Periodontitis and diabetes: a two-way relationship

Abstract

Periodontitis is a common chronic inflammatory disease characterised by destruction of the supporting structures of the teeth (the periodontal ligament and alveolar bone). It is highly prevalent (severe periodontitis affects 10-15% of adults) and has multiple negative impacts on quality of life. Epidemiological data confirm that diabetes is a major risk factor for periodontitis; susceptibility to periodontitis is increased by approximately threefold in people with diabetes. There is a clear relationship between degree of hyperglycaemia and severity of periodontitis. The mechanisms that underpin the links between these two conditions are not completely understood, but involve aspects of immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. Incidences of macroalbuminuria and end-stage renal disease are increased twofold and threefold, respectively, in diabetic individuals who also have severe periodontitis compared to diabetic individuals without severe periodontitis. Furthermore, the risk of cardiorenal mortality (ischaemic heart disease and diabetic nephropathy combined) is three times higher in diabetic people with severe periodontitis than in diabetic people without severe periodontitis. Treatment of periodontitis is associated with HbA(1c) reductions of approximately 0.4%. Oral and periodontal health should be promoted as integral components of diabetes management.

Fig. 1

Diagram of periodontal pocket in a patient with periodontitis. The pocket is the space between the root surface and the gingiva. In healthy gums, the base of the pocket is coincident with the cemento-enamel junction (CEJ, the boundary between the enamel crown and the root) and there is no attachment loss. In periodontitis, the base of the pocket migrates apically (i.e. away from the enamel crown towards the root tip), thereby creating a pocket. The base of the pocket is therefore apical to the CEJ, and attachment loss can be measured (in mm, using a periodontal probe) from the CEJ to the base of the pocket. Pocket depth (also called probing depth) is measured in mm from the top of the pocket (i.e. from the gingival margin) to the base of the pocket. In this example, the pocket depth might be 6 mm, with 4 mm loss of attachment (as indicated in this example, pocket depth is usually greater than attachment loss due to the inflammation-induced swelling of the gingiva). The direction of insertion of a periodontal probe is indicated

Fig. 2

Periodontitis (clinical appearance) in a 22-year-old man with poorly controlled type 1 diabetes and severe periodontitis. Note the generalised inflammation, abnormal gingival anatomy owing to tissue destruction, gingival recession, swelling and inflammation, spontaneous bleeding and abundant plaque deposits. The periodontal tissues around the lower incisors are particularly severely affected

Fig. 3

Periodontitis (radiographic appearance). a A 42-year-old man with type 2 diabetes and generalised severe periodontitis. There is extensive alveolar bone loss (generally 50–75% of the root length) affecting the entire dentition, with an irregular (uneven) pattern of bone loss. Some of the teeth have lost nearly all their supporting alveolar bone as a result of periodontitis progression, e.g. the upper molars (both right and left), and the four lower incisors, all of which are grossly mobile and which are retained in the oral cavity only by the soft tissue attachment (having lost 100% of their bone support). b A 21-year-old man with no periodontitis. Alveolar bone levels are normal, with the crest of the alveolar bone being in close proximity to the cemento-enamel junction (the boundary between the enamel crown and the root). Contrast with appearance in Fig. 3a

Fig. 4

Schematic representation of the proposed two-way relationship between diabetes and periodontitis. Exacerbated and dysregulated inflammatory responses are at the heart of the proposed two-way interaction between diabetes and periodontitis (purple box), and the hyperglycaemic state results in various proinflammatory effects that impact on multiple body systems, including the periodontal tissues. Adipokines produced by adipose tissue include proinflammatory mediators such as TNF-α, IL-6 and leptin. The hyperglycaemic state results in deposition of AGEs in the periodontal tissues (as well as elsewhere in the body), and binding of the receptor for AGE (RAGE) results in local cytokine release and altered inflammatory responses. Neutrophil function is also altered in the diabetic state, resulting in enhancement of the respiratory burst and delayed apoptosis (leading to increased periodontal tissue destruction). Local production of cytokines in the periodontal tissues may, in turn, affect glycaemic control through systemic exposure and an impact on insulin signalling (dotted arrow). All of these factors combine to contribute to dysregulated inflammatory responses that develop in the periodontal tissues in response to the chronic challenge by bacteria in the subgingival biofilm, and which are further exacerbated by smoking

Fig. 5

Forest plot to indicate outcome of periodontitis treatment on HbA_1c levels after 3–4 months. The effect for the mean percentage difference as a result of periodontal treatment was −0.40% (95% CI 0.78%, −0.01%), n = 244, representing a statistically significant reduction in HbA_1c (p = 0.04) as a result of the periodontal treatment. IV, inverse variance (from Simpson TC, Needleman I, Wild SH, Moles DR, Mills EJ Treatment of periodontal disease for glycaemic control in people with diabetes. Cochrane Database Syst Rev, 2010, Issue 5. Copyright Cochrane Collaboration, reproduced with permission)