Diet and Oral Health
- Author: Jeff Burgess, DDS, MSD; Chief Editor: Arlen D Meyers, MD, MBA more...
Diet can affect oral health via numerous mechanisms. Dietary deficiencies are known to cause several diseases that manifest as oral changes. In addition, certain foods have both beneficial and disease-causing capacity, potentially affecting the teeth, periodontal structures, and mucosa.
Dietary considerations are also important in the prevention and management of head and neck cancer.
This article discusses the impact of these dietary variables on multiple aspects of oral health.
Diet, Caries, and Dental Erosion
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.
Antonenko et al evaluated the association between oral health and calcium (Ca) and vitamin D nutritional status. The results of this study showed evidence of an association between high cariogenic risk and great severity of oral disease in the studied group of young women and low Ca intake. The authors suggest that an adequate nutritional status of Ca and vitamin D could be an additional factor that may help preserve a good oral health.
Diet and Periodontal Disease
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.[19, 20] 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.
Diet and Oral Cancer
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.[36, 37]
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.[42, 43, 44, 45] 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.
Diet and Other Oral Diseases
The pathogenesis of several oral conditions, including aphthous stomatitis, leukoplakia, plasma cell gingivitis (PCG), and allergy, has been associated with foods or food products.
Aphthous stomatitis, a condition characterized by multiple ulcers involving the unattached oral mucosa, has been linked to foods or food products such as chocolate, cheese, nuts, pineapple, citrus fruits, coffee, potatoes, figs, and gluten-containing products. The role of vitamin deficiency is mixed in the literature, but evidence supports the notion that deficiencies in iron, folate, and vitamin B-12 may play a role in the etiology of aphthous ulceration.
The issue of supplementation with vitamin B-12 continues to be controversial, but the results of at least one study suggest that management of aphthous ulceration with 1000 mcg/d has demonstrated a therapeutic benefit, regardless of presenting serum vitamin B-12 levels.
Cinnamon-flavoring agents have also been associated with oral mucosal changes, including erythematous patches, leukoplakia or keratosis, and ulceration. Lesions are typically confined to the buccal mucosa and the lateral borders of the tongue. Most commonly, cinnamon-flavored chewing gum is the cause of lesion formation. In contrast, cinnamon oil containing cinnamaldehyde has been found to suppress the growth of Candida species and may be useful in treating oral fungal lesions (candidiasis) in persons with HIV infection.
Several other oral mucosal conditions are associated with dietary factors. Although rare, PCG has been linked to the chewing of khat. PCG has also been observed in users of herbal toothpastes and mint, as well as red chili, black pepper, and cardamom.
The term oral allergy syndrome is used to characterize the oral symptom of intraoral itching reported in individuals with pollen allergies when they eat certain foods. The condition is said to arise from cross-reactivity of proteins in the food being eaten with the pollen proteins that cause the allergy.
The following is a list of foods that are suggested as having the capacity to cross-react with specific plant pollens (according to the American Academy of Allergy, Asthma, and Immunology [AAAAI]):
Ragweed pollen allergy reacts with bananas, melons (eg, honeydew, cantaloupe, watermelons), tomatoes, zucchini, sunflower seeds, dandelions, chamomile tea, and echinacea
Birch pollen allergy reacts with kiwi, apples, pears, peaches, plums, coriander, fennel, parsley, celery, cherries, carrots, hazelnuts, and almonds
Grass pollen allergy reacts with peaches, celery, tomatoes, melons, and oranges
Latex rubber allergy reacts with bananas, avocadoes, kiwi, chestnut, and papaya
Research supporting the above associations is scant. However, in patients who report oral itching not associated with obvious pathology, it might be worthwhile to inquire about the possibility of allergy and to refer the patient for allergy testing in such cases.
Oral Conditions and True Dietary Deficiency
Vitamin deficiency can alter the intraoral mucosa in distinctive ways.
One example is scurvy, a disease associated with a severe vitamin C (ascorbic acid) deficiency that occurs when food containing the vitamin is not eaten over a prolonged period. Although the condition has not generally been a problem in the 21st century, it does occur with starvation and has been observed in people of southeastern Africa. The oral signs associated with scurvy include severe bleeding of the gums, hyperplasia, and tooth loosening and loss.
