"Life style influences", including diet, effective oral hygiene, and smoking are pivotal to the occurrences of oral diseases.
Principal Oral Diseases affecting the populations are "Dental Caries and Periodontal Diseases" with etiological factors of sugar in the diet and bacterial dental plaque. Among the other oral problems, Oral cancer is a major concerning disease that affects although a minority, but the prevalence is increasing in some countries because of the classical risk factors of smoking and alcohol.
Many years of research have established that dietary factors are directly related to dental caries and erosion. Significant risk factors for these abnormalities include fat and sugar intake in both children and adults.[1, 2, 3, 4, 5, 6] In fact, not only does childhood sugar intake contribute to the development of caries, but the development of pediatric caries in children aged 5 years and younger is significantly associated with maternal weight and intake of sugar and fat by expectant mothers during pregnancy. Dietary habits and the risk of caries in children may also be confounded by maternal educational level.
Caries also occurs in adults, and its incidence appears to increase with age. In fact, incidence rates are similar to those observed in children. Numerous studies in Europe (Ireland, Netherlands, United Kingdom, France) and in the United states suggest that the dietary factors in children may be as important as they are in adults. In a recent study, severe tooth loss in older adults was found to be a key indicator of a compromised dietary quality. Evidence also shows that sport drinks may be increasing the incidence of dental erosion, which can precede caries in both child and adult athletes.
Specific dietary elements and related factors that have demonstrated significant potential for causing caries include the following:[12, 13]
Number of fruit-based sugary soft drinks imbibed
Frequency of fruit-based sugary drink intake
Length of time taken to consume acidic drinks
Eating processed starches as snacks (cooked starches: bread, crackers, cereal, chips/pretzels, pasta, fries)
Eating fermentable carbohydrates
Intake of long-lasting sources of sugars, such as hard candies, breath mints, and lollipops
Clearance properties of the carbohydrate
When the food is eaten
The level of salivation or lack thereof
The type of starch that is eaten
The co-presence of buffers, such as calcium taken with fermentable carbohydrates
Foods and dietary habits that should be recommended because of their minimal risk of caries potential or their caries risk reduction include the following:
Eating fruits such as apples, oranges, pears, and bananas
Eating vegetables such as carrots, celery, tomatoes, lettuce, cucumber, nuts, and crisps
Eating aged cheese or drinking milk
Eating eggs and yogurt
Imbibing xylitol-containing food products
Eating of sugar-containing foods with meals rather than between meals
Eating less sugar-containing food or carbohydrates
Drinking versus sipping sugary drinks
Rinsing with water after imbibing sugary snacks
Eating fruit instead of drinking unsweetened fruit juices that have sugar and that are acidic
Drinking sugar-free tea or coffee
Avoiding the intake of sugar or sticky carbohydrates before retiring to bed
Numerous foods have alleged anticaries activity. These include foods with added xylitol or fluoride, green tea, apple, red grape seeds, red wine, nutmeg, ajowan caraway, coffee, barley coffee, chicory, mushroom, cranberry, glycyrrhiza root, ethanolic extract of Myrtus communis, garlic aqueous extract, cocoa extracts, and propolis.[14, 15, 16] The extent to which these various anticaries foods or ingredients have been studied is limited, but some evidence does suggest an effect on the development of caries.
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.[18, 19] 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.
Deficiency in dietary magnesium has also recently been shown in at least one study to alter bone metabolism and stability around osseointegrated implants.
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.
The relationship between oral cancer and diet is complex.
Some specific dietary foods or formulations appear to cause oral squamous cell carcinoma. For example, in India and Asia, the chewing of areca nuts, betel nuts, paan, and gutka has been correlated with the development of oral cancer.
However, for other foods, the issue is more complex. As an example, in a large-scale, hospital-based, case-controlled study of 1387 eligible cases and 1459 frequency-matched controls in which numerous Cantonese-style foods were assessed, the results related to cancer causation were mixed. The consumption of Canton-style salted fish, preserved vegetables, and preserved/cured meat was shown to significantly increase the risk of nasopharyngeal cancer, with enhanced odds ratios of 2.45 (95% CI, 2.03-2.94), 3.17 (95% CI, 2.68-3.77) and 2.09 (95% CI, 1.22-3.60), respectively. Conversely, the consumption of fresh fruit was associated with reduced risk in a dose-dependent relationship (P = 0.001), and the consumption of Canton-style herbal tea and herbal slow-cooked soup was associated with decreased risk.
Although not a food, alcohol intake has also been shown to be associated with the development of oral cancer, particularly when it is used in combination with smoking. The theory is that alcohol dehydrates the mucosal cell walls, increasing permeation of the smoke carcinogens into the mucosa. Excessive alcohol use may also be associated with a lowering of the body’s ability to use antioxidants in fighting oral cancer development.
However, evidence suggests that the relationship between alcohol and smoking may be confounded by diet and specific micronutrients, although the evidence is limited. Petridou et al (2002) published a study in which 106 Greek patients (a society with a high incidence of smoking and alcohol use) with confirmed oral carcinoma and an equal number of control subjects matched for age and gender and dietary information were assessed for food frequency. After adjustment for numerous variables, including tobacco smoking and alcohol consumption, they found that the consumption of cereals, fruits, dairy products, and lipid in the form of olive oil and micronutrients including riboflavin, magnesium, and iron were found to be inversely associated with the risk of oral carcinoma. On the other hand, meat products were positively associated with risk. This study suggests that the risk of oral cancer in individuals who smoke and drink may be potentially altered by diet.
