Open access peer-reviewed chapter

Vitamin D Deficiency in Pediatric Dentistry

Written By

Elif Gül Aydin

Submitted: 26 August 2022 Reviewed: 01 December 2022 Published: 05 March 2023

DOI: 10.5772/intechopen.109278

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Vitamin D Deficiency - New Insights

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Abstract

Vitamin D (vitD) deficiency has essential effects on general health. It is known that oral and dental health is an integral part of public health, and there is a close relationship between them. From the development and eruption stages of the teeth to the formation of caries, vitD deficiency has accepted significant effects on oral health. It is essential to understand the role of vitD deficiency in early childhood caries (ECC), which is considered one of the most critical problems, especially in pediatric patients. Low vitD levels during pregnancy have even been reported to increase ECC risk in infancy. For this reason, care should be taken to ensure that the mother’s 25(OH)d level and later the child is in optimal conditions, starting from the pregnancy period, to improve the oral health status of children.

Keywords

  • pediatric dentistry
  • vitD deficiency
  • early childhood caries
  • primary teeth

1. Introduction

Today, within the framework of increasing holistic health understanding, it is seen that the interest in the relationship between oral and systemic health has improved. The relationship between dental caries and nutrition is known from when caries are defined. 25-hydroxyvitamin D (25(OH)D) <30 nmol/L is accepted as a vitamin D deficiency, and it is stated that it may be associated with poor oral health. The incidence of periodontal disease, dental caries, and enamel hypoplasia is increased with vitamin D deficiency. In addition, 25-hydroxyvitamin D or its metabolites are involved in the immunological response together with the antimicrobial peptides cathelicidin and defensins that play an immunological role.

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2. Vitamin D deficiency in pediatric dentistry

Tooth caries seen in children remain its place as a significant disease that affects more than 600 million children worldwide. Early childhood caries (ECC) is defined as the presence of one or more decayed (non-cavitated or cavitated lesions), missing or filled (due to caries) surfaces in any primary tooth of a child under 6 years of age [1]. Permanent teeth under the primary teeth play a protective place to come to their appropriate places in the mouth. Due to caries in these teeth, chronic pain, infections, and nutritional problems occur in children. These problems have a negative impact on the quality of life of children and families and increase the burden of community health programs. For this reason, they should be considered an integral part of general health.

Early childhood caries, like other types of caries, is a dynamic disease that starts with biofilm, can persist in the presence of sugar, is considered multifactorial, and occurs with the deterioration of the balance between demineralization and remineralization of dental hard tissues. Tooth decay occurs due to the biological, behavioral, and psychosocial factors associated with the individual’s environment. Common risk factors for ECC include improper infant feeding, exposure to sugar, poor oral hygiene, poverty, and late access to preventive dental care. ECC has common risk factors for other noncommunicable diseases associated with excessive sugar consumption, such as cardiovascular disease, diabetes, and obesity. Excessive sugar consumption causes prolonged acid production from the bacteria attached to the tooth and changes the composition of the oral microbiota and the pH of the biofilm. When this condition persists, the tooth structures demineralize [1]. Severe early childhood caries (S-ECC) is a more aggressive manifestation that frequently necessitates dental treatment under general anesthesia. Those with S-ECC often suffer from pain, sleep disturbance, behavior changes, and altered eating habits. In recent cross-sectional studies, children with S-ECC have been found to have lower vitamin D status, iron status, or anemia [2, 3, 4, 5, 6].

The relationship between nutrition, general health, and dental caries studies dates to the 1920s. The study by Mellanby and Pattison, published in 1928, provides the first evidence that vitamin D deficiency is associated with dental caries in children [7, 8]. A growing body of studies and evidence shows that low serum concentrations of 25-hydroxyvitamin D (25(OH)D) are associated with increased caries experience [2, 8, 9, 10, 11]. It has even been reported that low 25(OH)D levels in the mother during pregnancy increase the risk of ECC in children [9, 10, 12].

