Introduction
The oral cavity or mouth is often referred to as the ‘gateway to the body’. The mouth is composed of both hard (i.e. teeth) and soft (i.e. gingiva, tongue, oral mucosa) tissues, which process foodstuff in preparation for swallowing and subsequent digestion and enable communication via speech and facial expressions. More than just the absence of disease, oral health is a component of overall health and well-being(Reference Fisher, Berman and Buse1). Both the World Dental Federation’s definition:
includes the ability to speak, smile, smell, taste, touch, chew, swallow and convey a range of emotions through facial expressions with confidence and without pain, discomfort and disease of the craniofacial complex (Reference Glick, Williams and Kleinman2)
and the WHO’s definition:
state of the mouth, teeth and orofacial structures that enables individuals to perform essential functions such as eating, breathing and speaking, and encompasses psychosocial dimensions such as self-confidence, well-being and the ability to socialize and work without pain, discomfort and embarrassment (3)
of oral health acknowledge the fundamental role the oral cavity plays in both physiological and psychosocial health.
The objective of this review paper is to describe dietary risk factors common to both oral and systemic chronic diseases that contribute to multimorbidities. To do so, dietary and nutrient-risk factors for oral diseases, the functional outcomes of oral disease, implications of the impact of oral disease and dysfunction on well-being and oral dysfunction as a risk factor for unhealthy diets and nutrient deficits will be presented.
Oral diseases
Oral diseases are defined as an abnormality or condition that adversely impacts the physiological and psychosocial function of the oral cavity and/or causes oral pain. Oral diseases can impact the integrity and functions of the soft and hard tissues in and surrounding the mouth. Such diseases can affect oral motor and sensory functions including biting, chewing, swallowing and tasting foods as well as facial expressions and speaking. White et al. analysed data from the Adult Dental Health Survey conducted in 2009 and reported that 16 % of British adults experienced at least one oral impact (i.e. functional limitation, psychosocial discomfort, oral pain) frequently or very frequently during the previous 12 months with difficulty eating, avoiding smiling and difficulty cleaning teeth reported most frequently(Reference White, Tsakos and Pitts4). The four most common diet-related oral diseases are dental caries, periodontal disease, tooth wear and oral cancer.
Dental caries
Dental caries is a chronic, noncommunicable disease process during which oral bacteria ferment carbohydrates to produce acid at the tooth surface. The acid then dissolves the tooth’s enamel and/or dentine, leading to a white spot lesion which can progress to a cavitated lesion. Caries is a diet-dependent disease; without fermentable carbohydrates, caries does not occur(Reference Sheiham and James5). While sugars, particularly free sugars, are the primary substrate for oral bacteria, starches are also fermentable and, thereby, available as a substrate for oral bacteria. Modified starches (i.e. starches that have been altered, resulting in short glucose chains for their functional or sensory properties) are more cariogenic than the original starches(Reference Hancock, Zinn and Schofield6,Reference Al-Khatib, Duggal and Toumba7) . Modified starches are a common ingredient in ultra-processed (UP) snack foods (i.e. chips, crackers, energy bars). Bakery foods composed of starches and sugars and/or foods that stick to the teeth (i.e. taffy) are retained in the mouth, which increases their cariogenicity.
Caries risk is also impacted by food behaviours; caries risk is increased with longer exposure to fermentable carbohydrates. Exposure time can be defined as a function of the frequency and duration of an eating or drinking event. For example, a 12 oz sugar-sweetened beverage (SSB) might be consumed in 20 min or over 4 h. While the quantity and frequency of SSB consumed are the same, the exposure times are very different. Both holding foods and swishing beverages containing free sugars in the mouth increase contact with the sugars and extend the exposure time. Reduced oral motor skills leading to increased food pocketing and/or reduced food clearance can also increase exposure time. Adequate saliva is essential for clearing food debris from the mouth; hyposalivation and xerostomia (i.e. dry mouth) are associated with increased caries risk(Reference Flink, Tegelberg and Arnetz8).
