Journal of Dental Research and Review

: 2022  |  Volume : 9  |  Issue : 3  |  Page : 202--205

Vitamin D Deficiency and Its Effects on Enamel, Dentin, and Pulp: A Literature Review

Tapasya Karemore1, Mukta Motwani1, Vaibhav Karemore2,  
1 Department of Oral Medicine and Radiology, VSPM Dental College and Research Center, Nagpur, Maharashtra, India
2 Department of Periodontics and Implantology, Government dental college, Nagpur, Maharashtra, India

Correspondence Address:
Tapasya Karemore
Department of Oral Medicine and Radiology, VSPM Dental College and Research Center, Nagpur, Maharashtra


Vitamin D deficiency (VDD) is very common in the Indian subcontinent and many countries, in spite of plenty of sun exposure. Vitamin D has a definite influence on metabolism of bone and dental tissues. VDD causes a variety of bone deformities clinically represented as rickets and dental defects such as decreased enamel, dentin mineralization, and altered pulp morphology in children. Therefore, appropriate serum Vitamin D levels are required for the mineralization process of both teeth and bone. VDD may affect the teeth during intrauterine life and show changes in early childhood and may continue throughout life. Enamel, dentin, and pulp changes due to VDD can be diagnosed by clinical, microbiological, or histologic and radiologic examination. Knowledge of VDD-induced dental changes is necessary for early detection and in time corrections of defects produced. This review aims to collate the data available on the deficiency of Vitamin D observed among children and its manifestations affecting enamel, dentin, and pulp. To identify relevant articles, PubMed and Embase databases were searched for terms such as VDD (MesH terms), VDD (all fields), and dental enamel, dentin, and pulp (MesH and all fields). The related data searched includes peer-reviewed articles, randomized control trials, systematic reviews, and case reports for manuscript compilation.

How to cite this article:
Karemore T, Motwani M, Karemore V. Vitamin D Deficiency and Its Effects on Enamel, Dentin, and Pulp: A Literature Review.J Dent Res Rev 2022;9:202-205

How to cite this URL:
Karemore T, Motwani M, Karemore V. Vitamin D Deficiency and Its Effects on Enamel, Dentin, and Pulp: A Literature Review. J Dent Res Rev [serial online] 2022 [cited 2023 Jan 30 ];9:202-205
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Natural sunlight is a key source for synthesizing Vitamin D in the human body.[1] 7-dehydrocholesterol is converted by human skin into Vitamin D in presence of ultraviolet rays (B). Vitamin D is essential for various cell cycles, whereas its deficiency has a significant role in physiology of bones, cardiovascular systems, intestines, pancreas, immune system, muscles, and central nervous system.[1],[2] Mineral homeostasis is controlled by Vitamin D through intestinal and renal absorption of phosphorus and calcium and further used by mineralized tissues.[3] It has also been reported that Vitamin D not only helps to reduce the occurrence of cancer and viral diseases but also alleviates musculoskeletal pain and stabilizes mood disorders.[4],[5],[6]

Vitamin D deficiency (VDD) is prevalent in India and many countries, in spite of plenty of sun exposure.[7],[8],[9] In many studies, decreased levels of serum Vitamin D were observed among all age groups of males and females in various geographical regions. Apart from nutritional deficiency, other causes of VDD include fully covered clothing in tropical regions and the use of private transportation, discouraging regular exposure to the sun.[1],[10],[11],[12]

To maintain Vitamin D levels, the Indian Council of Medical Research has recommended daily outdoor activities in sun for normal healthy children and adults, although a daily 400 IU of Vitamin D dosage is suggested for specific medical conditions.[8],[13]

The form of Vitamin D, i.e., 1,25 dihydroxyvitamin D3 (1,25[OH] 2D3), has a significant role in regulating bone or osteoblasts metabolism due to the presence of Vitamin D receptors, that makes the cell a functional target of 1,25(OH) 2D3.[14] Secondly, VDD can reduce calcium and phosphorus absorption, it increases parathyroid hormone levels, in response, affecting bone homeostasis.[14],[15]

There are specific causes of VDD among different age groups with different clinical manifestations. In infants, VDD can be due to low maternal Vitamin D, decreased cutaneous synthesis, decreased dietary intake, and increased exclusive breastfeeding.[16]

Equally, in the older age group, nutritional deficiencies of Vitamin D and calcium, affect bone health adversely with increase the risk of fractures, especially in postmenopausal women.[2],[9],[17]

Children with VDD show difficulty in standing and walking due to muscle weakness while increased sway and more frequent falls with risk of fracture are reported in the elderly.[14],[18] Skeletal deformities due to VDD in children are commonly represented as rickets.[19],[20] Rickets usually occur during 6–24 months of age leading to changes in tooth structures with an increased incidence of dental caries.[21],[22],[23],[24] It can be said that this deficiency of Vitamin D and low calcium intake or high-phytate diet can be manifested as rickets globally.[2],[6],[16],[25]

In the general population, commonly observed long-term effects of early VDD include delayed teeth eruption, defective enamel, increased risk of caries and gingival inflammation,[5],[26] tooth loss,[27],[28],[29] and reduced postnatal growth[30], as Vitamin D or its metabolites act directly on ameloblasts and odontoblasts. Experimental study by Dhamo et al.[31] observed that VDD alters the mineralization of enamel and dentin and in contrast higher Vitamin D levels can affect the teeth calcification process, irreversibly. Therefore, optimum Vitamin D levels are required during the mineralization process of both teeth and bone.[32]

This review aims to collate the data available on the deficiency of Vitamin D among children and its consequences on enamel, dentin, and pulp structure. To identify relevant articles, PubMed and Embase databases were searched for terms such as VDD (MesH terms), VDD (all fields), and dental enamel, dentin, and pulp (MesH and all fields). The related data searched was from peer-reviewed articles in English and has included randomized controlled trials, systematic reviews, and case reports for manuscript compilation.