Marshall and Boyle (1996) reported on epidemiologic evidence linking nutrition and oral cancer. Case-control evidence suggests that some foods, including fruits and vegetables, may protect against oral cancer. Also noted is that the adverse effects of alcohol and smoking, as well as hygiene, may be confounded by dietary elements, suggesting a potential protective effect of some foods. In a recent study apparently supporting the risk-reducing effect of fruits and vegetables on oral squamous cell carcinoma, the vegetables that appear to be protective include the alliums, carrots, green vegetables, cruciferous vegetables, and tomatoes, and the greatest benefit accrues when these foods are eaten raw.[35, 36]
These findings are further supported by a comprehensive meta-analysis of 16 studies (15 case-control studies and 1 cohort study meeting the inclusion criteria) published until in which the effect of daily intake of fruit or vegetables was assessed for the relative risk of oral cancer. The combined computed adjusted odds ratio (OR) suggested that each portion of fruit consumed in a day significantly reduced the risk of oral cancer by 49%. For vegetable consumption, the overall reduced risk was 50%. However, as for the relationship between fruit and oral cancer, analysis suggested that the type of fruit consumed (citrus fruit consumption versus other types of fruit) and the interval of dietary recall (a methodology issue) appeared to influence the relative risk.
This meta-analysis suffered from several deficiencies, such as study heterogeneity (populations, study design, subject recall, data analysis). In addition, there were potential problems in using as a defining term ”oral cancer,” which, as the authors point out, might have included a heterogenous group of neoplasms.
The literature also suggests a potential effect of nutrient supplementations on the risk of oral cancer. Dennert et al (2011) studied the effect of various supplementations on several types of cancer.
Selenium is an antioxidant that is purported to be protective with respect to cancer. Forty-nine prospective observational and 6 randomized controlled trials pertaining to selenium and various cancers were reviewed and included in the analysis. Prior epidemiologic data suggest that selenium supplementation may be associated with an overall reduced cancer incidence and mortality, with the greatest risk reduction in men. However, this review found little evidence in supporting the use of selenium in reducing cancer risk.
In contrast, the relationship between selenium, zinc, and oral cancer has been confirmed by at least one case-controlled study involving 379 cases and 514 controls. Men with oral cancer were found to have lower nail selenium and zinc concentrations in nail clippings, but this was not the case among women. Smoking was associated with lower levels of both zinc and selenium. It should be appreciated, however, that the potential utility of selenium supplementation may be confounded by the type of selenium supplied (salts or organic), general nutrition and nutritional status, dilatory habits (eg, smoking and alcohol), other lifestyle factors, and dosage considerations. Selenium metabolism may also vary by sex. These potentially confounding variables have yet to be studied via appropriate research.
Other antioxidants are also reportedly helpful in preventing oral cancer, perhaps by protecting cell DNA from the effects of oxidative enzymes. In a study of nutrient-based dietary patterns and the risk of head and neck cancer based on pooled data from 5 case-controlled studies involving over 2452 cases and 5013 controls, Edefonti et al found that the “antioxidant vitamins and fiber” pattern of dietary intake was inversely related to oral and pharyngeal cancer (OR = 0.57; 95% CI, 0.43-0.76 for the highest versus the lowest score quintile). In addition, the fats pattern was inversely associated with oral and pharyngeal cancer (OR = 0.78; 95% CI, 0.63-0.97).
Antioxidant supplementation as a means of reducing cancer risk has been assessed in animal and human studies.[41, 42, 43, 44] The accumulating evidence suggests that various antioxidant substances may lower cancer risk and could be incorporated as supplements. Available antioxidant substances with some experimental validation include vitamin E (alpha-tocopherol [not upsilon-tocopherol]) and the carotenoids (beta-carotene, alpha-carotene, cryptoxanthin, lutein, and lycopene).
It should be appreciated that the most recent large-scale randomized clinical trials have reached inconsistent conclusions regarding antioxidants and their potential for preventing cancer. Nonetheless, foods that might be recommended to at-risk patients (eg, smokers, alcohol users) because they have substantial antioxidant properties include the following:
Beta-carotene - Potatoes, carrots, cantaloupe, squash, apricots, pumpkin, mangos, and some green leafy vegetables (collard greens, spinach, kale)
Vitamin A - Liver, sweet potatoes, carrots, milk, egg yolks, and mozzarella cheese
Vitamin C - Fruit, vegetables, cereals, beef, poultry, and fish
Selenium (a mineral) - Rice, wheat, meats, bread, Brazil nuts
Coffee may also include antioxidants.
In a study assessing the antioxidant enzymatic activity in saliva among patients with oral cancer and odontogenic cysts compared with healthy controls, subjects with oral cancer were found to exhibit lower total antioxidant capacity and salivary peroxidase and superoxide dismutase activity in their saliva than controls. The evidence was also interpreted as suggesting that the lower antioxidants levels in saliva among subjects with odontogenic cysts could indicate a role of antioxidants in the development of tumors (neoplastic transformation) that form within these structures.
Another aspect of diet and oral cancer is in disease management. Radiation and chemotherapy can cause severe mucosal deterioration and mucositis, ulceration, and significant oral pain; thus, patients undergoing treatment for oral and oropharyngeal cancer may experience significant disturbance in their dietary habits and undernourishment or frank malnutrition. In a study of 120 patients with oral cancer, one third experienced major food restrictions owing to side effects of cancer treatment; 39% were observed to suffer a less severe condition in which they could not eat less than 50% of the most commonly consumed food items. Hence, dietary planning for patients undergoing treatment for oral cancer is extremely important in the overall management of the disease.(mEDSCAPE RIGHTS OF ART.)