Vitamin B-12 deficiency anemia may result from poor gut absorption of vitamin B-12 secondary to removal of a portion of the intestines or stomach or consequent to gastrointestinal infection. The condition results in a loss of tongue papilla and a glossing of the dorsal surface of the tongue (termed atrophic glossitis)
Other deficiencies associated with oral mucosal changes include the following:
Vitamin A (retinol) deficiency - Mucosal dryness, atrophy, leukoplakia, angular cheilitis; lips appear to be “retreating” as the mucosal surface contracts back into the mouth
Vitamin B-2 (riboflavin) deficiency - Angular cheilitis, tongue swelling, atrophy and redness of the tongue, swelling and erythema of mucosa
Vitamin B-3 (niacin) deficiency - Mucosal stomatitis and glossitis; erythematous, smooth, raw tongue; initially, the tongue swells and then becomes atrophic; erosions and aphthouslike ulcers on the tongue and gingiva; early pellagra with increased salivary flow with salivary flow decreasing later; salivary gland swelling; burning mouth or burning tongue; angular cheilitis
Vitamin B-6 (pyridoxine) deficiency - Cheilitis and glossitis
Zinc deficiency - Lip crusting; oral ulcers, erosions, fissures; scaling rash of the lips; periorofacial erythematous rash
Folic acid deficiency - Angular cheilitis, ulcers, and glossitis
Malnutrition and Growth and Development
Severe starvation and malnutrition is a problem seen primarily in sub-Saharan African children aged 2-16 years. Malnutrition not only results in scurvy but also disturbs tooth development (delayed tooth eruption) and exacerbates infection and periodontal disease. Research does not support a relationship between tooth crowding and malnutrition.
A serious sequela of starvation is the development of cancrum oris (noma), a progressive gangrenous disease in which rapid and destructive tissue and bone necrosis causes significant facial morbidity and, in some cases, mortality.[63, 64]
Malnutrition may also increase the incidence of caries in primary teeth, enamel hypoplasia, salivary gland hypofunction, and delayed eruption.
Diet and Dry Mouth
Dry mouth can alter the type of food that is eaten, and some foods can contribute to dry mouth.
In a study assessing the association between dry mouth and beverage intake and dietary quality in 622 patients aged 60 years or older, the consumption of sugar-sweetened beverages was positively associated with dry mouth, although overall beverage consumption was not. Severe dry mouth was associated with a lower intake of whole grains and a higher intake of fruit. Patients were more likely to modify their eating behavior if dry mouth was severe.
Oral dryness can be caused by herbal supplements. These include ephedra, an herb used as a decongestant or stimulant; St. John’s Wort, used for depression, anxiety, and sleep; and kratom, an herb with psychoactive effects that is legal in the United States but banned in Thailand and Malaysia where it is harvested. Caffeinated drinks such as coffee, tea, and soda may cause or exacerbate dry mouth. For every cup of coffee consumed, the body dehydrates at about the same rate. Consumption of spicy foods and foods heavily salted may also contribute to dryness.
Foods that help to mitigate dry mouth include bananas, watermelon, and steamed vegetables. Chamomile and other noncaffeinated teas can also reduce perceived dryness. Xylitol adherent disks have also been shown to reduce perceived nighttime dryness. Sorbet has also been found to increase salivation.
Diet and Head/Neck Radiology and Chemotherapy
The oral mucositis and pain, xerostomia, and dysphagia that develop following radiation and chemotherapy for oropharyngeal cancer can profoundly affect subsequent dietary intake. Food and fluid restriction, if severe, increases the risk of malnutrition and mortality. Nutritional management following cancer treatment is imperative as a component of the overall care of the patient.
Posttherapy weight loss due to cancer treatment and subsequent oral problems is estimated to add an additional 10% to the pretherapy weight loss experienced by patients with oropharyngeal cancer. A greater than 20% loss of total body weight may increase the risk of additional toxicity and treatment time and a poorer clinical outcome, as well as the risk of mortality. Consequently, early intervention with nutritional supplementation via enteral support via nasoenteric or percutaneous endoscopic gastrostomy has been recommended in patients at high risk for weight loss.
Patients have been shown to benefit from nutritional counseling following cancer treatment. In terms of posttreatment quality of life, there is evidence that nutritional deterioration and intake deficits may be more relevant than the initial stage of the cancer itself. According to one study, after 3 months, nutritional counseling appeared to be the single best method of several strategies appearing capable of sustaining a meaningful effect on patient outcome. This study also found that early use of a mixture of foods and textures also modulated outcomes.
