#54121: Nutrition and Oral Health

Fat-soluble vitamins have several important roles in the maintenance of optimal oral health. These vitamins must bind to ingested lipids for absorption from the digestive tract, so any disease or medication that interferes with fat absorption can decrease the bioavailability of these nutrients and undermine a patient's systemic and oral health. Dental clinicians should take a holistic approach that includes adequate nutrition as an important component in the maintenance of their patient's oral health.

Vitamin A

Vitamin A is required for the proper functioning of the visual system and for the development and maintenance of epithelial cellular integrity; it also contributes to the proper function of the immune and reproductive systems [11]. Systemic deficiencies in vitamin A can cause retinal disorders such as night blindness and hyperkeratosis [12]. Deficiencies can also influence the development of teeth via impact on the cells that form the enamel (ameloblasts) and the dentin (odontoblasts). Sustained deficiency of vitamin A prior to the eruption of teeth can lead to enamel hypoplasia, defects in the formation of the enamel matrix, and incomplete calcification of the enamel and dentin. Odontoblasts can depart from their parallel linear arrangement and cause the degeneration and atrophy of ameloblasts. The regular spacing of teeth and the stimulation of osteoblasts (progenitor bone-forming cells) also depend on adequate intake of vitamin A [11].

Vitamin A deficiency beginning in utero and continuing to the early teenage years can negatively impact the development of enamel and dentin. Calcification of the deciduous teeth occurs first on the maxillary and mandibular central incisors at about 14 weeks' gestation, while the initial calcification of the deciduous molars ranges from 15 to 23 weeks' gestation. The initial calcification of the permanent maxillary and mandibular first molars occurs about the time of birth, while those of the maxillary and mandibular third molars ("wisdom teeth") can range from 7 to 10 years [13]. As such, maternal vitamin A deficiency during pregnancy has the potential to adversely affect the formation of offsprings' enamel and dentin. Childhood deficiencies may likewise result in irregularities in permanent teeth; a vitamin A deficiency that develops in early adolescence or later would have minimal or no impact or oral health.

Abnormalities in the formation of enamel and dentin can result in several problems. The enamel of deciduous teeth is thinner than that of the corresponding permanent teeth, and surface deformities in the enamel make these teeth more difficult to clean and more prone to decay. The normally smooth surface of enamel can become pitted and mottled and develop a "chalky" appearance. Surface irregularities promote the retention of plaque and increase the potential for the development of dental caries.

Restoring the carious lesions of teeth with abnormal formation of enamel and dentin can be a challenge, as can minimizing the development of recurrent carious lesions. Conventional composite (resin-based) restorations rely on a strong bond with the enamel for their retention. Enamel that is abnormally formed will have compromised bond strength with composite restorations, and these teeth are more prone to debonding, leakage, and recurrent caries. In these cases, it may be necessary to extend cavity preparations beyond the usual conservative boundaries in order to locate and include enamel that is properly formed [14]. This additional involvement of tooth structure may require the use of more involved, longer-term restorations, such as stainless-steel crowns on posterior deciduous teeth, polycarbonate crowns on anterior deciduous teeth, and ceramic or metallic (e.g., gold, semi-precious metal) restorations on permanent teeth. Given the potential difficulty in restoring carious deciduous teeth with abnormally formed enamel, clinicians may consider referral to a pedodontist. Adolescents and adults with enamel defects may require more frequent recall appointments given the heightened potential for carious lesions. Any patient with these issues should be provided with specific oral hygiene instructions regarding the use of fluoride-containing mouth rinses or gels placed in custom trays.

Excesses of vitamin A deficiency during pregnancy have been linked to facial deformities and other birth defects [10]. Pregnant women should consult with their obstetrician to determine the safest vitamin intake levels for her and her fetus.

Vitamin D

Vitamin D is unique among the vitamins in that it can be synthesized by the human body in reasonable quantities provided that there is adequate access to sunlight and that the skin, liver, and kidneys are functioning. It also has characteristics of a hormone, as its physiologic activity requires interaction with a receptor [1]. In humans, the two most important forms are vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol).

