Nutrition and Oral Health

Key Points

  • A bidirectional relationship exists between oral health and diet and nutrition. Diet and nutrition affect the health of the tissues in the mouth; and the health of the mouth affects nutrients consumed.
  • The consumption of sugars has been associated with an increased risk of developing dental caries.
  • The complex nature of periodontal disease makes it difficult to determine its relationship with diet and nutrition.
  • Frequent consumption of acidic food and beverages is associated with an increased risk of erosive tooth wear.


Diet and nutrition are significant influencers of oral health, and can affect the development and progression of oral diseases and conditions such as caries, periodontal disease, erosion, and others. While nutrition can be defined as the micro- (vitamins and minerals) and macro- (carbohydrates, protein, and fat) nutrients as they relate to the body’s dietary needs, diet refers to the specific foods consumed. The relationship that diet and nutrition have with oral health is bidirectional, as compromised integrity of the oral cavity can also influence an individual’s functional ability to eat.1

There are different types of nutrition studies such as epidemiological studies, case-control studies, and clinical trials. While all study types may be used to generate useful information, they differ in terms of reliability and how to interpret the data. For instance, epidemiological studies are primarily observational, meaning that the populations compared can differ from each other by any number of uncontrolled factors. They look for associations between nutritional factors and a given outcome in large populations. It is important to remember that finding an association is not the same as demonstrating causation. In case-control studies, two groups of closely matched subjects (by age, sex, race, etc.) that differ in the presence or absence of a particular condition of interest are compared to see what factors might differ between the groups, providing potential clues about cause and prevention of that condition. However, even though a number of variables are matched, the populations compared can differ in important ways. Clinical trials generally control for more factors, using a sample size calculated to be sufficient to detect a statistically significant change in the variable of interest.2 With any study involving nutrient intake or dietary patterns, it can be challenging to follow participants for a meaningful length of time.

A variety of dietary factors are hypothesized to influence the oral cavity, including macro- and micronutrients, vitamins, pH properties, as well as the behaviors associated with their consumption. Additionally, factors such as stage of development, specific medical conditions, and socioeconomic status may indicate particular diet and nutritional considerations. Older patients, for example, may experience tooth loss, reduced masticatory ability, and decreased appetite, which may, in turn, influence their nutritional status.3 A systematic review examined the association between food intake and oral health in elderly found that tooth loss in the older population was associated with changes in food intake and nutritional deficiency.4

Dental Caries

Dental caries is the most common disease worldwide. The term dental caries can be used to describe both the disease process and the cavitated or noncavitated lesions that form as a result of the disease process.5 The caries disease process is biofilm-mediated, sugar-driven, multifactorial, and dynamic in the phasic demineralization and remineralization of dental hard tissues.6

The relationship between caries and carbohydrates is fairly well understood; dental hard tissues are demineralized by acidic by-products produced by bacteria in biofilm (dental plaque) via fermentation of dietary carbohydrates.6 More specifically, there is a rapid fall in pH (to 5.5 or below) in tooth biofilm after carbohydrates are ingested. This lower pH can also affect the balance of microbes in the biofilm such that there is a higher proportion of acidic biofilm species, compounding tooth demineralization.7 Carbohydrate consumption is therefore an important nutritional factor in the development of caries.

For more information on dental caries, visit the ADA Oral Health Topics page on caries risk assessment and management.