Although no specific guidelines address the appropriate types of foods and textures that might be recommended to patients with oropharyngeal cancer, for those able to take food by mouth, a bland soft diet and liquid diet supplements are considered the most reasonable approaches for providing adequate nutritional. Mucositis is worsened by acidic, spicy, excessively salty, or course and dry food, and these products should be avoided. Oral moisture can be improved with sips of water, ice chips, or popsicles.
In cases of severe mucositis, parenteral nutritional support via a Hickman line may be necessary. The need for enteral support appears to be directly related to the extent of tumor involvement and severity of the initial disease, particularly for treatment extending beyond 12 months.
An important consideration with respect to diet is posttreatment dysphagia and its effect on what has been termed silent aspiration. Recent evidence suggests that this may be a more serious problem than previously thought. In one study, the problem was found to occur in 65.9% of patients. With respect to food consistency, it was found to occur in 65% of subjects who were taking thin fluids, 35% taking thick fluids, 12% on a pureed diet, and 6% on a soft diet.
Regardless of initial considerations regarding diet following radiation and chemotherapeutic treatment in patients with oropharyngeal cancer, the evidence suggests that there is an inverse relationship between reduction in chronic mucositis and improved oral intake and diet over time.
Wigen TI, Espelid I, Skaare AB, Wang NJ. Family characteristics and caries experience in preschool children. A longitudinal study from pregnancy to 5 years of age. Community Dent Oral Epidemiol. 2011 Aug. 39(4):311-7. [Medline].
Huew R, Waterhouse PJ, Moynihan PJ, Kometa S, Maguire A. Dental erosion and its association with diet in Libyan schoolchildren. Eur Arch Paediatr Dent. 2011 Oct. 12(5):234-40. [Medline].
Masson LF, Blackburn A, Sheehy C, Craig LC, Macdiarmid JI, Holmes BA. Sugar intake and dental decay: results from a national survey of children in Scotland. Br J Nutr. 2010 Nov. 104(10):1555-64. [Medline].
Hara AT, Zero DT. The caries environment: saliva, pellicle, diet, and hard tissue ultrastructure. Dent Clin North Am. 2010 Jul. 54(3):455-67. [Medline].
Papas AS, Joshi A, Palmer CA, Giunta JL, Dwyer JT. Relationship of diet to root caries. Am J Clin Nutr. 1995 Feb. 61(2):423S-429S. [Medline].
Masson LF, Blackburn A, Sheehy C, Craig LC, Macdiarmid JI, Holmes BA. Sugar intake and dental decay: results from a national survey of children in Scotland. Br J Nutr. 2010 Nov. 104(10):1555-64. [Medline].
Wigen TI, Wang NJ. Maternal health and lifestyle, and caries experience in preschool children. A longitudinal study from pregnancy to age 5 yr. Eur J Oral Sci. 2011 Dec. 119(6):463-8. [Medline]. [Full Text].
Barriuso Lapresa L, Sanz Barbero B, Hernando Arizaleta L. Prevalence of healthy oral habits in the child population resident in spain. An Pediatr (Barc). Oct, 2011[Epub ahead of pring].
Sheiham A. Dietary effects on dental diseases. Public Health Nutr. 2001 Apr. 4(2B):569-91. [Medline].
Savoca MR, Arcury TA, Leng X, Chen H, Bell RA, Anderson AM, et al. Severe tooth loss in older adults as a key indicator of compromised dietary quality. Public Health Nutr. 2010 Apr. 13(4):466-74. [Medline]. [Full Text].
Coombes JS. Sports drinks and dental erosion. Am J Dent. 2005 Apr. 18(2):101-4. [Medline].
Tanaka K, Miyake Y, Sasaki S. Intake of dairy products and the prevalence of dental caries in young children. J Dent. 2010 Jul. 38(7):579-83. [Medline].
Touger-Decker R, van Loveren C. Sugars and Dental Caries. Am J of Clin Nutrition. 2003. 78(4):881-892.
Gazzani G, Daglia M, Papetti A. Food components with anticaries activity. Curr Opin Biotechnol. 2011 Oct 24. [Medline].
Ferrazzano GF, Amato I, Ingenito A, Zarrelli A, Pinto G, Pollio A. Plant polyphenols and their anti-cariogenic properties: a review. Molecules. 2011 Feb 11. 16(2):1486-507. [Medline].