Normally, vitamin D is primarily stimulated by ultraviolet radiation, or sunlight, on the skin and then by hydroxylation in the liver and kidney. Vitamin D then acts to increase intestinal absorption of calcium and promote bone formation. Deficiency of vitamin D in children causes rickets, and adult deficiency results in osteomalacia [2]. Rickets is characterized by deficient mineralization at the growth plate, while osteomalacia is the result of impaired mineralization of the bone matrix (osteoid) [15]. Lateral bowing of the tibia and the femur is a common presentation of both conditions when they occur in younger patients. In older patients, osteomalacia increases the risk of fracture. Because it is not practical for many individuals to get adequate levels of vitamin D from exposure to sunlight, increasing vitamin D levels through diet and supplementation should be encouraged [2]. However, few foods naturally contain vitamin D. The flesh of fatty fish (such as trout, salmon, tuna, and mackerel) and fish liver oils are among the best sources. Beef liver, cheese, and egg yolks have small amounts of vitamin D, primarily in the form of vitamin D3 and its metabolite 25(OH)D3. In addition, in the United States, almost all of the milk supply is fortified with about 3 mcg/cup (120 IU), usually in the form of vitamin D3 [16].

Osteomalacia is a special concern for dental patients who require oral surgery. The pressure exerted during the elevation and forcep delivery of a tooth may exceed the limits of weakened bone, with an increased potential for fracture. Before any dental care is provided, clinicians should assess their ability to provide the care with an atraumatic technique that minimizes pressure on the supporting alveolar bone. Referral to an oral surgeon should be considered for patients with osteomalacia.

Smaller-than-normal molars and delayed eruption of teeth can also be manifestations of vitamin D deficiency [11]. Hypoplasia of the enamel can also develop in individuals with vitamin D deficiency and can be more diffuse than hypoplasia that develops from vitamin A deficiency [17]. The individual's age and the duration of the deficiency determine the teeth involved. Problems with increased retention of plaque, risk of caries, and the challenges of restoring teeth with enamel abnormalities are similar to those discussed related to vitamin A deficiency.

Vitamin E

Vitamin E is not a single molecule but a group of eight molecules that possess similar activity and that are divided into two major classes: the tocopherols and the tocotrienols. The tocopherols are more abundant in nature, with alpha-tocopherol being the most prevalent form and the focus of this section [1].

As a key extracellular antioxidant, vitamin E stabilizes the cell membrane by terminating the free radical reaction that precipitates cellular damage [18]. Free radicals have unpaired electrons available to bond with cellular chemical constituents, making them highly reactive. Most free radical activity occurs in the mitochondria, the cellular organelle that produces ATP [2]. Protracted free radical damage and the subsequent decreased energy production can impair cellular reproduction and renewal, especially in cells of the oral epithelium, which have a rapid turnover and the need for sustained replenishment.

Vitamin E deficiency is rare, because it is widely distributed in foods, including vegetable oils, nuts, seeds, green leafy vegetables, and fortified breakfast cereals. However, muscular and neurologic problems can develop in patients with inadequate levels of vitamin E [11].

No lesions are considered pathognomonic of vitamin E deficiency. However, high doses of vitamin E may increase the risk of bleeding [19]. This is a concern for dental patients for whom invasive treatment, such as oral or periodontal surgery, has been planned. The combination of excessive doses of vitamin E with antiplatelet medications (e.g., aspirin, clopidogrel) or anticoagulant medications (e.g., warfarin) can decrease the ability to obtain hemostasis during and after invasive dental procedures. In patients taking warfarin, hemorrhage may be treated with vitamin K injection, but newer anticoagulant medications (e.g., dabigatran, rivaroxaban, apixaban) do not have a reversal agent [20]. It is incumbent that vitamins and nutritional supplements are included with the patient's medical history, as patients can be unaware of their potential adverse drug interactions.