Investigations of caries epidemiology categorise the disease using terms such as caries experience, active decay or untreated caries. Caries experience includes active lesions, teeth that have been restored and teeth lost to the decay process. Active decay refers to lesions with active disease, and untreated caries refers to carious lesions with either active or arrested disease. The US Surgeon General’s 2000 report identified caries as the number one chronic disease of children in the USA(9), the 2015 Global Burden of Disease Study identified caries as the most prevalent condition in the world(10), and the National Institutes of Health’s 2021 Oral Health in America report also identified caries as the most prevalent chronic disease in children and adults(11). Decay among children in the UK is similarly high. According to the Children’s Dental Health Survey of 2013, 49 % of 5-year-olds had clinical decay experience in their primary teeth, and 34 % of 8-year-olds, 57 % of 12-year-olds and 63 % of 15-year-olds had clinical decay experience in their permanent teeth(Reference Pitts, Chadwick and Anderson12). White et al. reported that approximately 30 % of adults living in England had active caries extending into their dentine in 2009(Reference White, Tsakos and Pitts4). Douglas reported that upon clinic examination, 90 % of adults attending National Health Service clinics in 2018 had at least one filling with 27 % having untreated caries extending into the dentine(Reference Douglas, Jones and Dyer13).
Disparities in caries experience exist. Adults who regularly attend a dentist have lower caries experience, fewer teeth with active decay, fewer missing teeth and fewer filled or treated teeth than adults without regular dental attendance(Reference Aldossary, Harrison and Bernabé14). Individuals with higher social deprivation and limited access to care are at the highest risk of caries which reinforces the role of structural and upstream factors in oral health(Reference Rodriguez, Thakkar-Samtani and Heaton15,Reference de Abreu, Cruz and Borges-Oliveira16) .
Periodontal disease
Periodontitis is a chronic, noncommunicable, infectious disease resulting from the interaction of pathogenic bacteria and the host immune-inflammatory response. This results in an inflammatory state at the gingival margin leading to a loss of supporting alveolar bone and potential tooth loss. Periodontal disease is a nutrient-related disease; neither dietary nor nutrient factors cause periodontal disease, but they impact oral and systemic conditions favouring the disease process. The reverse is also true; the presence of cardiometabolic diseases including obesity, diabetes and CVD which are also inflammatory, nutrient-related diseases is associated with a greater incidence of periodontal disease. While there is no evidence of causality, prior research has demonstrated associations among these oral and systemic inflammatory disease processes(Reference Chaffee and Seston17–Reference Sanz, Ceriello and Buysschaert19). Malnutrition is known to disrupt the oral microbiome, impair tissue health and lead to a compromised immune system(Reference Enwonwu, Phillips and Falkler20–Reference Dommisch, Kuzmanova and Jönsson22). Vitamin C deficiencies are associated with increased gingival bleeding and periodontal disease(Reference Hujoel and Lingström23,Reference Chapple, Milward and Dietrich24) . Deficiencies of micronutrients including vitamins C, D and B12 have been associated with oral infections and periodontal disease(Reference Dommisch, Kuzmanova and Jönsson22,Reference Hujoel and Lingström23,Reference Chapple, Bouchard and Cagetti25) . Finally, low-quality diets that are nutrient poor have been associated with periodontal disease in both adolescents and adults(Reference Salazar, Laniado and Mossavar-Rahmani26,Reference Jauhiainen, Ylöstalo and Knuuttila27) .
The prevalence of periodontal disease in the UK was estimated at 37 % with 8 % of adults having severe disease in 2009(28). The presence of periodontal disease defined by bleeding, calculus or periodontal pockets of 4+ mm generally increased with age as 72 % of 16–24-year-olds, 80 % of 25–44-year-olds, 84 % of 45–54-year-olds and 90 % of 55+-year-olds reported some level of disease(Reference White, Tsakos and Pitts4). Disparities in periodontal disease exist with individuals of lower socioeconomic status, lower educational attainment and higher tobacco consumption at the highest risk(Reference de Abreu, Cruz and Borges-Oliveira16,Reference Tomar29) .
