Waist circumference and waist-to-height ratio are associated with periodontal pocketing-results of the Health 2000 Survey.

BACKGROUND: Body mass index (BMI) has been found to associate with different parameters of chronic periodontal disease in previous studies. It is reasonable to expect that central adiposity measures, such as waist circumference and waist-to-height ratio, which indirectly takes into account visceral fat, are more accurate measures of obesity-related oral health risks than BMI. The aim of this study was to examine whether central obesity is associated with periodontal pocketing, an indication of infectious chronic periodontal disease. METHODS: The study was based on a subpopulation from the national Health 2000 Survey in Finland. It included dentate, non-diabetic, never-smoking subjects aged 30-49 (n = 1287). The outcome variable was the number of teeth with deepened periodontal pockets (4 mm or more) and the number of teeth with deep periodontal pockets (6 mm or more). Central obesity was measured by means of waist circumference (WC) and waist-to-height ratio (WHtR). Poisson regression models were used to estimate prevalence rate ratios (PRR) and their 95% confidence intervals. RESULTS: Our main finding was that both WC and WHtR were associated with the number of teeth with deeper (4 mm or more) periodontal pockets; the PRR for the fifth quintile in WC was 1.5, CI: 1.2-1.9 and in WHtR 1.4, CI: 1.1-1.7, when compared to the lowest quintile. Corresponding figures for deep (6 mm or more) periodontal pockets were 2.3, CI: 0.9-6.1 for WC and 1.9, CI: 0.8-4.4 for WHtR. There were no essential differences in the strengths of the associations between WC and WHtR and the number of teeth with deepened periodontal pockets. CONCLUSION: Both central adipose measures-WC and WHtR-seem to be associated with periodontal pocketing in non-diabetic, never-smoking subjects aged 30-49 years old.

Role of insulin sensitivity and beta cell function in the development of periodontal disease in adults without diabetes.

AIM: The goal of this study was to explore whether insulin resistance and beta cell function are related to periodontal pocket formation, indicative of infectious periodontal disease in non-smoking adults without manifest diabetes. MATERIAL AND METHODS: We analysed data from a Health 2000 Survey consisting of dentate subjects without any indication of diabetes, aged between 30 and 64, who had never smoked and who had participated in the Follow-up Study on Finnish Adults' Oral Health about 4 years later (n = 157). The Homeostasis Model Assessment Indices were used to measure insulin resistance (HOMA-IR) and ß-cell function (HOMA-B). The development of periodontal disease was measured by means of the incidence of deepened periodontal pockets (4 mm deep or deeper) during the follow-up period. Incidence rate ratios (IRR) were estimated using Poisson regression models. RESULTS: Both HOMA-IR and HOMA-B indices were associated with periodontal pocket formation during the 4-year follow-up. CONCLUSION: The results of this follow-up study suggest that impaired glucose metabolism measured as insulin resistance and altered beta cell function predict the breakdown of periodontal tissues. Further studies about their role in the pathogenesis of periodontal diseases are needed.

Insulin sensitivity and periodontal infection in a non-diabetic, non-smoking adult population.

AIM: The aim of this study was to examine whether there is an association of insulin sensitivity with periodontal infection in a non-diabetic, non-smoking adult population. MATERIALS AND METHODS: A subpopulation of the Health 2000 Survey (effective n=2050) consisted of dentate subjects without any indication of diabetes, aged between 30 and 64, and who had never smoked. The outcome variable was periodontal infection measured by means of the number of teeth with deepened periodontal pockets. Insulin sensitivity was measured using the homeostasis model assessment index for insulin resistance. Poisson regression models were used to estimate the relative risks and 95% confidence intervals. RESULTS: We found that insulin sensitivity was associated with periodontal infection in the age group 30-49, but not in persons aged 50-64. Controlling for body weight made the association between insulin sensitivity and periodontal infection disappear. CONCLUSION: The lack of knowledge of the underlying causal model prevents making definite conclusions about the role of reduced insulin sensitivity in the pathogenesis of periodontal infection.