Vitamin K

Vitamin K exists in three main forms. Phylloquinone occurs naturally in green plants; menaquinone is produced by bacteria in the intestine; and menadione is the synthetic version used in animal feed [21]. In humans, the most significant role of vitamin K is its role in coagulation. It serves as a catalyst for the synthesis of blood-clotting factors, especially in the maintenance of clotting factor II (prothrombin). The conversion of prothrombin to thrombin transforms the soluble clotting factor I (fibrinogen) to the insoluble polymer fibrin, which forms the cross-linked fibrin mesh at the foundation of a blood clot. Deficiencies in vitamin K are rare, given its availability in food and endogenous production by intestinal bacteria. However, deficiency can occur if intestinal absorption is impaired due chronic gastrointestinal disease and/or resection or long-term use of broad-spectrum antibiotics.

Vitamin K deficiency can lead to issues with occult bleeding and hemorrhage during and after invasive dental procedures. Conversely, excessive vitamin K intake can impair the action of warfarin [22]. This can increase risk for an adverse cardiovascular or cerebrovascular event among patients who require anticoagulation therapy.

Vitamin K is also important for the formation of the proteins osteocalcin and periostin, which are integral to bone metabolism [12]. Low bone density can result in the development of osteoporosis, which is associated with increased risk of fracture. Decreased bone density of the maxillary or mandibular arch predisposes patients to fracture during extractions or from minimal force. Decreased bone density can also preclude the placement of implants.

Water-soluble vitamins are absorbed with water from the digestive tract, with an insignificant fraction stored in the lean tissue of the body. Ingested amounts that are not utilized by the body within approximately one hour of absorption are excreted in the urine [2]. Vitamins B and C are water-soluble, and each has an important role in oral and systemic health.

Vitamin B1 (Thiamine)

Thiamine plays a critical role in energy metabolism necessary for the growth, development, and function of cells [23]. As discussed, the rapid turnover of cells of the oral mucosa and epithelium relies on a consistent source of energy, and thiamine is an essential component of these reactions. Therefore, oral manifestations of a thiamine deficiency include prolonged healing and the diminished renewal of the surface layer of the oral mucosa and epithelium, which can result in tissue sloughing and surface ulcerations.

Perhaps the most serious systemic complication of a thiamine deficiency is beriberi, a disease characterized by peripheral neuropathy and wasting. It can cause irreversible neuromuscular disorders as well as defects in memory. Some cases of beriberi can progress to congestive heart failure and death [24]. A more common and serious manifestation of a thiamine deficiency is Wernicke-Korsakoff syndrome, which is up to 10 times more common in those with chronic alcoholism but can also affect patients with gastrointestinal disorders (e.g., hyperemesis gravidarum), hematologic malignancies, substance use disorders, or HIV/AIDS [25]. The syndrome consists of two phases. The first phase is acute and life-threatening and features a characteristic peripheral neuropathy. Approximately 20% of patients will die without treatment; those who survive develop Korsakoff psychosis [26]. Korsakoff psychosis features severe short-term memory loss, disorientation, and confusion between real and imagined memories (confabulation) [24].

The oral signs of a thiamine deficiency are not pathognomonic nor are they as severe as the systemic manifestations. However, dental professionals who treat patients with thiamine deficiency should be aware of potential drug-drug interactions and may need medical clearance prior to the initiation of dental treatment.

Vitamin B2 (Riboflavin)

Riboflavin is a component of coenzymes used in multiple metabolic pathways, including the regulation of cellular metabolism and the metabolism of carbohydrates, amino acids, and fats [27,28]. Riboflavin deficiency is rare in the United States, as it is fortified in many grains and cereals. Other possible food sources include eggs, organ meats, lean meats, milk, and green vegetables.

Riboflavin deficiency can result in both oral and systemic effects. Oral manifestations include angular cheilitis, an erythematous (red) tongue, and a burning/tingling oral sensation [29]. Angular cheilitis is a mixed fungal and bacterial infection that features bilateral involvement of the commissures of the lips. When riboflavin deficiency is the etiologic factor, angular cheilitis resolves when adequate intake is restored. Systemic manifestations of riboflavin deficiency include weakness, dermatitis, anemia, fatigue, personality changes, and cognitive dysfunction [30]. Developmental defects caused by riboflavin deficiency during pregnancy can have systemic and oral/maxillofacial manifestations in offspring, including cleft lip and palate abnormalities, congenital heart defects, and impaired growth [27].