Tooth wear
Three types of tooth wear are commonly recognised. Abrasion is a type of mechanical wear associated with repeated contact with non-tooth materials and is often observed in individuals with very high fibre diets, including high intakes of unprocessed whole grains, fruits and vegetables. Abfraction is another type of mechanical wear associated with bruxism (i.e. grinding one’s teeth) and/or uneven biting forces. Erosion is a chemical process during which surface enamel and/or dentine are lost with repeated exposure to either internal or external acids. Internal acids originate in the stomach with exposure due to gastro-oesophageal reflux, rumination or repeated vomiting as seen with eating disorders. Some ethnic and/or regional diets are high in acidic foods and beverages. Furthermore, behaviours such as pocketing or holding acidic foods (i.e. citrus products) or swishing acidic beverages prolong exposure to dietary acids and increase erosion risk.
The prevalence of any tooth wear was 77 % in British adults in 2009, with 15 % having moderate involvement(Reference White, Tsakos and Pitts4). The prevalence of erosion in the UK is higher than observed in other developed countries. In deciduous teeth, the prevalence ranged from 30 to 50 % and in permanent teeth from 20 to 45 %(30). In adults, the prevalence of erosion in the UK was high with 76 % of adults having any erosion in 2008, and 15 % of adults having moderate erosion defined as dentine involvement in 2009(30). Reported associations between tooth wear and the social determinants of health are limited; however, an environment consistent with social deprivation might lend to an increased association. For example, individuals with social deprivation tend to have less access to health care, lower diet quality and higher illicit drug use and favour the purchase of acidic beverages (cheaper than bottled water), all of which might increase the risk of tooth wear and/or erosion.
Oropharyngeal cancer
Oropharyngeal cancers (OPCs) represent cancers of the oral tissue; over 90 % of OPCs are squamous cell carcinomas(Reference Tan, Wang and Xu31). Treatment typically includes surgery, chemotherapy and/or radiation therapy, often concurrent, which can impact oral function, including mandibular opening, biting, chewing, food movement and swallowing. Surgical interventions can impact the structure, integrity and subsequent function of the mouth depending on the location and extent of surgery. For example, a palatal resection and subsequent placement of a palatal obturator will alter diet and speech patterns. In addition, sensory losses might impact taste and smell. The duration of these changes ranges from short term to lifelong depending on the cancer and nature and extent of treatment(Reference Ganzer, Touger-Decker and Parrot32). Dietary risk factors for oropharyngeal cancer include excessive alcohol exposure, high intakes of processed meats and low intakes of fruits and vegetables(Reference Rodríguez-Molinero, Miguelíñez-Medrán and Puente-Gutiérrez33).
Both the incidence and mortality of oropharyngeal cancer have increased in the UK during the past 20 years. The overall incidence has increased by almost 50 % with males and older adults having greater increases than females and younger adults, respectively(34). According to Public Health England’s Oral Cancer report, individuals in the most deprived income category or belonging to ‘other ethnic groups’ (i.e. not Black, White, Asian or Mixed) were at highest risk of oral cancer(34). Beyond dietary risk factors, smoking and sexually transmitted human papillomavirus are strong risk factors for oral cancer; these behaviours tend to be higher in individuals residing in disadvantaged communities(Reference de Abreu, Cruz and Borges-Oliveira16,Reference Allam and Windsor35) . Environmental pollution and occupational exposures also increase the risk of oral cancer and are thought to partially account for observed sex differences.