Types of Carbohydrates

The relationship between carbohydrates and dental caries depends on the type of carbohydrate (sugars or starches) consumed because the cariogenic potential (i.e., promoting the development of tooth decay) of a given carbohydrate is dependent on how efficiently it can be metabolized by the bacteria that ferment it.8 Sugars, specifically, are considered to be the most important drivers of caries development. The term free sugar includes all sugars added to food/beverages, as well as the naturally occurring sugars found in fruit juices and concentrates, honey, and natural syrups. Collectively, natural and free sugars (e.g., sucrose, glucose, fructose) are considered the primary necessary factors in the development of caries.8 Sucrose, a disaccharide of glucose and fructose, is the most cariogenic sugar.8 Sucrose acts as a substrate for the synthesis of intra- and extracellular polysaccharides in dental plaque.8-10 Additionally, dental plaque formed in the presence of sucrose has been shown to have lower concentrations of calcium, inorganic phosphate, and fluoride, which are the ions required to remineralize enamel and dentin.10, 11 Sucrose and its constituent monosaccharides, glucose and fructose, are also more cariogenic than starches because they enter the glycolytic pathway more rapidly and result in a more pronounced drop in pH.12 Although lactose is also a sugar, it is less cariogenic than sucrose, fructose, and glucose because its fermentation produces a smaller drop in pH.9, 13

Amount/Frequency of Sugar Intake

In addition to the type of sugar consumed, the amount consumed may affect caries development. A 2014 systematic review examining the effect of free sugar consumption on dental caries observed a consistent association between free sugar intake and caries development; higher incidence of caries was found in populations where free sugar intake was greater than 10% of total energy intake compared to those with free sugar intake of less than 10%.14 This systematic review informs the World Health Organization (WHO) guidelines for sugar intake, which recommends that free sugars be less than 10% of total energy intake, with a further reduction to less than 5% suggested.15

Frequency, or how often free sugars are consumed, may also play a role in caries development. Increased frequency of sugar consumption and additional snacking between meals have been hypothesized to be more important in predicting caries risk than total sugar consumption.16-18 A possible rationale for this concept is that it takes approximately 30 minutes for the pH to drop after an intake of sugar, so additional sugar intake within that 30-minute period is less harmful than additional intake after 30 minutes.16 It is, however, difficult to determine the relative contribution of amount of sugar and frequency of sugar consumption to dental caries risk, given that the two are highly interrelated.16, 19

The recent systematic reviews and guidelines mentioned above14, 15, 20 present data that support the association between sugar consumption and/or snacking with caries development. Although not evidence for causality, these reviews are consistent in their findings that increased free sugar consumption is associated with an increased risk of caries.

There is ongoing research to determine strategies to decrease the consumption of sugar-sweetened beverages (SSBs), as they are a significant contributor to free sugar consumption. A tax on SSBs is one strategy that has been attempted; studies suggest that taxation of SSBs may decrease SSB consumption, caries incidence, and caries-related costs. Although public acceptance and efficacy of this strategy are still unclear, a 2019 systematic review and meta-analysis21 found that the equivalent of a 10% tax on SSBs was associated with an average decline in SSB purchase and intake of 10.0%.21-23 In addition to interventions effective at the population level, there is a need for high-quality evaluations with long-term study designs examining efficacy.24

Early childhood caries (ECC) is the presence of one or more decayed, missing, or filled tooth surface in children under 6 years of age.25 ECC was formerly referred to as “baby bottle tooth decay” and is primarily due to prolonged exposure of the enamel to sweetened liquids causing caries in small children. To address ECC, both the Academy of Nutrition and Dietetics and American Academy of Pediatrics promulgate guidance limiting fruit juice consumption by babies and toddlers.25, 26

Limited income or access to food can have a negative impact on intake of fruits and vegetables, lean meat, whole grains, and dairy. This inadequate consumption of nutrient-dense foods combined with a lower health literacy and limited access to oral health care can put low-income populations at an increased risk for caries and other oral diseases.25

Foods such as milk and dairy products, apples, cranberries, tea, and high-fiber foods have been suggested to have cariostatic properties (i.e., inhibiting the development of caries), although more careful examination is needed.27 It has been postulated that the calcium in dairy products offsets some of the cariogenic properties of lactose by limiting enamel undersaturation during acidogenesis. As mentioned above, lactose fermentation also results in a smaller reduction in pH compared with other simple sugars. Data from studies examining the association between milk consumption and caries suggests milk consumption does not increase caries risk and may actually reduce it.28