Vitamin B3 (Niacin)

Niacin (also known as nicotinic acid) is a critical coenzyme in ATP production. Additionally, niacin has a role in oxidative reactions, DNA metabolism and repair, cellular signaling, and antioxidant protection [30].

Although uncommon in developed countries, when present (usually as a result of food scarcity) niacin deficiency may result in pellagra. Pellagra features a triad of clinical manifestations: a localized pigmented rash (dermatitis), gastroenteritis (diarrhea), and neurologic deficits (dementia) [31]. Dietary supplementation with niacin will reverse the condition. Other systemic manifestations of niacin deficiency include alopecia, muscle weakness, peripheral neuropathy, altered gait, depression, anxiety, and psychiatric symptoms [32].

Oral manifestations of niacin deficiency can involve several structures. Loss of the filiform and fungiform papilla of the tongue changes its appearance to be smooth and shiny. The oral mucosa can become erythematous, and the gingival tissues may resemble that of ulcerative gingivitis [11]. Pain can emanate from any of the affected tissues and can interfere with the patient's ability to eat, speak, and swallow. The ability to maintain oral hygiene may also be compromised. Fortunately, niacin supplementation will reverse these effects. Liquid nutritional supplementation, topical and/or systemic analgesics, and a bland diet may be required until the oral tissues are restored to health. The pain associated with these manifestations usually precludes elective dental treatment. Patients who present with oral and/or systemic signs and symptoms should be referred to their physician for further evaluation.

Vitamin B5 (Pantothenic Acid)

Pantothenic acid is a constituent of coenzyme A, which plays a significant role in oxidative metabolism and the provision of energy for the body. Coenzyme A also is involved in the synthesis of cholesterol, phospholipids, amino and fatty acids, and several neurotransmitters and steroid hormones [32].

Vitamin B5 deficiency is rare, as it is available in meat and poultry, fish, mushrooms, and whole grains and is synthesized by bacteria in the gastrointestinal tract. When a vitamin B5 deficiency does occur, systemic manifestations include peripheral neuropathy, dermatitis, diarrhea, encephalopathy, behavioral changes, and demyelination of axon (nerve) sheaths [30]. There are no oral lesions or developmental anomalies that are uniquely pathognomonic of vitamin B5 deficiency. However, coenzyme A cannot function without pantothenic acid, so a deficiency decreases cellular renewal of the oral epithelium and the oral mucosa. Prolonged healing of oral surgery sites, tissue sloughing, and oral ulcerations could develop with a protracted deficiency of this vitamin.

Vitamin B6 (Pyridoxine)

Pyridoxine is the precursor to pyridoxal, which is involved in the metabolism of proteins, carbohydrates, and fats. Pyridoxal also facilitates the release of glycogen stored in the muscles and liver and is a component in the synthesis of neurotransmitters such as dopamine, serotonin, and gamma aminobutyric acid (GABA) [19]. Deficiency of vitamin B6 alone is uncommon and usually occurs in conjunction with a deficiency of other B-complex vitamins. When such a deficiency occurs, systemic manifestations include anemia, fatigue, muscular twitching, irritability, depression, dementia, and convulsions [32].

Oral manifestations of a vitamin B6 deficiency typically involve the tongue. An initial sensation of burning of the tongue is followed by a reddening and hypertrophy of the filiform papilla. Pain and edema of the tongue may also develop. Angular cheilosis can also occur [11]. Diagnosis of a vitamin B6 deficiency cannot be made by based on the presence of systemic and/or oral manifestations alone. Dental patients with any such presentation should be referred for further evaluation.