Minerals, such as magnesium, calcium, and phosphorus, the essential structural components of the tooth, should be taken at sufficient levels with the diet. These minerals play a role by interacting with vitamins in strengthening the tooth structure. A deficiency of magnesium, calcium, and phosphorus in diet and nutrition content usually results in loose teeth and premature tooth loss. If magnesium deficiency occurs during the formation stages of teeth, delay in eruption times, enamel or dentin hypoplasia appear. Also, the alveolar bone becomes brittle, and the gingiva becomes hypertrophic. It is stated that magnesium strengthens the antimicrobial environment, reduces oral inflammation, and increases the flexibility of tooth enamel by increasing calcium absorption in the teeth [13, 14], especially vitD is related to calcium, magnesium, and zinc. Without magnesium, the immune system cannot activate vitamin D, and sufficient calcium absorption does not occur in the teeth. vitD is a hormone essential for the intestinal absorption of Calcium, Magnesium and Phosphate. Vitamin D helps regulate calcium and phosphate balance to maintain healthy bone function. Magnesium helps activate vitamin D, which helps regulate calcium and phosphate homeostasis, influencing bone growth and maintenance. There is a synergistic relationship between vitD and magnesium [13].

Several different mechanisms have been proposed to express the role of vitD among the factors reducing caries.

One of these mechanisms is to play a role in the formation, calcification, mineralization, and protection of teeth by affecting serum calcium, phosphate levels, and parathyroid hormone. The balance between calcium and phosphate levels is important for the formation, calcification, mineralization, and preservation of teeth, bone, hard tissue, maxilla, and mandible. Enamel and dentin defects-hypoplasia have been linked with hypocalcemia and hypophosphatemia [11, 15].

Dental caries and VDD (vitamin D deficiency) affect children worldwide. Changes in both enamel and dentin are observed in children with a VDD. Therefore, vitD has a significant role in forming oral hard tissue, comprising tooth enamel and dentin, and affects primary and permanent teeth development [8, 11, 16].

Vitamin D deficiency may cause defects in enamel and dentin and increase the risk of dental caries. In a systematic review of controlled clinical trials, 2827 children were included. As a result of this systematic review, the significant relationship found between vitamin D levels, and dental caries showed that vitamin D is a promising anticaries agent [4, 8, 17].

Vitamin D has a significant role in odontogenesis [11, 18]. The mechanism by which vitD excites the mineralization of tooth enamel involves binding to vitamin D receptors (VDR) expressed in both tooth and bone cells. VDR directs the transcription of several target genes, mostly defined by ameloblasts and odontoblasts [11, 15, 19]. It coordinates physiological functions by controlling calcium and phosphate metabolism, promotes growth, and induces necessary remodeling of the bones and teeth [4]. VDR stimulates the formation of structural gene products in dentin, together with calcium-binding proteins and diverse extracellular matrix proteins. The gene encoding VDR is positioned on chromosome 12q13.11 and comprises several polymorphisms [19]. The VDR gene adjusts the biological role of primary vitD metabolites; thus, having a vital role in the configuration of teeth, particularly in mineralizing dentin and enamel. Consequently, developmental deficiencies, for example, enamel hypoplasia, can result from VDD. Ultimately, vitD and VDR at the molecular level influence the tooth germ formation, supply the regulation of enamel and dentin structure and maturation, and organize the phases of dental crown growth [11, 15]. In addition to dental problems due to vitamin D deficiency, genetic polymorphism of VDR gene polymorphism has been associated with dental problems, such as external apical root resorption, periodontal diseases, dentinogenesis imperfecta, chronic periodontitis, and dental caries [20].

Tooth development and eruption are complex mechanisms involving the resorption of alveolar bone and the eruption pathway. A disorder in these processes causes persistent primary teeth and delays in permanent tooth eruption. It is stated that decreased vitamin D levels increase the rate of constant primary teeth and cause delays in eruption in permanent teeth. It was known that maternal vitamin D deficiency affects the formation and mineralization of primary teeth. It is considered among the dental effects of vitamin D deficiency, which cause tooth eruption delays in children [20].

