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The Relationship Between Periodontitis and Glycaemic Control in Type 2 Diabetes

Published Online: September 12th 2012 European Endocrinology, 2012;8(2):89-93 DOI: http://doi.org/10.17925/EE.2012.08.02.89
Authors: Edith M Allen, Iain L Chapple
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Abstract:
Overview

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

Article:

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
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 damage3,4 mediated by cytokines including interleukin-1 beta (IL-1β), 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 phagocytosis10 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.

Progression of untreated periodontitis can result in pain, aesthetic problems, functional difficulties and complete tooth loss in severe cases.13

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Disclosure

The authors have no conflicts of interest to declare.

Correspondence

Edith M Allen, Department of Restorative Dentistry, Cork University Dental School and Hospital, Wilton, Cork, Ireland. E: e.allen@ucc.ie

Received

2012-06-03T00:00:00

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