Ferrazzano GF, Roberto L, Amato I, Cantile T, Sangianantoni G, Ingenito A. Antimicrobial properties of green tea extract against cariogenic microflora: an in vivo study. J Med Food. 2011 Sep. 14(9):907-11. [Medline].
Yoo S, Murata RM, Duarte S. Antimicrobial traits of tea- and cranberry-derived polyphenols against Streptococcus mutans. Caries Res. 2011. 45(4):327-35. [Medline].
Antonenko O, Bryk G, Brito G, Pellegrini G, Zeni SN. Oral health in young women having a low calcium and vitamin D nutritional status. Clin Oral Investig. 2014 Oct 31. [Medline].
Bawadi HA, Khader YS, Haroun TF, Al-Omari M, Tayyem RF. The association between periodontal disease, physical activity and healthy diet among adults in Jordan. J Periodontal Res. 2011 Feb. 46(1):74-81. [Medline].
Russell SL, Posoter WJ. Protein-energy malnutrition during early childhood and periodontal disease in the permanent dentition of Haitian adolescents aged 12-19 years: a retrospective cohort study. Int J Paediatr Dent. 2010. May, 2010. 20(3):222-229.
Enwonwu CO. Interface of malnutrition and periodontal diseases. Am J Clin Nutr. 1995 Feb. 61(2):430S-436S. [Medline].
Enwonwu CO. Differential sex effects of nutritional status on inflammatory periodontal disease in non-human primates. Nutrition. 2010 Jan. 26(1):139; author reply 140. [Medline].
Esaki M, Morita M, Akhter R, Akino K, Honda O. Relationship between folic acid intake and gingival health in non-smoking adults in Japan. Oral Dis. 2010 Jan. 16(1):96-101. [Medline].
van der Velden U, Kuzmanova D, Chapple Il. Micronutritional approaches to periodontal therapy. J Clin Periodontol. Mar, 2011. 38Suppl 11:142-158.
Belluci MM, Giro G, del Barrio RA, Pereira RM, Marcantonio E Jr, Orrico SR. Effects of magnesium intake deficiency on bone metabolism and bone tissue around osseointegrated implants. Clin Oral Implants Res. 2011 Jul. 22(7):716-21. [Medline].
Willershausen B, Ross A, Försch M, Willershausen I, Mohaupt P, Callaway A. The influence of micronutrients on oral and general health. Eur J Med Res. 2011 Nov 10. 16(11):514-8. [Medline].
Slawik S, Staufenbiel I, Schilke R, Nicksch S, Weinspach K, Stiesch M. Probiotics affect the clinical inflammatory parameters of experimental gingivitis in humans. Eur J Clin Nutr. 2011 Jul. 65(7):857-63. [Medline].
Fentoğlu Ŏ Bk, Hicyilmaz H, et al. Pro-inflammatory cytokine levels in association between periodontal disease and hyperlipidaemia. J Clin Periodontol. Jan 2011. 38(1):8-16.
Iwasaki M, Yoshihara A, Moynihan P, Watanabe R, Taylor GW, Miyazaki H. Longitudinal relationship between dietary ?-3 fatty acids and periodontal disease. Nutrition. 2010 Nov-Dec. 26(11-12):1105-9. [Medline].
Fatty fish may prevent gum disease. Available at http://www.webmd.com/oral-health/news/20101026/fatty-fish-may-prevent-gum-disease. Accessed: 12/2/11.
Warnakulasuriya S, Trivedy C, Peters TJ. Areca nut use: an independent risk factor for oral cancer. BMJ. 2002 Apr 6. 324(7341):799-800. [Medline].
Jia WH, Luo XY, Feng BJ, Ruan HL, Bei JX, Liu WS. Traditional Cantonese diet and nasopharyngeal carcinoma risk: a large-scale case-control study in Guangdong, China. BMC Cancer. 2010. 10:446. [Medline].
Facts on Alcohol and Tobacco. Available at http://oralcancerfoundation.org/facts/alcohol_tobacco.htm. Accessed: 12/2/11.
Petridou E, Zavras Al, et al. The role of diet and specific micronutrients in the etiology of oral carcinoma. Cancer. Jun, 2002. 94(11):2981-8.
Marshall JR, Boyle P. Nutrition and oral cancer. Cancer Causes Control. 1996 Jan. 7(1):101-11. [Medline].
Latino-Martel P, Druesne-Pecollo N, Dumond A. [Nutritional factors and oral cancers]. Rev Stomatol Chir Maxillofac. 2011 Jun. 112(3):155-9. [Medline].