Vitamin B7 (Biotin)

Biotin is essential for the metabolism of carbohydrates, fatty acids, and the amino acid leucine [1]. Deficiency is rare, as this nutrient is available in multiple food sources (e.g., organ meats, eggs, fish, meat, seeds, nuts, sweet potatoes) and generally occurs as a deficiency with the other B-complex vitamins. Oral and systemic manifestations can occur but are not diagnostic. Systemic manifestations of a biotin deficiency can include peripheral neuropathy, pallor, fatigue, elevated cholesterol, eczematous rash, depression, lethargy, hallucinations, and seizures [30]. Oral manifestations include pallor of the tongue and a segmented atrophy of the lingual papilla that resembles benign migratory glossitis, also known as geographic tongue. This pattern can be limited to the lateral borders of the tongue or can be generalized to include the entire dorsum [33]. The exact cause of benign migratory glossitis has not been identified, and this temporary pathologic state is usually self-resolving. In patients with biotin deficiency, loss of the lingual papilla will resolve when adequate biotin levels are achieved.

Vitamin B9 (Folic Acid or Folate)

Vitamin B9 is known as both folic acid (the synthetic form that is found in dietary supplements) and folate (the naturally occurring form found in foods). Vitamin B9 is required for the synthesis of several coenzymes involved in metabolic processes essential in the production of DNA and RNA, especially in cells and tissues that are dividing rapidly. It also works in concert with vitamin B12 in the formation of red blood cells (erythrocytes) and supporting the function of iron in the body [33]. A deficiency of vitamin B9 can have serious adverse systemic effects. Megaloblastic anemia, characterized by larger-than-normal erythrocytes, can develop secondary to vitamin B9 deficiency and can lead to peripheral neuropathy, gastrointestinal problems, lethargy, altered taste perception, weakness, decreased appetite, and weight loss [34]. A deficiency during pregnancy can lead to neural birth defects, most prominently spina bifida. Spina bifida can lead to lifelong problems, including paralysis, learning disabilities, depression, memory impairment, and urinary and bowel dysfunction [33].

Oral manifestations of vitamin B9 deficiency are the result of compromised DNA and RNA, which decreases the production of new cells. This can cause protracted surgical site healing and tissue surface ulcerations. Vitamin B9 is also important in the production of white blood cells, a major component of the immune system [19]. This immune system dysfunction can result in the development of opportunistic oral infections and periodontal disease.

Vitamin B12 (Cyanocobalamin)

Vitamin B12 serves as a coenzyme for fat and carbohydrate metabolism and protein synthesis and is integral component in the production of red blood cells. The absorption of vitamin B12 from the gastrointestinal tract requires that it binds to intrinsic factor, a substance produced by the parietal cells of the stomach mucosa. Vitamin B12 is absorbed in the distal small bowel (terminal ileum), and persons with disease of the terminal ileus (e.g., Crohn disease, Whipple disease, celiac disease) are at risk for malabsorption of vitamin B12 and other nutrients. The primary natural sources of dietary vitamin B12 are animal products, including fish and shellfish, beef, poultry, pork, eggs, and dairy products [2]. However, fortified cereals also usually contain 100% of the recommended daily value of vitamin B12. Strict vegetarians and particularly vegans (who consume no animal products) are at an increased risk of insufficient intake of vitamin B12, and these patients may benefit from vitamin B12-fortified foods, oral vitamin B12 supplements, or vitamin B12 injections [1].

The most severe systemic complication of vitamin B12 deficiency is pernicious anemia. It is characterized by a decrease in red blood cells resulting from impaired intestinal absorption of vitamin B12, caused by autoimmunity against intrinsic factor or gastric parietal cells (which produce intrinsic factor). Intrinsic factor is necessary for the absorption of vitamin B12, and decreased production of intrinsic factor leads to reduced absorption of vitamin B12 [33].

Oral manifestations of a vitamin B12 deficiency are variable and can include angular cheilosis, oral ulcerations, hemorrhagic gingivitis, and detachment of the periodontal fibers [35]. The tongue may be painful and eventually lose its filiform and fungiform papillae, which can distort the patient's sense of taste [11]. The tongue may also develop a glossy, red surface that is prone to ulceration and can be very sensitive to temperature extremes and spicy foods. If these signs and symptoms are noted in the course of providing dental care, the patient should be referred for prompt medical evaluation.

