Nutrition and Oral Medicine (Nutrition and Health)

Chapter 10 / Emerging Research and Practices 173be significantly affected by transient blood sugar and nutrient levels. These and otherfindings point strongly to the need to reevaluate the role of nutrients in periodontaldiseases. The relation may be quite complex and not obvious to the casual observer.3.4. ObesitySaito et al. (41) reported a significant association between obesity and periodontitisand suggested that the latter may be exacerbated by some conditions associated withobesity. Subsequent studies by this group showed that waste–hip ratio (i.e., upper bodyobesity), body mass index (BMI), and body fat were significant risk indicators for periodontitisand, more specifically, that risk increased primarily in subjects with high waist–hip ratios and elevated BMI (27). Obesity is a known risk factor for Type 2 diabetes,cardiovascular disease, and other chronic diseases (42) and, not surprisingly, Grossi andGenco (30) reported the interrelationship between obesity, diabetes, and periodontaldisease. Preliminary studies at the Forsyth Institute (43) have shown that obese individuals,as determined by elevated BMI, were more likely to exhibit periodontitis and hadhigher proportions of B. forsythus in their subgingival plaque than nonobese individuals.Thus, the evidence for an association between obesity and periodontal disease appears tobe growing, although the nature of the association is not known at present. A number ofmechanisms are possible. Other systemic diseases may exacerbate the conditions thatfavor the development of periodontal disease as suggested by Saito and coworkers. Onthe other hand, periodontal disease may be yet another manifestation of a common set ofmechanisms involving increased caloric intake with a concomitant increased exposureto specific sugars or other nutrients, the uptake of specific fats, or the shared exposure toinflammatory mediators resulting from increased metabolic stresses. Obesity may resultin decreased blood flow to the periodontal tissues and may generally affect the hostimmune responses (44). Gemmell et al. (45) reported that adipose tissue can secretetumor necrosis factor (TNF)-, which mediates endotoxin-induced tissue injury in periodontaltissue, whereas Grossi and Genco (30) found that periodontal treatment resultedin improved diabetic control. These disparate observations, and others, tend to supportthe view that the interrelationship between periodontal disease and a variety of systemicconditions or diseases does indeed exist and is complex, and requires more careful study.3.5. Immune ResponsesIt has long been accepted that nutrients can have a profound effect on immune function(46). However, this relationship is most easily seen in instances of malnutrition (20).Thus, protein energy malnutrition is probably the most common cause of immunodeficiency,while scurvy leads to readily observable effects on the gingiva. In vitro studieshave supplemented clinical observations and have provided mechanisms whereby thespecific roles of given nutrients have been explained. The focus has generally been onantioxidants such as vitamin E and selenium as well as on vitamins A and D, zinc, andfatty acids. These have been shown to regulate immune function, and studies have shownthe benefits of increasing the intake of such nutrients. The review by Field et al. (46)covers specifics of some these findings, and reference to such observations (especiallythe interesting results with polyunsaturated fatty acids) have been made in this text. Twopoints stand out from many studies: (a) clinical studies on the efficacy of nutrient additiveson the immune system are complex, inconsistent, and difficult to interpret even