Some studies indicate that sugar alcohols such as xylitol and sorbitol used in chewing gums and as artificial sweeteners may have cariostatic effects, but overall findings are equivocal. Postulated mechanisms by which xylitol may reduce caries risk include simple substituting for fermentable carbohydrates,29 reducing the acidogenic potential,30 inhibiting the growth of Streptococcus mutans (plaque bacteria that contribute to tooth demineralization),31 or just increasing salivary flow (especially in the case of sugar-free chewing gums).32, 33 Although non-sugar sweetened gum is eligible for application to the ADA Seal of Acceptance, the ADA does not have a policy on the use of xylitol for caries prevention. The Council on Scientific Affairs expert panel report on Nonfluoride Caries-Preventive Agents concluded that evidence of xylitol’s benefit as an adjunctive therapy in children and adults who are at a high risk for developing caries is of low quality.34 For more information on chewing gum, visit the ADA Oral Health Topics page.

Vitamin D

Vitamin D influences the regulation of calcium and phosphate metabolism.35 According to some observational studies, higher prenatal intakes of vitamin D and prenatal serum vitamin D levels may be associated with reduced caries risk in children and infants.36, 37 Historical reports38 as well as a 2016 cross-sectional study suggest an association between dental caries and lower serum levels of vitamin D in children.39

Periodontal Disease

The American Academy of Periodontology defines periodontitis as “the inflammation of the periodontal tissues resulting in clinical attachment loss, alveolar bone loss, and periodontal pocketing.”40 It is caused by specific microorganisms in dental plaque and excessive host response to this bacterial challenge, resulting in progressive destruction of tooth-supporting apparatus (i.e., gingiva, periodontal ligament, and alveolar bone).41 The effect of nutrition status on the body’s immune response may modify factors affecting management of periodontal disease; however, the multifactorial nature of periodontal disease and nutritional status makes it difficult to determine such effects.25

Compared with caries, there are fewer studies exploring the relationship between nutrition and periodontal disease. Existing studies linking nutrition to periodontal disease have focused primarily on the intake of lipids and various micronutrients. However, the two systematic reviews examining the role of dietary minerals42 and lipids43 on the onset, severity/progression, and treatment of periodontal disease found insufficient evidence of any associations.

Dental Erosion

Dental erosion is clinically defined as “the progressive and irreversible loss of dental hard tissue caused by a chemical process of acid dissolution that does not involve bacteria,”44 and while acid reflux and some medications can contribute to erosive tooth wear, the most significant source of acid for tooth erosion is the diet.45 Specifically, frequency of consumption, patterns of consumption, and time in contact with acidic food or beverage influence erosive tooth wear.46 However, pH alone is not the only factor affecting how erosive a food/beverage may be. The pH and buffering capacity collectively determine how erosive a food or beverage is.47 Yogurt, for example, has a pH of about 4.0, but is not considered erosive due its high calcium content, which acts as a buffer.48

A meta-analysis conducted in 2012 found that soft drinks and chewable vitamin C tablets were both associated with the development of erosive tooth wear while juice, sports drinks, milk, and yogurt were not.49 This is somewhat at odds with a meta-analysis conducted in 2015 that found soft drinks and acidic snacks, as well as fruit juices, increased the odds for tooth erosion in children; and, in addition, found that intake of milk and yogurt was associated with a reduction in the occurrence of erosion.50

Dental erosion may also be caused by intrinsic factors such as stomach acid in those with gastroesophageal reflux disease (GERD) or individuals with who vomit frequently.51-53 Compared to erosion caused by extrinsic factors (i.e., dietary factors) which commonly affects the facial and occlusal surfaces of teeth, erosion caused by gastric acid primarily occurs on the palatal and occlusal surfaces of the anterior maxillary teeth and on the buccal and occlusal surfaces of the mandibular teeth.54

For more information on dental erosion, visit the ADA Oral Health Topics page on dental erosion.

