Gingivitis: Clinical signs, microbiology and pathogenesis Flashcards
(34 cards)
What are the periodontal structures?
Gingiva, PDL, cementum and alveolar bone
What are the different structures of the gingiva?
- Gingival margin
- Gingival sulcus
- Free gingiva
- Gingival/ marginal groove
- The attached gingiva
- Mucogingival junction
- Alveolar/ oral mucosa
What are the 5 signs of inflammation?
- Calor – heat
- Dolor – pain
- Rubor – redness
- Tumor – swelling
- Functio laesa – loss of function
What are the inflammation types of gingiva?
Acute:
• Acute Necrotising Ulcerative Gingivitis (ANUG)
• Primary Herpetic Gingivostomatitis
Chronic: Most other types of gingivitis tend to be chronic
What does the inflamed gingiva appear as?
- Red (erythema)
- Swollen (oedema)
- Shiny
- Soft
What are the clinical signs of gingivitis?
- Inflamed gingiva
- Bleeding on probing after 30 secs
- No bone destruction
Why is there bleeding on probing with gingivitis?
- Sulcus depths are increased
- Increased GCF flow
- Clinical signs are present within about 4-5 days of undisturbed plaque accumulation and maturation
Why is there no bone destruction with gingivitis?
- No breakdown of PDL fibres or bone destruction as part of the disease process
- Gingivitis is reversible with optimal oral hygiene and removal of any calcified plaque deposits
- No long term harm
What is the disease process of gingivitis?
Exaggerated host response to plaque
Interaction between microorganisms found in dental plaque biofilm and the tissues/ inflammatory cells of the host.
How does gingivitis all happen?
• Bacterial products from plaque stimulate epithelial cells to produce inflammatory mediators
→ Inflammatory response
→ Interleukins, prostaglandins, and destructive enzymes e.g. collagenases
• Fluid accumulates in tissues (clinical picture - red and swollen)
• PMNs infiltrate gingival tissues (also lymphocytes and macrophages)
• Neutrophils release destructive enzymes (collagenases) and other inflammatory mediators → positive feedback cycles
- If plaque is left on the teeth, the host continues its frustrated response to bacterial products
- Inflammation and destruction spreads to all the periodontal structures
- Ultimately, if unchecked, the inflammation would spread to the bone, which is resorbed by osteoclasts to make more room for the defence cells – i.e. periodontal disease
- This pathogenic process differs in extent and severity between individuals and the reasons are multifactorial, but there is clearly a strong genetic component to disease susceptibility
What resorbs bone to cause PD?
Osteoclasts resorb the bone – periodontal disease
What is a biofilm?
Biofilm - collection of organisms, held together with a matrix structure, on a surface or interface.
What is EM?
Extracellular matrix – dense mass of structure
Why are biofilms a problem? (7)
- Microorganisms are more resistant to attack
- Strength in greater no.’s
- Phenotype can change in biofilms
- Slow growth (lack of nutrients) means that antimicrobials (AM) targeting growth are ineffective
- Re-dox potential of biofilm deactivates AM
- Anaerobic bacteria predominate in the deeper layers (as oxygen is used by superficial bacteria)
- Bacteria in biofilm formation can be up to 1000 times more resistant to AM than planktonic form
Why must biofilms be disrupted mechanically?
Biofilms protect bacteria and therefore biofilm MUST be disrupted mechanically
What is the ecological/environmental plaque hypothesis?
- Not one specific pathogenic bacteria that causes disease
- The whole ‘biofilms’ virulence and the host response will dictate the progression to periodontitis
What the the 3 key factors of the oral microbiology with plaque related gingivitis?
- Gingivitis and subsequently periodontitis are not caused by one single bacterial species
- Initiation of disease results from an interplay between the bacteria present, the local environment and the host response
- Biofilms must be mechanically disrupted
What is the clinical presentation of ANUG?
- Painful, sloughing of gingival margin
- Ulceration
- Poor plaque control
What is the aetiology of ANUG?
- Fusospirochaetal complex
- Often immunocompromised, poor diet and general health
- Smokers
What is a Fusospirochaetal complex?
Trench mouth, a progressive painful infection with ulceration, swelling and sloughing off of dead tissue from the mouth and throat due to the spread of infection from the gums
What is the treatment of ANUG?
- Improvements in OH
- Scaling and debridement of teeth
- Antibiotics: Metronidazole 400mg TDS 3 days supply
- Hydrogen peroxide mouthwash 1.5 % w/v (peroxyl)
- CHX m/w 0.2% w/v
What is the function of the junctional epithelium?
Gives barrier and dense body of collagen fibres resist mastication
How is the junctional epithelium kept healthy?
- Intact epithelial barrier
- Shedding of epithelial cells
- Outflow of GCF
- Antimicrobial effects of antibodies
- Phagocytic function of neutrophils and macrophages
- Complement activity (attracting macrophages and neutrophils, cell lysis)
- Neutrophils and macrophages migrate through the JE into the sulcus
- GCF flows out through the gingival sulcus
- Collagen fibres maintain the form of the tissues and aid in attachment to the tooth
What is the junctional epithelium attached to?
Tooth surface