Moreover, vitD adjusts and adapts both the innate and adaptive immune systems. The immunological role of vitD is stimulating the arrangement of some antimicrobial peptides, for example, defensins and cathelicidin (LL-37), which defend against many pathogens, counting oral bacteria [4, 11, 12, 21]. Cathelicidin (LL-37 or hCAP-18) is controlled by vitD, which has antiendotoxin and antimicrobial properties [22]. Vitamin D induces cathelicidin (LL-37), which is found in the immune system. LL-37 exhibits both antimicrobial and antiendotoxin activity. It is stated that there is an inverse relationship between dental caries and LL-37, and the concentration of LL-37 is low in children with high caries activity. Epithelial antimicrobial peptides (LL-37 is one of them) are the protectors of the oral cavity. It is stated that these antimicrobial peptides have essential roles in reducing gingivitis in oral health. Therefore, vitamin D may be helpful in the treatment of periodontitis due to its direct effects on bone metabolism and possible anti-inflammatory effects on periodontopathogens [13].

Early tooth loss, bone resorption, and bleeding tendency increase in mineral deficiencies due to absorption disorders [13]. The chewing efficiency of individuals provides the highest nutrient intake efficiency. Prematurely lost teeth have adverse effects on diet selection and nutritional efficiency. Deterioration of nutritional efficiency also causes deficiencies in vitamin intake. The resulting vitamin deficiency also negatively affects the formation of dental hard tissue. Vitamin deficiencies in the developmental stages of teeth cause disorders in the formation of hard tissue of the tooth. Therefore, it has been stated that there is a strong positive correlation between vitamin deficiencies. Malnutrition and dental hard tissue hypoplasia increase the risk of dental caries in children during the primary dentition period [2, 23]. In addition, mineral deficiencies cause bleeding in the gums, delayed tooth eruption, periodontal disease, and destruction patterns in the alveolar bone [13, 23].

It is stated that dental health in children has started to decrease in industrialized countries due to identifying risk factors and developing preventive strategies. However, it was determined that while the prevalence of caries decreased, enamel defects began to increase. It is considered a global burden, with the majority of enamel defects rising to 38% in Western European countries [24]. Developmental enamel defects are present when the affected tooth erupts. When the tooth newly erupts, it may appear hypo mineralized, porous, and more yellow-brown opaque in color. These impacted teeth are susceptible to fracture easily, and the permanent first molars are affected quite frequently. Although these defects predispose to atypical and extensive caries, they may result in the loss of the relevant permanent teeth in the early period of life [25]. Even if the developmental enamel defects are mild, they cause pain in children due to dentin sensitivity, poor esthetic color, and caries susceptibility. Considering the effects of enamel defects on quality of life and health care utilization, a significant public health problem arises [24, 25, 26]. Developmental enamel defects are associated with the calcification processes of the teeth. Since calcifications of primary and permanent teeth occur in the early postnatal period following the intrauterine period, it is necessary to examine these periods while investigating the etiological factors. Studies indicate maternal disease, drug use during pregnancy, premature birth, birth complications, and early childhood diseases as the etiological factors of enamel defects [27]. However, these pieces of evidence are unfortunately insufficient and therefore preventable. Vitamin D plays a crucial role in enamel formation, and vitamin D deficiency is now also considered a common health challenge in westernized societies [4].

