PEM has been linked to periodontal disease. Enwonwu has outlined several mechanism to explain this link including: (1) decreased resistance of mucosa to colonization and invasion by pathogens; (2) impaired salivary flow and antibacterial properties; (3) reduced acute phase protein response in malnutrition; and (4) an increase in the prevalence and potency of pathogenic oral microorganism in PEM [72].

Vitamin C (ascorbic acid) is one of the most well-documented nutrients associated with periodontal health. Severe vitamin C deficiency is known to lead to scorbutic gingivitis (scurvy), characterized by ulcerative gingivitis and rapid periodontal pocket development with tooth exfoliation [73]. Vitamin C promotes a collagen formation and reduces the permeability of endotoxin from the oral mucosa [74]. Studies show that vitamin C enhances motility of polymorphonuclear leukocytes, and increases host immune responses [75, 76]. A reduction in bleeding on probing after supplementation with vitamin C was noted, suggesting that vitamin C may influence early stages of gingival inflammation [77]. Vitamin C may improve periodontal health by increasing bactericidal activity against Actinomyces viscosus [78].

Studies in animals have shown that a diet deficient in vitamin C increases susceptibility of the periodontium to chronic inflammation [79], and acute vitamin C deficiency increases the permeability of the gingival sulcular epithelium. The periodontal effects of vitamin C deficiency in humans are inconclusive. While some epidemiological and experimental evidence has failed to demonstrate significant etiological relationship between vitamin C deficiency and periodontal disease [80, 81], others have reported a direct relationship between gingival inflammation and vitamin C status [79, 82]. In healthy nonsmoking men aged 19–28 years, it was found that vitamin C deficiency contributed to the early stages of inflammation. This finding was noted even when controlling for changes in plaque accumulation or probing depths [77]. Leggott et al. [82] found a significant increase in gingival bleeding after a period with vitamin C depletion, without significant changes in plaque accumulation, probing pocket depth, or when attachment level were observed. Studies that examine vitamin C and its effect on the extracellular matrix and immunologic and inflammatory responses provide a rationale for hypothesizing that vitamin C is a risk factor for periodontal disease.

The role of dietary vitamin C as a contributing risk factor for periodontal disease has been investigated using data from the Third National Health and Nutrition Examination Survey (NHANES III) [73]. The periodontal health of 12,419 adult smokers and nonsmokers ages 20 or older was correlated to their dietary vitamin C intake. The dietary intake of vitamin C showed a statistically significant relationship to periodontal disease in current and former smokers as measured by clinical attachment. Those persons with the lowest intake of vitamin C, and who also smoke, are more likely to experience more severe periodontal disease, indicating a dose–response relationship.

A relationship between vitamin C and wound healing has been documented. In healthy young adult males, classified according to periodontal status, one single intravenous dose of 500 mg of ascorbic acid resulted in statistically significant correlations between gingival status and ascorbic acid concentrations in whole blood and urine [83]. In contrast, Woolfe et al. [84], found that an intake of 1 g vitamin C per day for 6 weeks in normal human subjects did not have an effect on the gingival response to initial therapy, and identical gingival responses to periodontal therapy were found in control and vitamin C—supplemented patients. Final blood vitamin C concentrations appeared to have increased minimally, suggesting that excesses of the vitamin were excreted in the urine. These data suggest that there is little to no value for OHCPs to recommend vitamin C supplementation for periodontal patients when the dietary reference intake (DRI) can be easily met through consumption of a healthy, balanced diet. (See Appendix for U.S. DRI reference).

Dietary calcium deficiency has been associated with changes in collagen synthesis and structure in oral connective tissue, and therefore thought to be a potential modulator for periodontal health [85]. Both animal and human studies suggest a relationship between calcium intake, bone mineral density (BMD), tooth loss [86], and resorption of the alveolar bone [85, 87, 88]; however, this relationship is not clearly elucidated.

In a double-blind study, calcium supplementation (1 g) for 180 d without any subsequent periodontal treatment did not influence the periodontal status of patients with moderate to advanced periodontal disease [89]. The periodontal status of patients with a low-calcium intake did not differ from those receiving adequate calcium. Other studies have reported positive associations between calcium supplementation and periodontal conditions [90, 91]. Periodontal disease has, in humans, been found to be reversed when the patients were given 1 g calcium per day for 180 d [91]. In a study of more than 12,000 adults, Nishida et al. [86] found a statistically significant association between lower dietary calcium intake and periodontal disease in young males and females and for older males. For the females with the lowest level of dietary calcium intake, there was a 54% greater risk of periodontal disease. See Chapter 16, Osteoporosis, for additional information on the role of Calcium and other nutrients in bone health.

Dietary omega-3 fatty acids, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) have anti-inflammatory actions that may benefit periodontal health. These long chain fatty acids are found in oily fish and also nuts and seeds, e.g., flaxseed. Though animal studies of the effect of omega 3 fatty acids on the periodontal tissue have shown mixed results, studies in humans are more convincing. Chapple [92] reviewed the literature and noted that shifts in nutritional status are independently associated with periodontal disease. The composition of fatty acids in inflamed gingival tissues is significantly different from that in healthy tissues [93]. Serum concentrations of omega 3 fatty acids have been shown to be lower in patients with alveolar bone loss compared with periodontally healthy subjects [94]. Furthermore, in a cohort study of older Japanese men, a lower intake of omega 3 fatty acids was significantly associated with greater development of periodontitis compared with a higher intake of omega 3 fatty acids. Those in the lowest cohort of DHA intake were at 1.5 times the risk than those in the highest tertile of intake after adjusting for confounders such as smoking, age, and body mass [95]. In the same cohort study, a high intake of saturated fatty acids was also significantly associated with a greater risk of periodontitis in nonsmokers [96]. Naqvi [97] compared periodontal status to the intake of omega-3 fatty acids in a cohort of 9,182 adults participating in NHANES from 1999–2004. He found that a higher dietary intake of DHA and EPA were associated with a lower prevalence of periodontal disease; however, the link with DHA was stronger than that for EPA in this study. These finding support other work that notes that oxidative stress is modulated by diet and infection, which has an impact on the extent and severity of periodontal disease.

Antioxidants, present in all body fluids and tissues, may protect against tissue-destructive effects of reactive oxygen species. In the periodontal environment, these oxygen species can lead to lipid peroxidation, protein degradation, DNA mutation, and bone resorption [98]. Examples of dietary antioxidants include, ascorbic acid (vitamin C), α-tocopherol (vitamin E), and β-carotene and other polyphenolic dietary components as well as uric acid, nonprotein thiols, and glutathione [99]. In periodontal disease, it has been found that P. gingivalis triggers the release of cytokines, resulting in increased activity of polymorphonucleocytes (PMN) and that increased oxidative damage to gingival tissue, periodontal ligament, and alveolar bone may occur [100]. A similar increase in PMN cells has been found after only 3 d plaque accumulation during experimental gingivitis [101].

Reduced salivary antioxidant activity in patients suffering from periodontal disease has been reported to result in reduced concentrations of antioxidants in both saliva [100] and gingival crevicular fluid [102, 103]. Iwasaki found that [104