Steinmetz KA, Potter JD. Vegetables, fruit, and cancer prevention: a review. J Am Diet Assoc. 1996 Oct. 96(10):1027-39. [Medline].
Pavia M, Pileggi C, Nobile CG, Angelillo IF. Association between fruit and vegetable consumption and oral cancer: a meta-analysis of observational studies. Am J Clin Nutr. 2006 May. 83(5):1126-34. [Medline].
Dennert G, Zwahlen M, Brinkman M, Vinceti M, Zeegers MPA, Horneber M. Selenium for preventing cancer (Review). Available at http://www.cochranejournalclub.com/selenium-preventing-cancer-clinical/pdf/CD005195.pdf. Accessed: 12/2/11.
Rogers MA, Thomas DB, Davis S, Weiss NS, Vaughan TL, Nevissi AE. A case-control study of oral cancer and pre-diagnostic concentrations of selenium and zinc in nail tissue. Int J Cancer. 1991 May 10. 48(2):182-8. [Medline].
Edefonti V, Hashibe M, Ambrogi F, Parpinel M, Bravi F, Talamini R. Nutrient-based dietary patterns and the risk of head and neck cancer: a pooled analysis in the International Head and Neck Cancer Epidemiology consortium. Ann Oncol. 2011 Nov 28. [Medline].
Dhanarasu S, Selvam M, Salama SM, Shanmugam M, Sethuraman P. Terminalia Arjuna (Roxb.) Modulates Circulatory Antioxidants on 7,12-dimethylbenz(a)anthracene- induced Hamster Buccal Pouch Carcinogenesis. Oman Med J. 2010 Oct. 25(4):276-81. [Medline].
Ljju VB, Jeena K, Kuttan R. An evaluation of antioxidant, anti-inflammatory, and antinociceptive activities of essential oil from Curcuma longa. Indian J Pharmacol. Sep, 2011. 43(5):526-31.
Korde SD, Basak A, Chaudhary M, Goyal M, Vagga A. Enhanced nitrosative and oxidative stress with decreased total antioxidant capacity in patients with oral precancer and oral squamous cell carcinoma. Oncology. 2011. 80(5-6):382-9. [Medline].
Suresh K, Manoharan S, Vijayaanand MA, Sugunadevi G. Chemopreventive and antioxidant efficacy of (6)-paradol in 7,12-dimethylbenz(a)anthracene induced hamster buccal pouch carcinogenesis. Pharmacol Rep. 2010 Nov-Dec. 62(6):1178-85. [Medline].
Garewal H. Antioxidants in oral cancer prevention. Am J Clin Nutr. 1995 Dec. 62(6 Suppl):1410S-1416S. [Medline].
National Cancer Institute. Antioxidants and Cancer Prevention: Fact Sheet. Available at http://www.cancer.gov/cancertopics/factsheet/prevention/antioxidants.
Giebultowicz J, Wroczynski P, Samolczk-Wanyura D. Comparison of antioxicant enzymes activity and the concentration of uric acid in the saliva of patients with oral cavity cancer, odontogenic cysts and healthy subjects. J Oral Pathol Med. April, 2011. Epub ahead of print:
Cruz ED, Toporcov TN, Rotundo LD, Biazevic MG, Brasileiro RS, Carvalho MB. Food restrictions of patients who are undergoing treatment for oral and oropharyngeal cancer. Eur J Oncol Nurs. 2011 Jul 15. [Medline].
Wardhana Datau EA. Recurrent aphthous stomatitis caused by food allergy. Acta Med Indones. 2010. 42(2):236-40.
Petersen MJ, Baughman RA. Recurrent aphthous stomatitis: primary care management. Nurse Pract. 1996 May. 21(5):36-40, 42, 47. [Medline].
Carrozzo M. Vitamin B12 for the treatment of recurrent aphthous stomatitis. Evid Based Dent. 2009. 10(4):114-5. [Medline].
Allen CM, Blozis GG. Oral mucosal reactions to cinnamon-flavored chewing gum. J Am Dent Assoc. 1988 May. 116(6):664-7. [Medline].
Cinnamon oil used for oral thrush. Available at http://www.livestrong.com/article/476698-cinnamon-oil-used-for-oral-thrush/#ixzz1fEPKe8gS).
Marker P, Krogdahi A. Plasma cell gingivitis apparently related to the use of khat: report of a case. British Dental Journal. 2002. 192:311-313.