Vitamin C (Ascorbic Acid)

Among all of the vitamins discussed in this course, the history of vitamin C is perhaps the most interesting. In the 18th century, scurvy was excessively common among sailors of the British Navy [1]. Scurvy is a disease caused by a vitamin C deficiency, with symptoms that include connective tissue defects (including gingivitis, loosening of teeth, rashes, internal bleeding, delayed wound healing), dermatitis, depression, and fatigue. Limes were found to be protective against scurvy, and in 1933, vitamin C was identified as the substance responsible for this action.

Vitamin C is involved in the synthesis of collagen, hormones, and amino acids. It is critical for the synthesis of connective tissues and for iron absorption and storage [19]. Vitamin C deficiency can have profound adverse effects on oral health, as it can impair collagen production and quality. A deficiency often firsts manifests as edematous, hemorrhagic, and painful gingival tissues [12].

The strength and resilience of the gingival tissues and the oral mucosa are impaired with a decreased production of collagen. These tissues are more prone to injury and take longer to heal after a traumatic incident or invasive dental procedure. Collagen deficiency can also impair the structure of the oral mucosa and its ability to support partial or complete dentures. The periodontal ligament and alveolar bone may display decreased ability to support the teeth in their sockets, leading to an increase in mobility and tooth loss.

Further compromise of the oral structure may occur as the intercellular cement in the connective tissues bone and dentin become defective [36]. Capillary integrity is weakened and vascular permeability is increased, with extravasation of blood into the interstitial hard and soft tissues. The lining of the gingival sulcular epithelium is also weakened; this compromises the epithelial attachment and results in apical migration of the periodontal attachment, a deepened periodontal pocket, and tooth loss [10].

Vitamin C deficiency during pregnancy or during childhood or adolescence may cause atrophy of the ameloblasts and odontoblasts [37]. The age at which the deficiency occurs and the duration of the deficiency will determine the degree of enamel and dentin malformation and the impact on oral health. The enamel of deciduous teeth is relatively thin, and any malformation of this layer can increase the potential for rapidly advancing caries. Although the enamel of permanent teeth is proportionately much thicker, malformation nonetheless increases the potential for plaque retention, caries, and periodontal disease.

Fluoride is the ionized form of fluorine and is the mineral most associated with oral health and the reduction of carious lesions in children and adults. The Centers for Disease Control and Prevention (CDC) has named community water fluoridation one of the 10 great public health achievements of the 20th century, given the substantial decline in carious lesions since the program began in 1962 [38]. As of 2020, approximately 73% of people in the United States are served by fluoridated community water systems [38].

The American Dental Association recommends people at risk of developing dental caries receive 2.26% fluoride varnish or 1.23% fluoride (acidulated phosphate fluoride) gel, or a prescription-strength, home-use 0.5% fluoride gel or paste or 0.09% fluoride mouthrinse for those 6 years of age or older.

(https://jada.ada.org/article/S0002-8177%2814%2960659-0/fulltext Last Accessed: October 10, 2023)

Strength of Recommendation: In Favor (for patients 6 to 18 years of age)/Expert Opinion For (for patients older than 18 years of age)

Fluoride exerts an anticaries effect by forming fluoroapatite and inhibiting bacterial growth and adhesion, thereby strengthening enamel and cementum [12]. Developing teeth incorporate fluoride via foods, fluoride supplements, and water absorbed from the gastrointestinal tract. However, ingested fluorides are no longer useful after the development of the teeth is complete (usually by the middle to late teenage years) [39]. At this stage, the benefits of fluoride are limited to topical application via dentifrices, gels/pastes, varnishes, and mouth rinses [40]. Residual fluoride in the saliva and the dental plaque decrease the risk of caries by encouraging the remineralization of tooth surfaces [41]. Some restorative materials (e.g., glass ionomers) contain fluoride and release it slowly, thus decreasing the potential for recurrent caries at the tooth-restoration junction [42]. The benefits of fluoride are balanced by the potential risks [41].

