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Diabetes and Periodontal Disease The Relationship Between Periodontitis and Glycaemic Control in Type 2 Diabetes Edith M Allen 1 and Iain L Chapple 2 1. Lecturer, Department of Restorative Dentistry, Cork University Dental School and Hospital, Cork, Ireland; 2. Professor of Periodontology and Consultant in Restorative Dentistry, Periodontal Research Group, School of Dentistry, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK Abstract Periodontitis is a chronic, inflammatory condition in the tissues surrounding teeth that is stimulated by dental plaque bacteria and results in the destruction of tooth supporting tissues. Type 2 diabetes is associated with an increased prevalence and severity of periodontitis that is related to underlying glycaemic control. It has been suggested that the presence of chronic periodontal inflammation has a converse and negative effect on glycaemic control in diabetes with most evidence emerging from studies of type 2 diabetes. This article reviews the evidence from cohort, prospective and meta-analysis studies that have been conducted to examine the relationship between periodontitis and glycaemic control in type 2 diabetes and suggests underlying pathogenic mechanisms that may explain the relationship between these conditions. Keywords Periodontitis, diabetes, glycaemic control Disclosure: The authors have no conflicts of interest to declare. Received: 3 June 2012 Accepted: 20 August 2012 Citation: European Endocrinology, 2012;8(2):89–93 Correspondence: Edith M Allen, Department of Restorative Dentistry, Cork University Dental School and Hospital, Wilton, Cork, Ireland. E: Periodontitis is a bacteria-related, chronic inflammation that results in destruction of the bone and connective tissue support of teeth forming periodontal pockets between the tooth and gingival soft tissue. 1 It is initiated by inadequate oral hygiene and the development of a biofilm colonised with pathogenic bacteria on the tooth surface that results in direct damage to local tissues by bacterial virulence factors (see Figures 1 and 2). 2 The stimulation, an inflammatory/immune response to the offending bacteria, is further associated with indirect tissue damage 3,4 mediated by cytokines including interleukin-1 beta (IL-1β), 5 IL-6, tumour necrosis factor-alpha (TNF-α) prostaglandins and collagenolytic enzymes. 6,7 Oxidative damage to the tissues is also a feature of the periodontitis lesion, 8,9 thought to result from hyper-reactive neutrophils generating excessive reactive oxygen species (ROS) during bacterial phagocytosis 10 causing both direct damage and stimulating redox-sensitive pro-inflammatory transcription factors. Individuals vary in their susceptibility to periodontitis and the key determinant appears to be a phenotype coding for a particularly exaggerated inflammatory and immune response to pathogenic bacteria. 11 Within worldwide populations, periodontitis is a common condition with a prevalence of between 5 to 20 %. 12 The rate of progression varies among individuals but the most common form of the disease has a chronic, slowly progressing nature and patients may be burdened by the chronic inflammatory condition for years or decades before diagnosis and treatment. © TOUCH BRIEFINGS 2012 Progression of untreated periodontitis can result in pain, aesthetic problems, functional difficulties and complete tooth loss in severe cases. 13 Systemic Effects of Periodontitis There is evidence of an ‘over-spill’ from chronic periodontal lesions to more peripheral tissues; plasma levels of periodontitis-associated markers including IL-6, TNF-α, and high-sensitivity C-reactive protein (hsCRP) are elevated 14,15 and systemic oxidative status is compromised in patients with periodontitis compared with healthy controls. 16–18 Indeed, pro-inflammatory cytokines released at the diseased periodontal site 19,20 translocating to distant sites via the circulation, are thought to induce changes in vascular endothelium and increase the risk for cardiovascular disease. 21,22 A recent cross-sectional study of more than 6,000 adults reported that participants with diabetes and periodontitis had an increased likelihood of intimal media thickening and coronary heart disease (CHD). 23 Periodontal treatment lowers systemic levels of inflammatory markers 24 and improves haemostatic parameters in cardiac patients. 25 Diabetes and Periodontitis There is substantial evidence from cross-sectional and prospective studies that people with types 1 and 2 diabetes have more than double the risk of developing periodontitis; 26–36 reviewed by Taylor and Borgnakke. 37 Diabetes can also result in more severe periodontal destruction than in matched non-diabetes groups. 38,39 The increased risk for periodontitis is dependent on glycaemic control 40 and not the duration of diabetes. 41 89