Outcome of oral diseases
Well-being
The presence of oral disease can lead to oral dysfunction with subsequent implications for overall quality of life and well-being. Tooth or other hard or soft tissue loss can impact one’s ability to communicate by impairing articulation and facial expressions. Pain and/or embarrassment associated with diseased or missing teeth or soft tissue can also impair eating, socialization and communication, contribute to sleep difficulties and increase the risk of mental health concerns(Reference Peres, Macpherson and Weyant36,Reference Zelig, Jones and Touger-Decker37) . Oral disease and/or dysfunction can contribute to alterations in diet intake and quality, lower self-esteem, reduced employment opportunities and less social engagement particularly in public-facing roles. Furthermore, oral disease and dysfunction have been associated with other chronic diseases, including impaired cognition, obesity and obesity-related diseases, type 2 diabetes and pregnancy gingivitis(Reference Wu, Luo and Tan38–Reference Dörfer, Benz and Aida40). Individuals with the highest social deprivation are at greatest risk of untreated oral disease and dysfunction(Reference de Abreu, Cruz and Borges-Oliveira16,Reference Peres, Macpherson and Weyant36) .
Oral function
Oral disease and dysfunction can alter food choices. Missing teeth reduce one’s ability to bite and/or chew food; opposing pairs of molar teeth or stable, well-fitting dentures are necessary to chew food. Dentures alone significantly reduce biting and chewing function compared to complete dentition(Reference Moynihan and Varghese41). Missing or damaged soft tissues (i.e. tongue, oral mucosa) reduce one’s ability to retain and move food within the mouth, form a bolus and swallow. Oral pain associated with soft tissue disorders, including burning mouth syndrome, and hard tissues disorders, such as temporal mandibular joint disorders, can also interfere with eating. Oral dysfunction and/or pain favour an increased reliance on texture-modified foods and beverages, including UP foods of low nutrient and higher energy density.
Increased reliance on foods and beverages of lower nutrient density and quality contributes to lower-quality diets inconsistent with Eatwell Guide recommendations(42). Food choices and nutrient profiles inconsistent with Eatwell Guide recommendations increase the risk of both oral and systemic chronic diseases (Fig. 1). Specifically, dietary patterns characterised by foods high in free sugars such as SSBs are associated with an increased risk of dental caries, obesity and cardiometabolic disease (including type 2 diabetes)(Reference Moynihan and Kelly43–Reference Vos, Kaar and Welsh46). Dietary patterns characterised by foods high in animal and saturated fats are associated with an increased risk of obesity, cardiometabolic disease and cancer(Reference Peterson, Flock and Richter47–Reference Ubago-Guisado, Rodríguez-Barranco and Ching-López49). Low intakes of whole grains and fresh fruits and vegetables are associated with periodontal disease, obesity, cardiometabolic disease and cancer(Reference Chapple, Milward and Dietrich24,Reference Chapple, Bouchard and Cagetti25,Reference Peterson, Flock and Richter47,Reference Ubago-Guisado, Rodríguez-Barranco and Ching-López49,Reference Papadimitriou, Markozannes and Kallenopoulou50) . Diets low in dairy or dairy alternatives are associated with periodontal disease and osteoporosis(Reference Adegboye, Christensen and Holm-Pedersen51–Reference Weaver, Gordon and Janz54). Finally, nutrient-poor diets can lead to malnutrition.
Fig. 1. Non-compliance with Eatwell guidance.
Poor compliance with Eatwell Guide recommendations is associated with an increased risk of both oral and systemic diseases and increases the risk of multimorbidity throughout the lifespan. This begs the question – with respect to oral health and multimorbidity, is diet the chicken or the egg? (Fig. 2) A less healthful diet characterised by high intakes of added sugars and UP foods increases the risk of both oral and systemic chronic diseases, while oral disease contributes to oral dysfunction which further increases the risk of an unhealthy diet.
Fig. 2. Is diet the chicken or the egg?
Iowa Fluoride Study
The Iowa Fluoride Study (IFS) enables the evaluation of associations among dietary intakes, dental caries and growth measures in a birth cohort throughout childhood and adolescence(Reference Levy, Warren and Davis55,Reference Levy, Warren and Broffitt56) . The IFS was initially designed to evaluate the sources of fluoride intake and risk of dental fluorosis in a cohort recruited between 1992 and 1995 from east-central Iowa in the USA and followed longitudinally through 2019. IFS objectives evolved and included evaluating associations among dietary intakes, caries and growth measures.