There are levels at which chronic fluoride ingestion can be associated with adverse effects. The maximum allowable concentration of fluoride in community water systems, also known as the maximum contaminant level (MCL), is 4.0 mg/liter [43]. This level is nearly six times the recommended level for community water systems. As of 2023, the U.S. Environmental Protection Agency was in the process of reviewing the maximum amount of fluoride allowed in drinking water [41]. Ingestion of fluoride at the MCL for a long period of time can lead to the development of dental and skeletal fluorosis [44]. The most common adverse effect associated with the long-term ingestion of fluoride in excess of 2 mg/liter is dental fluorosis [45]. Mild forms of dental fluorosis feature small white spots or streaks in the dental enamel (i.e., mottled enamel). Severe forms of dental fluorosis feature brown or black pits in the enamel. These are not carious lesions but may require composite restorations, as surface pitting will enhance the retention of plaque and increase the potential for the development of caries. In more severe cases, all the enamel may be damaged [46]. A study published by the Centers for Disease Control and Prevention found that approximately 23% of the U.S. population between 6 and 49 years of age had some form of dental fluorosis; 16.0% had very mild fluorosis, 4.8% had mild fluorosis, 2.0% had moderate fluorosis, and less than 1% had severe fluorosis [47]. An additional 16.5% were classified as having questionable or possible dental fluorosis. This same study found that the rates of dental fluorosis among adolescents (12 to 15 years of age) significantly increased between 1986–1987 and 1999–2004. Skeletal fluorosis is characterized by pain and stiffness in major joints and an increased risk for fractures. This condition is rare in the United States [46].

Calcium is the most abundant mineral in the human body and accounts for about 40% of its mineral composition; approximately 99% of this calcium is sequestered in the bones and teeth [1]. Calcium plays a role in the formation of teeth and bone, muscle contraction, coagulation, cardiac rhythm maintenance, and enzyme reactions.

Calcium metabolism is under hormonal control; parathyroid hormone raises serum calcium levels while calcitonin lowers levels. Approximately 65% of bone mass is inorganic hydroxyapatites (mineral salts), most of which is composed of highly condensed calcium phosphate crystals [2]. The enamel layer of teeth consists of a 96% inorganic matrix, with about 25% of this matrix composed of calcium [48]. Ameloblasts release both calcium and phosphate, so deficiencies in calcium during tooth development stages (including in utero) can cause incomplete tooth calcification, dental malformation, and increased caries risk after tooth eruption [10].

Calcium deficiency can decrease the density of alveolar bone, compromising its ability to support and retain teeth. Patients with nutritional deficiencies of calcium and vitamin D also are at increased risk of osteoporosis. When the extraskeletal calcium level is inadequate, bone tissues are resorbed in an attempt to maintain equilibrium. To prevent excessive skeletal calcium loss, an adequate amount of calcium, as well as vitamin D, must be ingested.

Men 50 to 70 years of age should obtain at least 1,000 mg/day of elemental calcium; women 51 years of age and older and men 71 years of age and older require 1,200 mg/day of elemental calcium [49]. National nutrition surveys have revealed that many individuals in the United States consume less than half of the recommended daily amount of calcium in their diet [49]. Dietary supplements may be necessary. Intakes in excess of 1,200–1,500 mg per day provide limited benefit and may increase the risk of developing kidney stones or cardiovascular disease in at-risk individuals [49]. The upper safe limit for total calcium intake is 2,500 mg/day [49,50,51].

Calcium supplements are especially necessary in more fragile, older patients; however, the problem of reduced calcium absorption is more acute in older persons. This may be overcome by increasing overall calcium intake and maintaining adequate levels of vitamin D [50]. The best way to increase calcium intake is through diet (e.g., consumption of dairy products), because supplements are not always absorbed well. To increase absorption, supplements should be taken with meals [50]. For patients on acid-reducing medications, calcium citrate should be used because calcium carbonate requires an acidic environment.

