Background. Periodontitis results from an inappropriate host response to pathogenic biofilms. Because traditional management approaches have failed to reduce disease prevalence, the research focus has shifted toward managing host-mediated inflammation. In this article, the author reviews the role of nutrition in the development and resolution of inflammation.
Methods. The author reviewed the biomedical literature to elucidate mechanisms by which dietary factors affect inflammatory processes and to establish what evidence exists for macronutritional and micronutritional modulation of inflammation at a cellular and molecular level.
Conclusions. Hyperinflammation characterizes the periodontitis phenotype, and oxidative stress is a key orchestration point for the diverse signaling pathways, which control inflammation. Oxidative stress is modulated by diet, as well as by infection. Recent research has demonstrated that subtle shifts in nutritional status are associated independently with the prevalence of periodontitis. Moreover, the results of contemporary animal and human studies have demonstrated the role of specific micronutrients in the modulation of the host’s inflammatory response by reducing inflammatory biomarkers and bone loss.
Clinical Implications. The scientific community is starting to realize the health benefits of diets containing foods naturally rich in antioxidants and omega-3 polyunsaturated fatty acids, as well as the dangers of diets that are high in refined carbohydrates. Nutritional intervention studies in patients with inflammatory periodontitis are needed to evaluate the effect of nutritional approaches to periodontal management.
B: Nuclear factor–kappa B. • OH: Hydroxyl radical. • oxLDL: Oxidized low-densitylipoproteins. • 
-3PUFAs: Omega-3 polyunsaturated fatty acids. • PPARs: Peroxisome proliferator–activated receptors. • PUFA: Polyunsaturated fatty acid. • ROS: Reactive oxygen species. • TLR: Toll-like receptor. • TNF: Tumor necrosis factor. • TNF
: Tumor necrosis factor alpha.
