href="#ulink_0ecb7df4-1479-5670-9d91-eb6df1e845a6">35 analysed data from almost 14,000 men and women from the third NHANES in the United States and observed that subjects older than 45 years with severe periodontitis were 2.31 times more likely to have metabolic syndrome, defined by concurrence of hypertension, atherogenic lipid profiles, obesity and insulin resistance; compared to unaffected individuals after adjusting for confounders. Furthermore, diagnosis of metabolic syndrome increased by 1.12 times per 10% increase in gingival bleeding and 1.13 times per 10% increase in the proportion of periodontal pockets. Morita et al36 followed up more than 3000 Japanese workers for 5 years and assessed the incidence of periodontitis. They observed a significant association between BMI and the development of periodontal pockets of greater than 4 mm, and the hazard ratios for women were higher than they were for men. However, this study used partial-mouth recording and the Community Periodontal Index to assess periodontal status, which would underestimate the true periodontal status. Merchant et al37 observed in 39,461 males that individuals who maintained a normal weight, pursued regular exercise, and consumed a diet in conformity with the Dietary Guidelines for Americans and the Food Guide Pyramid recommendations, were 40% less likely to have periodontitis.
In addition, periodontal pathogen populations seem to be altered in obese subjects. For example, Haffajee and Socransky38 observed an overgrowth of Tannerella forsythia in the biofilms of periodontally healthy obese individuals that might put them at risk for initiation of periodontitis. They also observed that the ORs of overweight and obese subjects exhibiting periodontitis were 3.1 (95% CI 1.9 to 4.8) and 5.3 (95% CI 2.8 to 9.5), respectively, when compared with subjects with normal BMI. Logistic regression analysis indicated an OR of 2.3 (95% CI 1.2 to 4.5) for an obese subject to exhibit periodontitis after adjusting for age, gender and smoking status. In a recent study, Maciel et al39 observed that obese male subjects with periodontitis harboured higher levels and/or higher proportions of periodontal pathogens, such as Aggregatibacter actinomycetemcomitans, Eubacterium nodatum, Fusobacterium nucleatum subspecies vincentii, Parvimonas micra, Prevotella intermedia, T. forsythia, Prevotella melaninogenica and Treponema socranskii when compared to normal weight subjects with periodontitis. Furthermore, the healthy sites of the obese subjects also exhibited higher proportions of some of the pathogens than the normal weight counterparts39.
In terms of treatment outcome, Suvan et al40 investigated the predictive role of overweight/obesity on clinical response following non-surgical periodontal therapy in 260 adults. On re-evaluation, i.e., after 8 weeks, they observed that obesity was an independent predictor of poorer periodontal treatment outcomes. These patients had, on average, 3.2% (95% CI 0.7% to 5.6%) more sites with probing depths greater than 4 mm when compared with normal weight subjects after adjustment for the baseline. For every BMI increase of 10 kg/m2, the mean percentage of sites with probing depths greater than 4 mm increased by 2.5% (95% CI 1.10% to 3.80%). No differences were found in bleeding on probing. It is worth pointing out that the magnitude of this association was similar to that of smoking, which was also linked to a worse clinical periodontal outcome40. However, Palomo41 stated that this study had limitations inherent in the study design. The confounders for periodontitis, such as smoking and diabetes, were not part of the exclusion criteria. Instead, statistical analysis was undertaken to account for them, increasing the risk for false-positive associations. Thus, a poor outcome after periodontal therapy in the obese patients of this study may in fact not be fully attributed to the BMI alone41.
It is difficult and complex to unravel the relative contributions of obesity and metabolic status, including hyperglycaemia, to periodontitis. Positive association between obesity and periodontitis has been consistently shown in recent meta-analyses. However, few of them have a prospective or a longitudinal design, and these relationships appear to be modest26. Taken together, there is significant evidence of an association between overweight/obesity and the prevalence, extent and severity of periodontitis, as well as periodontal treatment outcomes in children, adolescents and adults. However, the magnitude and mechanisms of this association require further clarification. The available evidence comes mainly from cross-sectional, experimental and longitudinal studies, respectively33,42. The difficulty to reach a final conclusion is related to the difficulty to evaluate the mechanisms underlying the association between them, because most of the studies involved a cross-sectional design. In addition, there is heterogeneity in the definition of obesity in most of the studies, which evaluate the degree of obesity by calculating BMI, however some of them also include wait-circumference, waist-hip ratio and, in some cases, percentage body fat. In order to confirm the causal relationship and the pathophysiological mechanism involved in the association between obesity and periodontitis, further prospective studies are needed33,42.
SUMMARY
● A potential association between obesity and periodontitis was first reported in 1977.
● There are several confounding and risk factors related to obesity that should be adjusted for in future studies and biologically clarified to elucidate the association between obesity and periodontitis.
● Data from NHANES show that subjects older were 2.31 times more likely to have metabolic syndrome.
● 1% increment in waist-to-height ratio was associated with a 3% increase in the hazard of having periodontitis progression in a 2012 study.
● The overall level of evidence is low; therefore, an association cannot yet be confirmed.
1.2.2 Periodontitis and DM
Diabetes is one of the largest global health emergencies of the 21st century. In 2015, the International Diabetes Federation estimated that 415 million people worldwide have diabetes43. Despite better awareness and new developments in the treatment of diabetes and prevention, an unrelenting increase has been observed in the number of people with the disease. By 2040, an increase to 642 million is expected, where a major concern is low- and middle-income countries and in those countries that have experienced rapid economic growth44. The number could be higher, since there are numerous people from many countries that have the disease undiagnosed (especially in Africa, where it is estimated that more than 65% of individuals with diabetes remain undiagnosed)45.
The percentage of adults with diabetes increased with age, reaching a high of 25.2% among those aged 65 years or older46. The age-adjusted prevalence of diagnosed and undiagnosed diabetes is higher among Asians, non-Hispanic blacks, and Hispanics, respectively46. According to the ADA, the estimated costs associated with diabetes in the United States in 2002 totalled US $132 billion, with direct medical costs of US $92 billion and indirect costs (disability, loss in work productivity and premature mortality) of US $40 billion47. T1DM, previously referred to insulin-dependent diabetes or juvenile-onset diabetes, results from a cell-mediated autoimmune destruction of the insulin-producing