Do patients with aggressive periodontitis have evidence of diabetes? A pilot studyJournal of Periodontal Research

About

Authors
R. C. Davies, K. M. Jaedicke, H. E. Barksby, P. Jitprasertwong, R. M. Al-Shahwani, J. J. Taylor, P. M. Preshaw
Year
2011
DOI
10.1111/j.1600-0765.2011.01388.x
Subject
Periodontics

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Text

Do patients with aggressive periodontitis have evidence of diabetes? A pilot study

R. C. Davies, K. M. Jaedicke,

H. E. Barksby, P. Jitprasertwong,

R. M. Al-Shahwani, J. J. Taylor,

P. M. Preshaw

School of Dental Sciences and Institute of

Cellular Medicine, Newcastle University,

Newcastle upon Tyne, UK

Aggressive periodontitis is a specific form of periodontal disease. Clinically, it is distinguishable from other forms of periodontal disease primarily by its rapid rate of destruction and progression, its early age of onset or detection, its specific patterns of destruction and its familial aggregation. The aetiology and pathogenesis of aggressive periodontitis is not entirely clear, but there is evidence that specific microbiological, immunological and genetic features exist which are distinct to aggressive periodontitis (1).

Substantial research has linked diabetes with chronic periodontitis, but studies focusing on aggressive periodontitis are limited. It is widely

Davies RC, Jaedicke KM, Barksby HE, Jitprasertwong P, Al-Shahwani RM, Taylor

JJ, Preshaw PM. Do patients with aggressive periodontitis have evidence of diabetes?

A pilot study. J Periodont Res 2011; 46: 663–672.  2011 John Wiley & Sons A/S

Background and Objective: Complex relationships exist between diabetes and periodontal disease. Diabetes is accepted as a risk factor for periodontal disease, and recent evidence supports the existence of a bidirectional relationship between these two diseases. It has been hypothesized that inflammation, lipids and adipokines may mediate these relationships. However, research regarding the above relationships with respect to aggressive periodontitis is very limited. This pilot study aimed to investigate whether patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes and have altered serum levels of inflammatory mediators, lipids and adipokines.

Material and Methods: Glycaemic control markers (random plasma glucose and glycated haemoglobin), inflammatory mediators (high-sensitivity C-reactive protein, tumour necrosis factor-a, interleukin-1b, interleukin-6, interferon-c and interleukin-18), lipids (triglycerides, total cholesterol and high-density lipoproteincholesterol) and adipokines (leptin, adiponectin and resistin) were measured in serum samples from 30 patients with aggressive periodontitis and 30 age- and sexmatched periodontally healthy control subjects, none of whom had a previous diagnosis of diabetes.

Results: Levels of glycaemic control markers, inflammatory mediators, lipids and adipokines were not significantly different (p > 0.05) between the aggressive periodontitis patients and healthy subjects for unadjusted and adjusted analyses (adjusting for body mass index, smoking, ethnicity, age and sex). The p-value for the adjusted analysis of adiponectin in female aggressive periodontitis patients compared with the female control subjects reached 0.064, the mean adiponectin level being lower in the female aggressive periodontitis patients (4.94 vs. 5.97 lg/ mL).

Conclusion: This pilot study provided no evidence to suggest that patients with aggressive periodontitis (not previously diagnosed with diabetes) have evidence of diabetes or altered serum levels of inflammatory mediators, lipids and adipokines.

Philip Preshaw, BDS, FDSRCSEd, PhD, School of Dental Sciences, Newcastle University,

Framlington Place, Newcastle upon Tyne NE2 4BW, UK

Tel: +44 191 222 8193

Fax: +44 191 232 5144 e-mail: p.m.preshaw@newcastle.ac.uk

Key words: aggressive periodontitis; periodontal disease; diabetes; adipokine

Accepted for publication May 10, 2011

J Periodont Res 2011; 46: 663–672

All rights reserved  2011 John Wiley & Sons A/S

JOURNAL OF PERIODONTAL RESEARCH doi:10.1111/j.1600-0765.2011.01388.x accepted that people with diabetes exhibit an increased prevalence and severity of periodontal disease and that the severity of periodontal disease correlates with levels of diabetes control (2). Furthermore, in nondiabetic people, increased fasting plasma glucose and glycated haemoglobin (HbA1c) levels have been found to be significantly associated with periodontal disease (3,4). With regard to aggressive periodontitis, research is limited to a study by Nibali et al. (5) who found that a sample of nondiabetic patients with either aggressive periodontitis or severe chronic periodontitis exhibited higher nonfasting glucose levels than healthy control subjects. Anecdotally, some dentists consider testing for diabetes in patients presenting with aggressive periodontitis.

Conventionally, research has focused on a unidirectional relationship between diabetes and periodontal disease, in which diabetes predisposes to periodontal disease, and features observed in diabetes, such as defective polymorphonuclear neutrophils, altered vascular function and altered collagen metabolism, have been proposed to explain this relationship (6).

However, in recent years, evidence has supported the existence of a bidirectional relationship between diabetes and periodontal disease (7,8), and it has been proposed that common susceptibility may exist between these two diseases (9,10). Hypotheses have developed regarding a role for inflammation, dyslipidaemia and adipokines in these relationships (5,10–17).

Both periodontal disease and diabetes have been associated with increased levels of systemic inflammatory mediators (18–21). Moreover, some evidence has suggested that diabetes may predispose to periodontitis by inducing a heightened inflammatory response (22), that low-grade systemic inflammation can result from periodontitis (7,23), that inflammation influences the pathogenesis of diabetes (24) and that systemic inflammation induced in periodontitis may be sufficient to influence the pathogenesis of diabetes (7). Preliminary research has also begun to investigate whether a common inflammatory genetic basis exists between diabetes and periodontal disease (9). Many inflammatory mediators could potentially mediate the relationship between diabetes and periodontal disease. Specifically, highsensitivity C-reactive protein (hs-CRP), tumour necrosis factor-a (TNF-a), interleukin-1b (IL-1b), interferon-c (IFN-c), interleukin-6 (IL-6) and interleukin-18 (IL-18) have all been implicated in the pathogenesis of both diabetes and periodontal disease (18,25–32). However, it is currently unclear whether systemic levels of the above mediators are raised in patients with periodontal disease. Investigations involving patients with aggressive periodontitis in particular are lacking.