Periodontics Flashcards
Why do we need a classification system for gingivitis?
The classification systems are necessary in order to provide a framework in which to scientifically study the aetiology, pathogenesis and treatment.
What is gingivitis?
It is generally regarded as site-specific inflammatory condition initiated by dental biofilm accumulation and characterized by gingival redness and oedema and the absence of periodontal attachment loss
How does gingivitis diagnosed?
It is a purely diagnosed condition. Use signs and symptoms. Look, feel and SMELL it. Listen to the patient – do their gums bleed? Are they experiencing soreness in gums? Increased BOP? Halitosis smell? Discomfort on probing?
What if you see any bone loss in the radiograph and think it is gingivitis?
NO IT IS PERIODONTITIS. Any attachment loss = periodontitis (except for reduced periodontium).
What is the prevalence of gingivitis and periodontitis?
Gingivitis of some degree – 95% of the population
Periodontitis – 60-65% of over 65 population
How do we define cases of gingivitis in an intact periodontium?
Localised gingivitis : Probing attachment loss – No, Radiographic bone loss – No, BOP score – between 10% and 30%
Generalised gingivitis: Probing attachment loss – No, Radiographic bone loss – No, BOP score – above 30%
How do we define cases of gingivitis in a reduced periodontium without history of periodontitis?
Localized gingivitis: Probing attachment loss – Yes, Radiographic bone loss – Possible, Probing depth all sites – less than 3mm, BOP score – between 10% to 30%
Generalised gingivitis: Probing attachment loss – Yes, Radiographic bone loss – Possible, Probing depth all sites – less than 3 mm, BOP score – above 30%
How do we right diagnostic statement for gingivitis?
- Extend - localised of generalised
- Disease - gingivitis
- Specification - biofilm induced, mediated by pregnancy or leukaemia
What is the pathogenesis of gingivitis? (Initial reaction)
- Biofilm accumulates
- Biofilm produces metabolites (fatty acids), peptides (FMLP) and LPS
- Junctional epithelium cells stimulated to synthesize inflammatory mediators (cytokines)
- Free nerve peptides produce neuropeptides and histamine in response to cytokines
- Perivascular mast cells release even more histamine
- This cause an increase in local vascular activity
- Endothelium releases IL-8 into vessels to attract PMNs
What is the pathogenesis of gingivitis? (PMNs migration)
- Mast cells release histamine
- Direct activation – LSP or OMP react with endothelial cells
- Indirect activation – after contact with LPS/OMP macrophages release proinflammatory cytokines
- ELAM-1 is expressed
- Contact between leucocytes adhesion receptor integrin beta 2 with endothelial Integrin ICAM-1
- PMNs leave vessel by amoeboid diapedesis
- PMNs follow gradient of chemotactic factors
What is the pathogenesis of gingivitis? (Post PMNs migration)
- Biofilm stimulates JE cells to produce cytokine IL-8
- IL-8 is a chemo-attractant for PMNs
- PMNs follow IL-8 concentration gradient
- PMNs reach the sulcus
- Complement and antibodies support phagocytosis of bacteria and their products
What is the pathogenesis of gingivitis? (Early gingivitis)
- PMNs form dense layer over biofilm
- PMNS and tissues release pro-inflammatory cytokines nad enzymes
- Activation of macrophages (more proinflammatory things)
- Lymphocytes infiltrating connective tissues (T cells mostly)
- Increase in vascular dilation
- Lateral proliferation of junctional epithelium basal cells
What is the pathogenesis of gingivitis? (Established gingivitis)
- Intense PMN infiltration in junction epithelium
- Lymphocytes dominate the infiltrate
- Activated T cells coordinate the response via cytokines
- B cell differentiation and conversion to plasma cells
- Plasma cells produce Igs and cytokines
- Activated fibroblasts produce MMP and TIMP instead of collagen
- Loss of collagen fibres to provide space for expanding infiltrate
- Lateral proliferation and apical migration of junction epithelium (creation of pseudopocket)
Why do we say that gingivitis “takes two”?
Because gingivitis take 2 important factors to develop –1 the microbes and 2 the host response to the microbes
What is a risk factor?
It is something that increases the chance of developing a disease or disorder
What are the two categories of risk factors of gingivitis?
- Systemic
- Local
What are the systemic risk factor for gingivitis?
It is something that modifies disease expression and may influence disease progression by altering the host’s immune response
What are some of the systemic risk factors for gingivitis?
- Smoking
- Hyperglycemia
- Nutritional factors
- Pharmacological agents
- Sex hormones
- Hematological conditions
What are the impacts of smoking on gingival tissues
- Decrease immunoglobulin G2 production
- Chronic reduction in blood flow and vascularity – THIS ALSO REDUCES THE BOP AND POTENTIALLY REDUCING POCKET DEPTH
3Increase prevalence of potential periodontal pathogens
- Shift in neutrophil function towards destructive activities
- Negative effects on cytokine and growth factor production
- Inhibition of fibroblast growth attachment and collagen production
How does hyperglycaemia impact gingivitis?
Hyperglycaemia causes a production of advanced glycation end products or (AGE) which causes immune disfunction, cellular stress & increase of proinflammatory cytokines.
What is the local risk factor for gingivitis?
It is the retention biofilm or prevent its removal and predispose for disease progression
What are some of the local factor for gingivitis?
- Dental plaque retention
- Oral dryness
What is DIGO?
Drug Induced Gingival Overgrowth
What are some of the medication associated with DIGO?
- Calcium channel blocker
- Immuno-suppressants
- Anticonvulsants
How do you treat patients with DIGO?
- Biofilm control
- Surgical excision
- Drug substitution
What are signs of necrotising gingivitis?
- Necrosis of papilla
- HELLA BOP
- Pain on probing
- Halitosis
- Lympadenopathy
What causes necrotising gingivitis?
It is caused by opportunistic bacteria but it is also influenced by systemic factors
What are the treatments of necrotising gingivitis?
- Debriment under LA
- Local Irrigation with Chlorhexidine 0.2%
- Antibiotic Therapy – Metronidazole 400mg orally, 12-hourly, 3-5 days
- Analgesics
- Review
- potentil referral to a Specialist or GP
What are some of the classifications of the non-biofilm induced gingival disease
- Genetic developmental disorders
- Specific infections
- Inflammatory and immune conditions and lesions
- Reactive processes
- Neoplasms
- Endocrine nutritional and metabolic diseases
- Traumatic lesions
- Gingival pigmentation
What is supra- and subgingival debridement?
It is the removal or disruption of dental deposits and plaque-retentive calculus from tooth surfaces and within the periodontal pockets space without deliberate removal of cementum as done in root planning and often in dental scaling
What is the relevance of debridement in treating periodontal disease?
As biofilm matures, the opportunities to shift from healthy biofilm to pathogenic increases.
Debridement allows for removal of the biofilm or destruction of the bio-environment which encourages the growth of less pathogenic species of bacteria within the biofilm.
What is the rationale of removal of supra and subgingival calculus?
- This eliminate a potential colonisation site for the pathogenic bacteria
- This allows the patient to perform oral hygiene techniques appropriately
What are the instruments available for debridement at the ADH for supragingival removal?
- Sickle Scaler – anterior
- McCall’s Scaler – universal
- Ultrasonic scaler – regular or fine tip
- Gracey Curettes – with limitations around the contact point
What instruments can be used for debridement at the ADH for subgingival removal?
- Ultrasonic scaler – XF tip
- Gracey Curettes