Calcium Intake

Calcium is a mineral found in many foods, and is essential for forming and maintaining healthy bones and teeth,55 including hydroxyapatite, the primary calcium phosphate mineral in bone and enamel. Dietary calcium is absorbed from the intestine into the blood, from human or animal milk and dairy products (e.g., cheese, yogurt), or foods fortified with calcium (in accord with eCFR §104.20). The 2015-2020 Dietary Guidelines for Americans recommend 700 mg of calcium per day as the recommended dietary allowance (RDA) for children aged 1-3 years, and 1000 mg of calcium per day for children aged 4-8 years.56

In the United States, an estimated 72 percent of calcium intake occurs from consumption of dairy and products to which dairy has been added.55 Numerous varieties of plant-based milk alternatives, including products made with soy, almonds, oats, nuts, potato, flaxseed or hemp, are a growing segment of the consumer marketplace.57 Many exist in forms fortified with one or more nutrients, often including calcium.58-60 However, a technical report from national health and nutrition organizations concludes that plant milks/non-dairy beverages are not recommended from 0-12 months of age; and that unsweetened plant milks/non-dairy beverages other than soy milk are not recommended for exclusive consumption in place of dairy milk.61

Other Oral Health Conditions

Oral and Oropharyngeal Cancer

With the exception of heavy alcohol consumption, which is associated with an increased risk of developing oral cancer,62 other than generalized findings, no direct relation between diet and oral and oropharyngeal cancer risk has been identified. If consistent with what is observed with other cancers, the consumption of fruits and vegetables may be protective.1 A meta-analysis showed a lower risk of oral cancer associated with increased fruit and vegetable consumption,63 and a large prospective observational study64 found total fruit and vegetable intake was associated with a reduced head and neck cancer risk.

For more information on oral and oropharyngeal cancer, visit the ADA Oral Health Topics page on cancer of the head and neck.

Aphthous Ulcers

There is a lack of rigorous studies examining the role of diet in the management of recurrent aphthous stomatitis (RAS), also known as canker sores. Reported dietary triggers include hard, acidic, and salty substances as well as alcoholic and carbonated beverages.65 Preliminary data suggest that zinc deficiency is more common in those with RAS than healthy individuals without them66 and that zinc-supplementation improved RAS resolution in zinc-deficient individuals.67


Xerostomia (dry mouth) and its associated effects on oral health and overall quality of life may be exacerbated by dietary factors such as dry or acidic foods, caffeine, and alcohol.68

For more information on dry mouth, visit the ADA Oral Health Topics page on xerostomia/dry mouth.

ADA Policy on Diet and Nutrition
Policies and Recommendations on Diet and Nutrition Read the ADA policy and recommendations on diet and nutrition.