Mothers of infants were recruited at birth for their child’s participation and completed extensive questionnaires querying fluoride intakes and oral hygiene behaviours, beverage frequency questionnaires and 3-d diet records at 3–6-month intervals through 8 years of age. Beginning with age 9, dietary data were collected using FFQs. Caries were identified at clinical exams at 5, 9, 13 and 17 years of age, and anthropometric outcomes were measured at clinical exams at 5, 9, 11, 13, 15 and 17 years of age.
During the 1990s, the scientific literature examining associations between soda-pop beverages and caries was inconclusive with few studies supporting an association between SSB and caries. Using IFS data, Marshall et al. explored associations among ages 1–5 years of individual sugared beverages intakes, nutrient intakes and overall diet quality and caries experience at 5 years of age(Reference Marshall, Levy and Broffitt57). They reported that 1–5-year intake of sugared soda-pop and reconstituted powdered beverages increased caries risk. Additional analyses of these data explored the timing (i.e. meal, snack) of 1–5-year food and beverage intakes and caries experience at 5 years of age(Reference Marshall, Broffitt and Eichenberger-Gilmore58). Higher frequencies of snack and total eating events at ages 1–5 years and higher intakes of SSB beginning at age 2 years were associated with increased caries experience. Both studies reported that consumption of 100 % juice was not associated with caries experience in this population; these results are consistent with other studies(Reference Kolker, Yuan and Burt59,Reference Vargas, Dye and Kolasny60) . Investigation of associations among beverage intakes and diet quality in this cohort found that milk intakes were inversely associated with SSB intakes at 1–5 years(Reference Marshall, Eichenberger-Gilmore and Broffitt61). Furthermore, higher diet quality was associated with lower 100 % juice and SSB intakes.
Hypotheses supported by cross-sectional studies in the oral health literature suggested that caries was associated with an increased risk of obesity(Reference Reifsnider, Mobley and Mendez62–Reference Willerhausen, Haas and Krummenauer64). IFS data were used to determine if caries and obesity were associated at age 5 years and, if so, to explore the role of diet and socioeconomic factors as additional risk factors(Reference Marshall, Eichenberger-Gilmore and Broffitt65). Children with caries experience had lower family incomes, less educated parents, heavier mothers and higher 1–5-year soda-pop intakes than children without caries at 5 years of age. Children who were overweight had heavier parents and less educated fathers than children of normal weight or were at risk of being overweight. Mother’s education replaced soda-pop intake in the final model supporting an association between being at risk of overweight and caries experience suggesting that social determinants of health are associated with both diseases.
Associations between childhood and adolescent beverage intakes, oral hygiene behaviours and age 17 caries experience were also explored using IFS data(Reference Marshall, Curtis and Cavanaugh66). Multivariable models were developed adjusting for other beverage intakes, fluoride intake, toothbrushing frequency, sex and socioeconomic status. In the final model, each additional 8 oz of SSB increased the new caries rate by 42 %, while each additional 8 oz of 100 % juice or water/sugar-free beverage decreased new caries rates by 53 and 39 %, respectively, and each additional toothbrushing event decreased new caries rates by 43 %.
Finally, associations between childhood and adolescent beverage intakes and growth measures at age 17 were explored using IFS data. In a linear mixed model adjusted for diet quality, energy intake and socioeconomic status, each additional 8 oz of milk consumed daily throughout childhood and adolescence was associated with a 0·39 cm increase in height(Reference Marshall, Curtis and Cavanaugh67). Linear mixed models adjusted for energy intake, diet quality and socioeconomic status were also used to investigate associations between beverage intakes and BMI z-scores throughout childhood and adolescence(Reference Marshall, Curtis and Cavanaugh68). Each additional 8 oz of SSB consumed per day increased the BMI z-score 0·050 units; 100 % juice and milk consumption were not associated with BMI z-scores.