Anil S. Plasma cell gingivitis among herbal toothpaste users: a report of three cases. J Contemp Dent Pract. 2007 May 1. 8(4):60-6. [Medline].
lubow RM, Cooley RL, et al. Plasma-cell gingivitis. Report of a case. J Periodontol. 1995. 55(4):235-41.
Gargiulo AV, Ladone JA, Ladone PA, Toto PD. Case report: plasma cell gingivitis A. CDS Rev. 1995 Apr. 88(3):22-3. [Medline].
Oral Allergy Sydrome Foods. Available at http://www.webmd.com/allergies/features/oral-allergy-syndrome-foods. Accessed: 12/02/11.
Dolberg OJ, Elis A, Lishner M. Scurvy in the 21st century. Isr Med Assoc J. 2010 Mar. 12(3):183-4. [Medline].
scurvy. Available at http://www.nlm.nih.gov/medlineplus/ency/article/000355.htm.
Thomaz EB, Cangussu MC, da Silva AA, Assis AM. Is malnutrition associated with crowding in permanent dentition?. Int J Environ Res Public Health. 2010 Sep. 7(9):3531-44. [Medline].
Chiandussi S, Luzzati R, Tirelli G, Di Lenarda R, Biasotto M. Cancrum oris in developed countries. Aging Clin Exp Res. 2009 Dec. 21(6):475-7. [Medline].
Phillips RS, Enwonwu CO, Falkler WA. Pro- versus anti-inflammatory cytokine profile in African children with acute oro-facial noma (cancrum oris, noma). Eur Cytokine Netw. 2005 Jan-Mar. 16(1):70-7. [Medline].
Psoter WJ, Reid BC, Katz RV. Malnutrition and dental caries: a review of the literature. Caries Res. 2005 Nov-Dec. 39(6):441-7. [Medline].
Quandt SA, Savoca MR, Leng X, Chen H, Bell RA, Gilbert GH. Dry mouth and dietary quality in older adults in north Carolina. J Am Geriatr Soc. 2011 Mar. 59(3):439-45. [Medline].
Herbs that cause dry mouth. Available at http://www.livestrong.com/article/271040-herbs-that-cause-dry-mouth/#ixzz1fM6vd28H. Accessed: 12/02/11.
Crogan NL. Managing xerostomia in nursing homes: pilot testing of the Sorbet Increases Salivation intervention. J Am Med Dir Assoc. 2011 Mar. 12(3):212-6. [Medline].
Wood K. Audit of nutritional guidelines for head and neck cancer patients undergoing radiotherapy. J Hum Nutr Diet. 2005 Oct. 18(5):343-51. [Medline].
Colasanto JM, Prasad P, Nash MA, Decker RH, Wilson LD. Nutritional support of patients undergoing radiation therapy for head and neck cancer. Oncology (Williston Park). 2005 Mar. 19(3):371-9; discussion 380-2, 387. [Medline].
Ravasco P. Nutritional support in head and neck cancer: how and why?. Anticancer Drugs. 2011 Aug. 22(7):639-46. [Medline].
Nathaniel S Treister, DMD, DMSc. Chemotherapy-Induced Oral Mucositis Treatment & Management. Available at http://emedicine.medscape.com/article/1079570-treatment#a1130.
Lalla RV, Sonis ST, Peterson DE. Management of oral mucositis in patients who have cancer. Dent Clin North Am. 2008 Jan. 52(1):61-77, viii. [Medline].
Chapuy CI, Annino DJ, Snavely A, Li Y, Tishler RB, Norris CM. Swallowing function following postchemoradiotherapy neck dissection: review of findings and analysis of contributing factors. Otolaryngol Head Neck Surg. 2011 Sep. 145(3):428-34. [Medline].
Ng LK, Lee KY, Chiu SN, Ku PK, van Hasselt CA, Tong MC. Silent aspiration and swallowing physiology after radiotherapy in patients with nasopharyngeal carcinoma. Head Neck. 2011 Sep. 33(9):1335-9. [Medline].
Pauloski BR, Rademaker AW, Logemann JA, Lundy D, Bernstein M, McBreen C. Relation of mucous membrane alterations to oral intake during the first year after treatment for head and neck cancer. Head Neck. 2011 Jun. 33(6):774-9. [Medline].
Touger-Decker R, van Loveren C. Sugars and Dental Caries. American Journal of Clinical Nutrition. 2003. 78(4):881S-892S.