American Dental Association
Adopted 2016

  1. Touger-Decker R, Mobley C. Position of the Academy of Nutrition and Dietetics: oral health and nutrition. J Acad Nutr Diet 2013;113(5):693-701.
  2. Library of Rush University Medical Center. Clinical Nutrition: Types of Nutrition Studies. Accessed October 11, 2021.
  3. Najeeb S, Zafar MS, Khurshid Z, Zohaib S, Almas K. The role of nutrition in periodontal health: An update. Nutrients 2016;8(9).
  4. Kazemi S, Savabi G, Khazaei S, et al. Association between food intake and oral health in elderly: SEPAHAN systematic review no. 8. Dent Res J (Isfahan) 2011;8(Suppl 1):S15-20.
  5. Selwitz RH, Ismail AI, Pitts NB. Dental caries. Lancet 2007;369(9555):51-9.
  6. Pitts NB, Zero DT, Marsh PD, et al. Dental caries. Nat Rev Dis Primers 2017;3:17030.
  7. Tinanoff N, Baez RJ, Diaz Guillory C, et al. Early childhood caries epidemiology, aetiology, risk assessment, societal burden, management, education, and policy: Global perspective. Int J Paediatr Dent 2019;29(3):238-48.
  8. Sheiham A, James WP. Diet and Dental Caries: The Pivotal Role of Free Sugars Reemphasized. J Dent Res 2015;94(10):1341-7.
  9. Palacios C, Rivas-Tumanyan S, Morou-Bermudez E, et al. Association between Type, Amount, and Pattern of Carbohydrate Consumption with Dental Caries in 12-Year-Olds in Puerto Rico. Caries Res 2016;50(6):560-70.
  10. Cury JA, Rebelo MA, Del Bel Cury AA, Derbyshire MT, Tabchoury CP. Biochemical composition and cariogenicity of dental plaque formed in the presence of sucrose or glucose and fructose. Caries Res 2000;34(6):491-7.
  11. Paes Leme AF, Koo H, Bellato CM, Bedi G, Cury JA. The role of sucrose in cariogenic dental biofilm formation--new insight. J Dent Res 2006;85(10):878-87.
  12. Bibby BG, Krobicka A. An in vitro method for making repeated pH measurements on human dental plaque. J Dent Res 1984;63(6):906-9.
  13. Johansson I, Lif Holgerson P. Milk and oral health. Nestle Nutr Workshop Ser Pediatr Program 2011;67:55-66.
  14. Moynihan PJ, Kelly SA. Effect on caries of restricting sugars intake: systematic review to inform WHO guidelines. J Dent Res 2014;93(1):8-18.
  15. Moynihan P. Sugars and dental caries: evidence for setting a recommended threshold for intake. Adv Nutr 2016;7(1):149-56.
  16. van Loveren C. Sugar Restriction for Caries Prevention: Amount and Frequency. Which Is More Important? Caries Res 2019;53(2):168-75.
  17. Rodrigues CS, Sheiham A. The relationships between dietary guidelines, sugar intake and caries in primary teeth in low income Brazilian 3-year-olds: a longitudinal study. Int J Paediatr Dent 2000;10(1):47-55.
  18. Feldens CA, Giugliani ER, Vigo A, Vitolo MR. Early feeding practices and severe early childhood caries in four-year-old children from southern Brazil: a birth cohort study. Caries Res 2010;44(5):445-52.
  19. Bernabe E, Vehkalahti MM, Sheiham A, Lundqvist A, Suominen AL. The Shape of the Dose-Response Relationship between Sugars and Caries in Adults. J Dent Res 2016;95(2):167-72.
  20. World Health Organization. Guideline: Sugars Intake for Adults and Children. Geneva: World Health Organization 2015. Accessed October 11, 2021.
  21. Teng AM, Jones AC, Mizdrak A, et al. Impact of sugar-sweetened beverage taxes on purchases and dietary intake: Systematic review and meta-analysis. Obes Rev 2019.
  22. Schwendicke F, Thomson WM, Broadbent JM, Stolpe M. Effects of Taxing Sugar-Sweetened Beverages on Caries and Treatment Costs. J Dent Res 2016;95(12):1327-32.
  23. Jevdjevic M, Trescher AL, Rovers M, Listl S. The caries-related cost and effects of a tax on sugar-sweetened beverages. Public Health 2019;169:125-32.
  24. von Philipsborn P, Stratil JM, Burns J, et al. Environmental interventions to reduce the consumption of sugar-sweetened beverages and their effects on health. Cochrane Database Syst Rev 2019;6:CD012292.
