S3 Recognising gingival conditions (gingivitis) Flashcards
Define gingivitis.
An inflammatory lesion resulting from interactions between dental plaque biofilm and the host’s immune inflammatory response which remains contained within the gingivae and does not extend to the periodontal attachment (cementum, bone, PDL unaffected).
Reversible.
What are the clinical features of gingivitis?
- Oedema
- Bleeding on gentle probing
- Erythema
- Discomfort on gentle probing
- Primarily asymptomatic (some pts experience sensitivity on probing or when brushing their teeth)
Explain the disease process with regards to gingivitis.
- Initial gingival lesion (2-4 days, not clinically evident): increased vascularity, capillary permeability, GCF, PMNs, less CT
- Early gingival lesion (5-7 days, mild gingivitis): collagen destruction/lost tissue tone, damage to fibroblasts, hyperplasia of JE basal cells
- Established gingival lesion (2-3 weeks, obvious gingivitis): lymphocyte/plasma cell lesion, some rete peg proliferation in SE, inflammatory cytokines, deepened gingival sulcus
What microorganisms are present in gingivitis?
- Mostly orange complex microorganisms: Parviromonas micra, Fusobacterium nucleatum, Prevotella intermedia, Tannerella forsythia, C. rectus
- Some red complex microorganisms: Porphyromonas gingivalis, Treponema denticola
How did the 2017 world workshop classify the 2 types of gingivitis?
- Dental plaque-induced
- Non-dental plaque-induced
What are the 3 types of patients with plaque induced gingivitis?
- Intact periodontium: no loss of attachment
- Reduced periodontium in a non-perio patient: minor loss of attachment, may be due to gingivla biotype, toothbrushing or habit etc.
- Reduced periodontium in a successfully teated periodontitis patient: loss of attachment, tissue inflammation but not at the base of a pocket
How is gingivitis classified according to distribution?
- Localised: 10-30% BoP
- Generalised > 30% BoP
- Gingival health < 10% BoP
How is plaque induced gingivitis classified by mechanism?
- Gingivitis associated with biofilm alone (poor OHI causing gingivitis)
- Gingivitis mediated by systemic or local risk factors (e.g. smoking, poor diet, hormones)
- Drug induced gingival enlargement
Give examples of systemic and local risk factors for gingivitis.
- Retentive factors e.g. overhanging margins
- Xerostomia
- Smoking
- Hyperglycaemia
- Nutrition
- Sex steroid hormones
- Haematological conditions
Describe smoking as a systemic risk factor for gingivitis.
- Nicotine induced peripheral vasoconstriction
- Masked gingival inflammation, reduced BoP
- Gingival fibrosis: pale and thickened gums
- Lower volumes of GCF
Describe hyperglycaemia as a systemic risk factor for gingivitis.
- Poorer innate immune repsonse
- Less polymorphonuclear leukocytes
- More inflammatory mediators (IL-1β and MMP-8)
- Increased BV permeability, changes to vascular walls, increased blood volume in vessels, vasculutis (BV inflammation)
Describe poor nutrition as a systemic risk factor for gingivitis.
- Vit C deficiency: increased oxidative stress, less collagen = more bleeding, less ability to repair damage to tissues
- High carbohydrate diet: more plaque accumulation
Describe xerostomia as a systemic risk factor for gingivitis.
- E.g. poorly controlled diabetes, anxiety, Sjogren’s, antidepressants, antihypertensives
- More plaque accumulation = increased risk of gingival inflammation
- Glossy, stretched out tissues
Describe sex steroid hormones as a systemic risk factor for gingivitis.
- Cytoplasm of gingival cells contain specific high affinity, low capacity receptors for oestrogen and testosterone
- Oestrogen has a stimulatory effect on the metabolism of collagen, stimulates angiogenesis and decreases keratinisation of the gingival epithelium
- Progesterone has a major effect in levels of pro-inflammatory mediators, gingival vasculature and permeability
- Puberty gingivitis (will see excessive gingival inflammation relative to the amount of plaque in these patients)
- Menstrual cycle (research suggests that when women ovulate, there is an increase in GCF, not noticeable in majority of women)
- Pregnancy (higher prevalence and severity of gingivitis relative to amount of plaque), pregnancy related granulomas-these symptoms are intensified in the 2nd and 3rd trimesters
- Oral contraceptives, historical contraceptives, dose of contraceptives has now decreased so gingival effects are not frequently seen
Describe haematological conditions as a systemic risk factor for gingivitis.
- Leukaemia: abundant dysfunctional immature leukocytes
- Neutropenia: low PMNs
- HIV/AIDS: low CD4 positive T cells