The IFS results support the hypothesis that SSB intakes increase the risk of both caries and obesity during childhood and adolescence and that SSB intakes are associated with lower diet quality and intakes of the nutrient-dense beverage milk. In addition, the association observed between milk intakes and height is of concern and might reflect unknown social determinants of health impacting one’s growth potential.
Chronological diet-related chronic disease framework
Chronic diseases that increase the risk of multimorbidity throughout the lifespan develop over time, with signs and symptoms observed during later stages of disease processes. Dietary risk factors for chronic diseases contributing to multimorbidity overlap and precede the onset of visual signs and symptoms of disease. Therefore, it is reasonable to consider the development of diet-related chronic diseases over the lifespan (Fig. 3). Dental caries can present within months of tooth eruption and/or the transition to a diet high in free sugars and are likely the first chronic disease to be observed. Obesity is usually the first systemic chronic disease to manifest and may present during childhood or adolescence. Cardiometabolic diseases (including type 2 diabetes) and periodontal disease typically present during late adolescence or adulthood. Finally, diet-related cancers and osteoporosis typically present during adulthood, but a lifetime of poor dietary habits contributes to disease risk.
Fig. 3. Timeline of diet-related multimorbidities.
Considering the lifetime presentation of diet-related oral and systemic chronic diseases, we must consider the question – ‘are early childhood caries (ECC) our canary in the coal mine?’ That is, are ECC the early presentation of food choices and dietary behaviours that increase the risk of both oral and systemic diseases throughout the lifespan? ECC are defined as the presence of a carious lesion in the primary tooth of a child under 5 years of age(69); the primary diet-related risk factor for ECC is frequent exposure to free sugars, including high intakes of SSBs. Furthermore, a diet high in free sugars is usually characterised by energy-dense, nutrient-poor, UP foods(Reference Rauber, da Costa Louzada and Steele70). Unchecked, the dietary habits contributing to ECC likely continue throughout childhood and adolescence. This same diet increases the risk of obesity, cardiometabolic diseases, periodontal disease and cancers. Thus, ECC might be an early indicator of diet-related chronic disease risk.
If we accept the hypothesis that ECC are a marker of diet-related chronic disease risk, then diagnosis of ECC presents an opportunity to disrupt the disease process. Disrupting the disease process through dietary intervention is a challenge as the child lives within a family and a community. Food choices and dietary behaviours are typically similar within families and the community within which one lives often determines available food choices. However, promoting healthier dietary behaviours for the family and community might have a halo effect by reducing existing chronic disease both within the family and community. To successfully disrupt the disease process, a healthcare team composed of nutritionists, oral healthcare professionals, medical providers, social workers and community workers will be necessary to address the food choices and dietary behaviours at the individual, family and community levels(Reference Fisher, Berman and Buse1). Consistent dietary counselling and messaging by the healthcare team and community to promote and enable healthier dietary behaviours have the potential to reduce the risk of oral diseases, obesity, cardiometabolic diseases and cancers. Disparities exist in the presentation of ECC as children living in poverty with limited access to care are at the highest risk. To ensure success, efforts to improve dietary behaviours and reduce ECC and other chronic diseases contributing to multimorbidity will require structural solutions addressing the social determinants of health.
Summary
Dental caries, periodontal disease, tooth wear, edentulism and oral cancer are diet- and nutrient-related chronic diseases. Oral dysfunction resulting from oral disease increases the likelihood of energy-dense, nutrient-poor diets which subsequently increase the risk of systemic chronic diseases contributing to multimorbidity. ECC are an early manifestation of unhealthy diets that increase the risk of chronic diseases throughout the lifespan. As such, ECC present an opportunity for early dietary intervention to disrupt the trajectory of the disease process and prevent diet-related chronic disease.
Financial support
This research received no specific grant from any funding agency, commercial or not-for-profit sectors.
Author contributions
TAM conceptualised the presentation organisation, drafted the initial manuscript and edited and approved the final manuscript. RTD provided contextual feedback for the presentation and manuscript, edited the manuscript and approved the final manuscript.
Competing interests
The authors declare none.