A randomized controlled study conducted with high-dose vitamin D supplementary to mothers during pregnancy and early postpartum showed an inverse relationship between high-dose vitamin D intake and the formation of enamel defects. In other words, high-dose vitamin D supplementation taken during pregnancy and early postpartum showed a 50% reducing effect on enamel defects in 6-year-old children [26]. It is on the agenda to recommend vitamin D supplementation as a primary preventive measure for enamel defects, potentially impacting dental health. Considering the crucial role of vitamin D in enamel mineralization [19, 28], the biological relationship between vitamin D supplementation and these enamel defects is considered reasonable. Vitamin D has an effect on the function of ameloblasts and the mineralization of enamel in the early stages of tooth formation. It is stated that high-dose vitamin D supplementation has a protective effect on the structural strength and development of enamel [26].

Vitamin D is also very effective, along with minerals, in protecting oral health. Vitamin D helps maintain the calcium-phosphate balance and contributes to the shaping of the bone. The beneficial effects of vitamin D on oral health are not only limited to the direct impact on tooth mineralization. Still, they are also exerted through anti-inflammatory functions and the ability to stimulate the production of antimicrobial peptides. It also has essential functions by showing anti-inflammatory effects. It is reported that with sufficient Vit-D levels, the onset and progression of caries in the tooth structure can be stopped, caries can be formed, and enamel loss can be prevented [4, 11, 13].

Early childhood caries affects not only dental health but also has severe effects on general health. Malnutrition, iron deficiency anemia, and VDD are seen in children with ECC because their nutritional status is affected [11, 17]. When the relationship between vitamin D levels and caries was evaluated, it was determined that the incidence of dental caries was higher in the children of mothers with low serum vitamin D during pregnancy, and there was a strong correlation between vitamin D levels and DMFT scores in the early childhood period of children up to 6 years of age [3]. It is stated that the incidence of caries in the permanent first molar teeth is lower in children with serum vitamin D levels greater than 50 nmol in the 10–11 years of early adolescence period [3]. Similarly, in children aged 6–17 years, it was determined that every 10 mg/ml increase in serum vitamin D resulted in a 0.66 decrease in DMFT scores. It is also expected that malnutrition and related vitamin deficiencies increase the incidence of enamel hypoplasia [2, 5, 9, 11]. According to the results of an observational study, the rate of dental caries was found to be more than three times higher in 6-year-old children of mothers with 25 OHD deficiency in the third trimester of pregnancy compared to the children of mothers with adequate 25 OHD levels in the third trimester of pregnancy [3].

Vitamin D use may have a role in the protection of caries early in life. According to meta-analysis studies, it is thought to be a promising caries prevention agent, given that Vit-D supplementation relates to a 47% reduction in caries in children [3, 17]. Considering intrauterine life, an essential and critical stage for the development of teeth, and vitamin D deficiency during pregnancy plays a crucial role in the susceptibility to enamel hypoplasia and caries [2, 11, 23].

Improving vitD levels in children from an early stage appears to be an essential task. This requires awareness of pregnancy. Pregnant women should have their vitD levels tested routinely during the first trimester of pregnancy, and the risk of VDD, VDD, and vitD ingestion should be evaluated. Prenatal vitD levels appear to influence the development of primary dentition and ECC [3, 9, 11, 23]. In addition, a study found that pregnant women’s poor oral hygiene and low vitamin D levels were positively correlated with preterm birth and low birth weight [29].

Vitamin D is an essential hormone for absorbing calcium, magnesium, and phosphorus from the intestine, which is necessary for properly mineralizing bones and teeth. Although there are no applications in children, it has been shown that coating the implant surfaces with vitD during dental implant application increases osteointegration. In addition, intraperitoneal application of vitD creates positive effects (such as facilitating acceleration) on tooth movements during orthodontic treatment [13].

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3. Conclusions

When evaluated from a holistic perspective, it should be kept in mind that oral health is also a part of general health. When seeking solutions for dental problems in children, the vitamin values of individuals should be considered. Increasing social awareness in the fight against ECC and evaluating vitamin D deficiency is essential.

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Conflict of interest

The authors declare no conflict of interest.

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Written By

Elif Gül Aydin

Submitted: 26 August 2022 Reviewed: 01 December 2022 Published: 05 March 2023