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niche that encourages increased plaque accumulation. 7 These include: a. Dental plaque biofilm retention factors (including certain tooth anatomical factors) – facilitate plaque accumulation at and apical to the gingival margin, enabling biofilm adherence and maturation and increasing the difficulty of mechanical plaque removal. Several clinical studies providing a moderate level of evidence have demonstrated that subgingival resto- ration margins may be detrimental to gingival health. 15,16 b. Oral dryness is a clinical condition often associated with symp- toms of xerostomia. Oral dryness manifesting as a lack of sali- vary flow, availability, or changes in quality of saliva, leading to reduced cleansing of tooth surfaces is associated with reduced dental plaque biofilm removal and enhanced gingival inflamma- tion. Common causes include medications that have anti‐para- sympathetic action, Sjögrens syndrome when the salivary acini are replaced by fibrosis following autoimmune destruction, and mouth breathing in people who may have enhanced gingival display and/or an incompetent lip seal. 17
• Dental plaque biofilm‐induced gingivitis • Non–dental plaque‐induced gingival diseases
Dental plaque biofilm‐induced gingivitis is defined at the site level as “ an inflammatory lesion resulting from interactions between the dental plaque biofilm and the host's immune‐inflammatory response, which re‐ mains contained within the gingiva and does not extend to the periodontal attachment (cementum, periodontal ligament and alveolar bone). Such in‐ flammation remains confined to the gingiva and does not extend beyond the mucogingival junction and is reversible by reducing levels of dental plaque at and apical to the gingival margin ”. Depending on whether dental plaque biofilm‐induced gingival inflammation occurs on an intact or reduced periodontium, or in a patient diagnosed with periodontitis, gingivitis can be further clas- sified as: • Gingivitis on an intact periodontium • Gingivitis on a reduced periodontium in a non‐periodontitis pa- tient (e.g., recession, crown lengthening) • Gingival inflammation on a reduced periodontium in a success- fully treated periodontitis patient (Note that recurrent periodon- titis cannot be ruled out in this case) Since the 1999 classification, there have been advances in knowl- edge of the microbiome and the gingival transcriptome. Gingivitis is a non‐specific inflammatory condition and is therefore a consequence of sustained plaque biofilm accumulation at and apical to the gingi- val margin. 7 Longitudinal studies have demonstrated that sites that do not progress to attachment loss are characterized by less gingival inflammation over time, whereas those sites that do progress have persistently greater levels of gingival inflammation. 8‒14 Therefore, gingivitis is a major risk factor, and a necessary pre‐requisite, for peri- odontitis. The management of gingivitis is thus a primary prevention strategy for periodontitis. Periodontitis patients who are currently stable but develop gingival inflammation at specific sites should remain on periodontal mainte- nance and should be closely monitored during periodontal maintenance for any reactivation of periodontitis. Such patients may not be managed in the same way as non‐periodontitis patients with gingivitis. What are the determinants of the rate of development of gingivitis, its severity and extent? The threshold of plaque accumulation necessary to induce gingival inflammation and impact upon its rate of progression at specific sites or at a whole mouth level varies between individuals according to both local risk factors, known as predisposing factors, and systemic risk factors, referred to as modifying factors, respectively. 1. Local risk factors (predisposing factors) Local risk factors for gingivitis are those that encourage plaque accumulation at a specific site by either inhibiting its removal during daily oral hygiene practices, and/or creating a biological
2. Systemic risk factors (modifying factors)
Systemic risk or modifying factors are those characteristics pres- ent in an individual, which negatively influence the immune‐in- flammatory response to a given dental plaque biofilm burden, resulting in exaggerated or “hyper” inflammation. Examples include: a. Smoking – is one of the major lifestyle/behavioral risk factors for periodontitis, but which also has profound effects upon the gingival tissues. Systemic circulatory uptake of components of cigarette smoke as well as local uptake are reported to induce microvascular vasoconstriction and fibrosis. This can mask clini- cal signs of gingivitis, such as bleeding on probing, despite a sig- nificant underlying pathological inflammatory cell infiltrate. 18 b. Metabolic factors – hyperglycemia in people with or without diabetes. Excess glucose is toxic and directly induces mitochon- drial stress and an enhanced respiratory burst in inflammatory cells that may activate various proinflammatory mediator cas- cades. Formation of advanced glycation end‐products (AGEs) may also result in AGE binding to its cell surface receptor (RAGE), which activates proinflammatory signaling cascades and downstream proinflammatory events. 19 c. Nutritional factors – Severe Vitamin C deficiency, or scurvy, results in compromised antioxidant micronutrient defenses to oxidative stress and also negatively impacts collagen synthe- sis, resulting in weakened capillary blood vessel walls and a consequent propensity to enhanced gingival bleeding. 20 d. Pharmacological agents (prescription, non‐prescription, and recreational agents) – can act via diverse mechanisms to in- crease susceptibility to gingivitis. This may include drugs that reduce salivary flow, drugs that impact endocrine function (see below), and drugs that may induce gingival enlargement and pseudo‐pocketing.
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