodeficiency
- overhanging restorations
- alcohol
- stress
Risk factors increase the chance of progression!
As plaque biofilm accumulates and matures, evidence of inflammation increases with evidence of?
- increased gingival crevicular fluid (GCF) flow
- increase in inflammatory and immune cellular infiltrate in the connective tissue underlying Junctional Epithelium
- fewer fibroblasts in the gingival connective tissue underlying JE
- reduction in collagen content in the inflamed connective tissue under JE
What publication classifies the histopathological changes which take place during progression from gingivitis to periodontitis?
What are the 4 phases?
Page and Schroeder
Initial lesions
Early lesions
Established lesions
Advanced lesions
What are the key findings in initial lesion?
- occurs within 24-48 hours of plaque accumulation
- plaque mainly gram positive aerobic bacteria
- vasodilation of blood vessels, increased number of neutrophils/monocytes, and GCF production
- tissue damage minimal
- inflammatory infiltrate confined to small area of connective tissue below JE
- bacterial factors/antigens initiate an inflamatory response
What are the key findings in early lesion?
- no clinical findings yet!
- occurs approx after 1 week
- immunoglobulin production and cytokines released
- increase in size of inflammatory infiltrate - mainly PMNs and lymphocytes
- loss of fibroblasts and collagen in infiltrated area
- increased GCF
- Neutrophils accumulate in gingival crevice
- swelling of gingva resulting in a deeper gingival crevice
- favours growth of gram negative bacteria with associated release of endotoxins and enzymes which cause more tissue damage
What are the key findings in an established lesion?
- corresponds to clinically obvious gingivitis
- gingival connective tissue largely replaced by inflammatory infiltrate
- JE replaced by ulcerated, leaky pocket epithelium, but no LOA
- large numbers of PMN and plaque biofilm building up subgingivally
- bacterial products cause damage: directly by enzymes and indirectly by triggering host response - release of cytokines, complement, enzymes (PMN release MMP 8 and MMP 9 resulting in connective tissue damage)
- continued loss of collagen in the gingival connective tissue
What are the key findings in an advanced lesion?
- inflammatory infiltrate extends apically and laterally, compromises >50% plasma cells
- continued loss of collagen
- ulceration and migration of JE apically to root surface = LOA
- this stage corresponds to periodontitis
- advancing inflammatory front where host tries to stop spread of invading bacteria, leading to breakdown of PDL and bone loss seen with osteoclasts on periosteal and endosteal surfaces of crestal bone
- the apically advancing periodontal pocket creates the ideal environment for the growth of periodontal pathogens Gram negative anaerobes (GNABs)
What is the role of the host response?
- protection of the host against local microbial attack
- prevention of spread of micro-organisms if manage to invade tissue
What does tissue damage to periodontal ligament involve?
Bone resportion?
- destruction of PDL fibres inserting into the bone and cementum
- loss of extracellular matrix
- fibroblast damage
- loss of the surface cementoblast layer
Bone resorption:
- mediated by both host-derived and bacterial factors
- majority of bone loss due to release of factors produced by host response such as cytokines (IL-1), prostaglandins (PGE2), which lead to activation of osteoclasts