  25. Academy of Nutrition and Dietetics. Practice Paper of the Academy of Nutrition and Dietetics: Oral Health and Nutrition. June 2014. Accessed August 27, 2019.
  26. Heyman MB, Abrams SA. Fruit Juice in Infants, Children, and Adolescents: Current Recommendations. Pediatrics 2017;139(6).
  27. Moynihan P. Foods and dietary factors that prevent dental caries. Quintessence Int 2007;38(4):320-4.
  28. Bradshaw DJ, Lynch RJ. Diet and the microbial aetiology of dental caries: new paradigms. Int Dent J 2013;63 Suppl 2:64-72.
  29. Van Loveren C. Sugar alcohols: what is the evidence for caries-preventive and caries-therapeutic effects? Caries Res 2004;38(3):286-93.
  30. Bradshaw DJ, Marsh PD. Effect of sugar alcohols on the composition and metabolism of a mixed culture of oral bacteria grown in a chemostat. Caries Res 1994;28(4):251-6.
  31. Vadeboncoeur C, Bourgeau G, Mayrand D, Trahan L. Control of sugar utilization in the oral bacteria Streptococcus salivarius and Streptococcus sanguis by the phosphoenolpyruvate: glucose phosphotransferase system. Arch Oral Biol 1983;28(2):123-31.
  32. Dowd FJ. Saliva and dental caries. Dent Clin North Am 1999;43(4):579-97.
  33. Janket SJ, Benwait J, Isaac P, Ackerson LK, Meurman JH. Oral and Systemic Effects of Xylitol Consumption. Caries Res 2019:1-11.
  34. Rethman MP, Beltran-Aguilar ED, Billings RJ, et al. Nonfluoride caries-preventive agents: executive summary of evidence-based clinical recommendations. J Am Dent Assoc 2011;142(9):1065-71.
  35. Esposito S, Leonardi A, Lanciotti L, et al. Vitamin D and growth hormone in children: a review of the current scientific knowledge. Journal of Translational Medicine 2019;17(1):87.
  36. Tanaka K, Hitsumoto S, Miyake Y, et al. Higher vitamin D intake during pregnancy is associated with reduced risk of dental caries in young Japanese children. Ann Epidemiol 2015;25(8):620-25.
  37. Schroth RJ, Lavelle C, Tate R, et al. Prenatal vitamin D and dental caries in infants. Pediatrics 2014;133(5):e1277-e84.
  38. Mellanby M, Pattison CL. The Action of Vitamin D in Preventing the Spread and Promoting the Arrest of Caries in Children. Br Med J 1928;2(3545):1079-82.
  39. Schroth RJ, Rabbani R, Loewen G, Moffatt ME. Vitamin D and Dental Caries in Children. J Dent Res 2016;95(2):173-9.
  40. American Academy of Periodontology. AAP Connect: Periodontitis. Accessed October 11, 2021.
  41. Genco RJ, Williams RC. Periodontal disease and overall health: a clinician’s guide. Yardley, Pennsylvania, USA: Professional Audience Communications Inc 2010:254-63.
  42. Varela-Lopez A, Giampieri F, Bullon P, Battino M, Quiles JL. A Systematic Review on the Implication of Minerals in the Onset, Severity and Treatment of Periodontal Disease. Molecules 2016;21(9).
  43. Varela-Lopez A, Giampieri F, Bullon P, Battino M, Quiles JL. Role of Lipids in the Onset, Progression and Treatment of Periodontal Disease. A Systematic Review of Studies in Humans. Int J Mol Sci 2016;17(8).
  44. Ganss C, Lussi A. Diagnosis of erosive tooth wear. Monogr Oral Sci 2006;20:32-43.
  45. Kargul B, Bakkal M. Prevalence, Etiology, Risk Factors, Diagnosis, and Preventive Strategies of Dental Erosion: Literature Review (Part l & Part II). Acta Stomatologica Croatica 2009;43(3).
  46. Salas MM, Nascimento GG, Huysmans MC, Demarco FF. Estimated prevalence of erosive tooth wear in permanent teeth of children and adolescents: An epidemiological systematic review and meta-regression analysis. Journal of dentistry 2015;43(1):42-50.
  47. Buzalaf MAR, Magalhaes AC, Rios D. Prevention of erosive tooth wear: targeting nutritional and patient-related risks factors. Br Dent J 2018;224(5):371-78.
  48. Carvalho TS, Colon P, Ganss C, et al. Consensus Report of the European Federation of Conservative Dentistry: Erosive tooth wear diagnosis and management. Swiss Dent J 2016;126(4):342-6.
