In most industrialized countries there is an “obesity epidemic”, one of the consequences of which is an overwhelming increase in type 2 diabetes mellitus (DM), not only in adults, but also in children and adolescents, and Australia is no exception. Obesity is also a risk factor for hypertension, dyslipidaemia, CHD and stroke, and there is now evidence that obesity is also associated with periodontitis.41 The most commonly used indicator of obesity is body mass index (BMI) (weight in kg/(height in m2)), with a BMI ≥ 25 kg/m2 considered overweight and ≥ 30 kg/m2 considered obese. Indeed, BMI together with extensive periodontal disease has been related to increased CRP levels in otherwise healthy middle-aged adults.29 However, BMI has its limitations as it does not assess body fat distribution and so abdominal obesity is generally regarded as a better indicator of disease risk. This is assessed by waist circumference, which should be less than 102 cm for men and 88 cm for women.42 In this context, it is interesting to note that high waist circumference was associated with periodontitis in young adults aged 18–34 years, but not in older adults.43 Abdominal obesity in conjunction with glucose intolerance, hypertension and dyslipidaemia has been termed metabolic syndrome or insulin resistance syndrome and is an indicator of increased risk for cardiovascular disease.44 The cause of metabolic syndrome is not known, however, it is now recognized that adipose tissue can produce a number of hormones and cytokines that contribute to systemic inflammation and insulin resistance, which in turn can lead to the development of type 2 diabetes and cardiovascular disease.45,46 Of particular interest in recent years is the adipocytokine, leptin, which controls appetite on the one hand, and has immune regulatory functions on the other, such as the production of inflammatory cytokines. Obesity is associated with reduced sensitivity to the appetite suppressing effects of leptin, leading in turn to higher levels.47 Infection and inflammation can also lead to higher leptin levels.41 As raised serum leptin concentration can enhance atherosclerosis it is, therefore, a potential risk factor for CVD.48 However, whether periodontal inflammation has any effect on leptin levels, or vice versa, remains to be determined, especially in view of the epidemiological association between obesity and periodontitis. Nevertheless, a recent study suggests that overweight and obese individuals who are periodontally healthy may be at risk for initiation and progression of periodontal disease due to an overgrowth of Tannerella forsythia in subgingival plaque.49 Thus, clinicians need to be aware that patients with abdominal obesity, as well as carrying a greater burden of systemic inflammation, may also have a greater burden of infection, placing them, not only at greater risk for periodontitis, but also compounding their risk for CVD.
The National Heart Foundation Guidelines40 recommend that overweight or obese adults without known CVD or who are not known to be at high risk for CVD should be assessed for absolute CVD risk using the Framingham Risk Equation, even though the predictive value has not been specifically assessed in this population. In this situation, the Framingham Risk Equation may underestimate CVD risk as it does not take into account obesity or overweight status, especially abdominal or central obesity. Notwithstanding the influence of obesity, as discussed above, until there is evidence to the contrary, periodontitis should be regarded as a modifiable risk factor in those found to have high absolute CVD risk.