Any food product that contributes to the growth of dental plaque has the potential to cause inflammation associated with periodontal disease that results from bacterial buildup in tooth biofilm (plaque). One of the sugars most responsible for enhancing plaque production from Streptococcus mutans and Streptococcus sobrinus bacteria is sucrose. Degradation of sucrose- and glucose-containing foods mediates the buildup of the disease-causing plaque matrix. The long-term presence of plaque initiates a gingival inflammatory response that contributes to periodontal pocketing, inoculation of the space by anaerobic bacteria, and alveolar bone loss.
A poor diet may also be associated with the development of periodontal disease independent of sugar intake. An inadequate diet modifies the oral microbial ecology via several mechanisms, including alteration of the antibacterial and physicochemical properties of saliva. This allows periodontal disease to progress more rapidly than would occur otherwise. Gender differences may also interact with diet, contributing to the progression of periodontal disease.
Antioxidant deficiency has also been postulated as a cause of periodontal disease. However, the evidence for a significant association between low levels of antioxidants such as vitamin C, beta-carotene, and alpha-tocopherol (vitamin E) and periodontal disease has not been established sufficiently to support their prescription as preventive of periodontal disease. The dietary intake of folic acid and its effect on periodontal disease as manifested by gingival bleeding has been recently investigated, and the evidence suggests that this deficiency may be associated with this specific variable (gingival bleeding). However, a significant relationship was not found between the community periodontal index, a more general marker of disease, and folic acid levels.
A recent review of the evidence for nutritional exposures in the etiology of periodontitis suggests that, in some cases, inadequate levels of vitamin D and calcium may contribute to periodontal disease and that nutritional intervention may be of some benefit. The authors of this review suggest that, for the prevention and treatment of periodontal disease, daily nutritional intake should include antioxidants, vitamin D, and calcium in the form of vegetables, berries, and fruits or by phytonutrient supplementation. As is the case with antioxidants, the authors state that the current evidence is insufficient to support a recommendation regarding mono-antioxidant vitamin supplements.
In another study, a combination of micronutrients (Orthomol Vital m/f) taken for 3 months slightly improved gingival health among individuals exposed to high stress as compared to controls. This pilot study provides limited evidence for the association between dietary micronutrients and periodontal disease. However, as the authors suggest, studies involving a greater number of subjects are necessary before final conclusions can be made supporting the use of micronutrient supplements in the dietary management of periodontal disease.
The effect of a probiotic milk drink on the expression of clinical inflammatory factors expressed by oral gingival tissue during several phases of plaque-induced gingivitis was recently evaluated in a study of 28 adults with healthy gingiva. Subjects were divided into two groups—14 given probiotic milk and 14 controls. After 28 days, a daily consumption of probiotic milk was found to reduce the markers of periodontal disease, including the level of gingival crevicular fluid and the volume and bleeding upon probing.
A fatty diet may also affect periodontal status. Hyperlipidemia, an excessive amount of lipids (total cholesterol, LDL cholesterol, HDL cholesterol, triglycerides) in the blood has been associated with increased gingival bleeding upon probing, probing pocket depth, the clinical attachment level, and serum levels of proinflammatory cytokines. These data suggest a potential association between lipid intake and periodontal disease.
Dietary docosahexaenoic acid (DHA) is an omega-3 fatty acid found in cold-water oceanic fish or in a manufactured product from microalgae. Low DHA intake was significantly associated with an increased number of periodontal disease events in a study reported by Iwasaki et al (2010).In another study, supplementation with polyunsaturated fatty acids such as omega-3s appeared to improve and potentially prevent periodontitis. Results of this study suggest another possible dietary intervention that might be delivered as part of the overall management of periodontal disease. Additional research is needed to confirm these preliminary findings.