  49. Li H, Zou Y, Ding G. Dietary factors associated with dental erosion: a meta-analysis. PLoS One 2012;7(8):e42626.
  50. Salas MM, Nascimento GG, Vargas-Ferreira F, et al. Diet influenced tooth erosion prevalence in children and adolescents: Results of a meta-analysis and meta-regression. J Dent 2015;43(8):865-75.
  51. Johansson AK, Norring C, Unell L, Johansson A. Eating disorders and oral health: a matched case-control study. Eur J Oral Sci 2012;120(1):61-8.
  52. Manarte P, Manso MC, Souza D, Frias-Bulhosa J, Gago S. Dental erosion in alcoholic patients under addiction rehabilitation therapy. Med Oral Patol Oral Cir Bucal 2009;14(8):e376-83.
  53. Kanzow P, Wegehaupt FJ, Attin T, Wiegand A. Etiology and pathogenesis of dental erosion. Quintessence Int 2016;47(4):275-8.
  54. Lazarchik DA, Filler SJ. Dental erosion: predominant oral lesion in gastroesophageal reflux disease. Am J Gastroenterol 2000;95(8 Suppl):S33-8.
  55. Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium. Dietary Reference Intakes for Calcium and Vitamin D. 2, Overview of Calcium. Washington (DC): National Academies Press (US) 2011. Accessed October 11, 2021.
  56. U.S. Department of Health and Human Services and U.S. Department of Agriculture. Dietary Guidelines for Americans 2015–2020. 8th Edition.  December 2015. Accessed October 11, 2021.
  57. Sethi S, Tyagi SK, Anurag RK. Plant-based milk alternatives an emerging segment of functional beverages: a review. J Food Sci Technol 2016;53(9):3408-23.
  58. Thorning TK, Raben A, Tholstrup T, et al. Milk and dairy products: good or bad for human health? An assessment of the totality of scientific evidence. Food Nutr Res 2016;60:32527.
  59. Verduci E, D'Elios S, Cerrato L, et al. Cow's Milk Substitutes for Children: Nutritional Aspects of Milk from Different Mammalian Species, Special Formula and Plant-Based Beverages. Nutrients 2019;11(8): 1739.
  60. Vanga SK, Raghavan V. How well do plant based alternatives fare nutritionally compared to cow's milk? J Food Sci Technol 2018;55(1):10-20.
  61. Lott M CE, Welker Duffy E, Story M, Daniels S.  Healthy beverage consumption in early childhood: recommendations from key national health and nutrition organizations. Technical scientific report. 2019.
  62. Chi AC, Day TA, Neville BW. Oral cavity and oropharyngeal squamous cell carcinoma - an update. CA Cancer J Clin 2015;65(5):401-21.
  63. 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;83(5):1126-34.
  64. Freedman ND, Park Y, Subar AF, et al. Fruit and vegetable intake and head and neck cancer risk in a large United States prospective cohort study. Int J Cancer 2008;122(10):2330-6.
  65. Altenburg A, El-Haj N, Micheli C, et al. The treatment of chronic recurrent oral aphthous ulcers. Dtsch Arztebl Int 2014;111(40):665-73.
  66. Ozler GS. Zinc deficiency in patients with recurrent aphthous stomatitis: a pilot study. J Laryngol Otol 2014;128(6):531-3.
  67. Yıldırımyan N, Özalp Ö, Şatır S, Altay M, Sindel A. Recurrent Aphthous Stomatitis as a Result of Zinc Deficiency. Oral Health Prev Dent 2019:1-4.
  68. Napenas JJ, Brennan MT, Fox PC. Diagnosis and treatment of xerostomia (dry mouth). Odontology 2009;97(2):76-83.

Other Resources
Materials from the Academy of Nutrition and Dietetics on how to eat a healthy diet

U.S. Department of Agriculture’s MyPlate
Topic Updated: October 11, 2021

Prepared by:

Department of Scientific Information, Evidence Synthesis & Translation Research, ADA Science & Research Institute, LLC.


Content on the Oral Health Topics section of is for informational purposes only.  Content is neither intended to nor does it establish a standard of care or the official policy or position of the ADA; and is not a substitute for professional judgment, advice, diagnosis, or treatment.  ADA is not responsible for information on external websites linked to this website.