Periodontology Flashcards
What is the clinical presentation of a patient with symbiosis?
Patient will have clinical gingival health
What is the clinical presentation of a patient with dysbiosis?
Patient will have reversible gingivitis OR irreversible periodontitis
What causes the transition from symbiosis to dysbiosis in patients? Is this the same for everyone?
Mainly due to plaque accumulation No- the amount of plaque and length needed to cause disease varies between people due to different susceptibilities and risk factors
What factor of plaque is most important in causing gingivitis?
The quality of plaque (i.e. components) is more important than its quantity
What is the benefit of diagnosing periodontal disease early?
Patient will respond better to periodontal therapy, such as: - OHI - Scale and polish - Smoking cessation
What do epidemiological (population) studies show about the incidence of periodontitis?
Periodontitis occurs as a SPECTRUM In any given population: 1. 10% will have severe, destructive periodontitis with tooth loss 2. 10% never get disease despite poor OHI 3. 80% have slowly progressing periodontitis if enough treatment is given, plus potential tooth loss
Can we cure periodontitis?
Periodontitis is incurable but can be stabilised
What does the 2017 Periodontal Classification say about treating periodontal disease?
We can only stabilise periodontitis by ensuring the patient stays in clinical gingival health However if conditions favour disease progression occur (such as smoking/poor OHI) clinical health can be lost. This tips the ‘scale’, meaning disease will return and progress
What are the 3 models of periodontitis progression?
- Continuous Rate Theory 2. Random Burst Theory 3. Asynchronus Multiple Burst Theory
Describe the Continuous Rate Theory (4)
Sites in mouth are either active or inactive Disease progression is constant unless active sites are treated Different active sites might deteriorate faster than others This theory not really believed today
Describe the Random Burst Theory
Sites can be active or inactive Active sites have random or EPISODIC bursts of periodontal destruction. These are then followed by periods of no activity, called QUIESCENE Some sites can self-repair during quiescene, before bursts happen again. Different sites are active at different times and can progress differently. This is because they are each their own different micro-environments with different: - Plaque levels - Root anatomy - Levels of calculus - Different bacterial strains
Describe the Asynchronous Multiple Burst Theory: How does it differ from the RBT? What does this imply?
Similar to the RBT, however multiple active sites will breakdown within short defined periods of time Implies that some transient factor causes multiple sites to breakdown at the same time: - Stress - Illness -Other risk factors Activity is then followed by long periods of quiescence
What is RAL?
Rapid Attachment Loss: This is extensive loss of attachment in a short time period. Detected by manual periodontal probes
What is GAL?
Gradual Attachment Loss: Small amounts of loss of attachment over time in either; 1. Lots of mini-bursts 2. Slow and continuous 2) is detected by an electronic probe called a Florida probe
Who is more commonly affected by RAL?
More common in patients with high susceptibility to periodontal disease
Who is more commonly affected by GAL?
Slow and gradual process; more common in patients with low susceptibility to disease
Can a patient only have GAL or RAL?
NO- both can occur at different sites in the same mouth
When do we carry out RSD?
Root Surface Debridements (RSD) are done in: True pockets 4mm or greater, with BOP and/or sub gingival calculus in patient with good OHI
How do we overtreat patients?
Only 30% of sites with BOP will go on to have further LOA, but dentists must treat all pockets. This is because we don’t know what specific pockets will go on to have LOA
What are the risk factors for periodontitis? (8)
Primary factor is dental plaque 1. Genetics 2. Smoking 3. Uncontrolled diabetes 4. Immunodeficiency 5. Overhanging restorations 6. Stress 7. Alcohol
What is present histologically in patients with clinical health?
Inflammatory cells- mostly neutrophils in the gingival connective tissue. This shows the concept of physiological immune surveillance
What happens when the plaque biofilm accumulates?
Gingival inflammation also increases: 1. Increased GCF flow 2. Increase in inflammatory and immune cellular infiltrate in connective tissue underlying the junctional epithelium 3. Fewer fibroblasts in the gingival connective tissue under junctional epithelium 4. Decrease in collagen content of infiltrated C.T. underneath the junctional epithelium
What did Page and Schroeder (1976) show?
They classified the histopathological changes in gingivitis progressing to periodontitis
How did Page and Schroeder show this? (4)
By dividing lesions into 4 phases: 1. Initial lesion 2. Early lesion 3. Established lesion 4. Advanced lesion
What lesions are found in: early stages of gingivitis clinically apparent gingivitis periodontitis
early stages of periodontitis: initial and early lesions clinically apparent gingivitis: established lesions periodontitis: advanced lesions
when do initial lesions happen? describe plaque’s properties here (3)
within 24-48 hours of plaque build-up plaque is mainly gram-positive, aerobic and saccharolytic
what happens histologically in initial lesions?
Vasodilation Increased neutrophils GCF formation Minimal tissue damage as infiltrate is confined to small area of connective tissue under the junctional epithelium