While calcium deficiencies can cause problems with oral and systemic health, the use of supplements is not without adverse consequences. Calcium supplements can decrease the absorption of iron, zinc, and magnesium, deficiencies of which can lead to renal insufficiency, neuropsychiatric problems, and xerostomia [22].

Zinc is an essential trace mineral that serves as a cofactor in many enzyme-controlled processes, functions as an antioxidant, and reduces bacterial toxins [12]. Zinc is necessary for new tissue formation and immune system (particularly antibody) function, actions that are essential to the prevention of oral infections and periodontal disease [10]. Zinc has been added to oral health products to help control plaque and calculus formation and to reduce halitosis. It has the ability to persist for several hours in the saliva and plaque. Low levels of zinc are anticariogenic, as it can inhibit enamel demineralization and promote remineralization [52]. Zinc deficiencies can cause prolonged healing of surgical sites, delayed replenishment of the gingival and mucosal surface layers, and compromised immune function.

Concern about zinc levels has generally focused on systemic complications from excessive ingestion rather than a deficiency. Aside from nutritional supplements, the most common source of excess zinc is denture adhesive pastes, powders, or pads. Many patients who use partial or complete dentures use an adhesive to provide additional retention for eating and speaking. While properly fabricated prostheses should require no or little adhesive, over time the mucosa and underlying bone atrophy, which can compromise retention and function. Ideally, the existing prostheses should be relined or replaced to reflect the patient's current oral topography. However, the cost can be prohibitive for some, leading to a reliance on adhesive. The cumulative ingestion of zinc from denture adhesives and dietary sources can result in a systemic excess, with the competitive inhibition of copper absorption the primary concern. Zinc and copper use similar metabolic pathways for absorption from the gastrointestinal tract. Therefore, an increase in zinc in the digestive tract will decrease the amount of copper absorbed; when this is sustained, a copper deficiency (hypocupremia) can develop [53]. Symptoms of hypocupremia develop gradually and can include anemia, gait and balance problems, and paresthesias in the extremities [54]. Patients with excessive zinc are often older and may attribute these issues to conditions common with aging. It is therefore essential for dental professionals to educate their patients about the potential systemic complications of sustained ingestion of zinc-containing denture adhesives. Zinc-free denture adhesives have been developed and are the preferred formulations, when possible.

Phosphorus is the second most abundant mineral in the body, and approximately 85% of phosphorus is located in bone [1]. It is found in smaller amounts in tissues throughout the body and is a major component of ATP. It is essential for bone and tooth formation, maintenance of the body's acid-base balance (necessary for RNA and DNA synthesis), and for energy production and storage. Phosphate is the common inorganic form of phosphorus and consists of one phosphorus atom bonded with four oxygen atoms. This negatively charged ion (anion) is capable of bonding with a positively charged ion (cation), such as calcium.

Calcium phosphate is a major constituent of both teeth and bone, so phosphorus deficiency during dental development can adversely affect the formation of the inorganic matrices of both enamel and dentin. Malformation of the enamel surface can predispose it to the retention of plaque and the associated increased potential caries and periodontal disease. This effect of phosphorus deficiency ceases to be an issue after early adolescence, when dental development is complete [48].

Bone is dynamic tissue that undergoes changes throughout life. Phosphorus deficiency at any stage of life can interfere with the subtle but constant process of bone remodeling. The formation of new bone in the matrix of an extraction site can be compromised in patients with phosphorus deficiency. Similarly, the repair and the replacement of the alveolar bone that supports the teeth can be adversely affected.

Deficiencies of phosphorus are rare, as this mineral found in many foods, including dairy products, meats and poultry, fish, eggs, nuts, legumes, vegetables, and grains. However, conditions such as diabetes, malnutrition/anorexia, and alcohol use disorder can decrease phosphorus levels in the body. Certain gastrointestinal conditions, such as Crohn disease and celiac disease, can compromise a patient's ability to absorb phosphorus and other nutrients. Symptoms of a phosphorus deficiency are not pathognomonic but include anxiety, fragile bones, fatigue, irregular breathing, numbness, and weight change [55]. Referral to a physician is advisable when phosphorus deficiency is suspected.