The effect of VDD on enamel, dentin, and pulp was found to be a significant fact to be reviewed and by reanalyzing the fact, measures for prevention of ill effects of VDD on dental structures would be possible to consider.

The effects of VDD on enamel, dentin, and pulp are discussed separately, as follows.


Hypophosphatemic Vitamin D-resistant rickets was observed with hypoplastic enamel in individuals with inherited metabolic deficiency of Vitamin D. This inherited form manifested as hypoplastic enamel in both, deciduous and permanent dentitions in children.[33]

It is also studied that hypoplastic enamel has a significant risk for developing dental caries in the primary dentition.[33],[34]

Zerofsky et al.[27] compared the effect of deficiency of Vitamin D on bone density, growth, immune function, and dental health[35] among healthy children diagnosed with rickets. This study concluded that children with VDD-induced rickets had greater chances of malformed enamel and a tendency for fracture.

Kuhnisch et al.[3] analyzed the relationship between serum 25-hydroxyvitamin D (25[OH] D) status, molar incisor hypomineralization (MIH), and caries in primary and permanent teeth. It was found that MIH is common in the initial years of life and can be associated with dental caries. The author concluded that decreased serum Vitamin D levels showed an association with MIH.

Reed et al.[33] evaluated the correlation between Vitamin D concentrations of mothers during pregnancy and enamel changes in infants' teeth developed in utero. Crowns of primary maxillary central incisors are formed by birth and erupted by 12–18 months of age, hence can be used as a record of VDD during pregnancy. In this pilot study, it was observed that the pattern of hypoplastic or malformed enamel reflects the levels of Vitamin D during pregnancy with a specific gestational week.[36]

van der Tas et al.[37] also studied serum Vitamin D levels during fetal, postnatal, and childhood periods and its association with hypomineralization of teeth. In contrast to previous studies, this study concluded that Vitamin D concentrations are not associated with the presence of hypomineralization of teeth.

Dhamo et al.[31] investigated the correlation of mothers' and neonates' Vitamin D concentrations with the development of teeth among 10-year-old children in the Netherlands where the author suggested that sufficient concentration of Vitamin D in the prenatal period minimizes the chances of hypomineralization and decay of dental structures in children.


Similar to the bone, the active form of Vitamin D, 1,25-dihydroxyvitamin D3 is significant for dental tissues for metabolism[38] which was inferred by deficiency-induced defective dentin formation and delayed tooth eruption through various studies.[39],[40]

Rebeiro et al.[41] analyzed the structure of enamel and dentin among affected by X-linked hypophosphatemic rickets (XLHR) individuals using micro-CT (mCT). The author also evaluated the association of mineralization defects, tooth position, and gender with XLHR. It is also studied that mCT, a method with high-resolution and minimum destruction, can be used for microstructural analysis of small bodies including mineral density, volume, and mineralization pattern.[42]

It is observed that spontaneous recurring abscesses involving noncarious primary and permanent teeth are the classic oral clinical feature associated with familial hypophosphatemic rickets. These teeth usually show deficient dentin mineralization. It is also hypothesized that bacterial invasion of pulp through mineralization defects in enamel and dentin leads to abscess formation.[43],[44] These changes also were confirmed by various histologic and radiologic investigations.[45]

Veselka et al.[32] also correlated the onset and duration of VDD with the appearance of interglobular dentin (IGD) using mCT. A comparison of severity of IGD affecting various age groups of males and females was done by mCT and histological analysis observed that females had a less severe pattern of IGD than males suggesting that males experienced more severe episodes of VDD.

Even after replenishment of Vitamin D, dentin mineralization defects remain visible as dentin, once formed does not turnover, like bone. This helps to analyze the common sociocultural practices and growth of the disease, developed in past within different age and sex groups.[32]

In addition to radiographic evaluation of VDD-induced dental changes, Brickley et al.[46] studied about effects on dentin due to past VDD. It is suggested that changes in dentin structure or IGD formation would guide to investigate the previous episodes of VDD. IGD can be well preserved in archeological teeth and can be considered to evaluate the number and severity of periods of VDD.[47]

It was found that the neonatal line also differentiates between prenatal and postnatal VDD events can be used as a guide to understand the correlation between mother and infant status for changes which were induced due to alteration in calcium and phosphate metabolism.[47]


Woo et al.[38] investigated the effect of Vitamin D on dentin and mineralization of human dental pulp cells (HDPCs). In this study, the author found that an active form of Vitamin D can affect odontoblastic differentiation genes through mRNA and protein expression. The author stated that differentiation of HDPC is promoted by Vitamin D through extracellular signal-regulated kinase activation.

To analyze this experiment clinically, D'Ortenzio et al.[48] studied past VDD-induced coronal pulp changes among living and archeological individuals using radiographs of permanent molars. The study stated that VDD could lead to disturbance in the metabolism of the microstructure of developing tooth dentin. Histologically, this dentin showed bubble-like spaces near incremental lines in the dentinal matrix similar to IGD. Dental pulp has odontoblasts which mature and also produce dentin. It is observed that very few odontoblasts are active in permanent teeth at a certain time leading to a slow rate of dentin formation and longer tooth development period, usually 3–6 years. Any change or deficiency due to endocrine and nutritional factors, therefore, gets a longer duration for it to show its impact. In such conditions, VDD can show the absence of secondary dentin formation in affected teeth ultimately causing morphological alterations or shape deformity in the coronal pulp.[39]

Various studies conducted so far to correlate VDD and enamel hypomineralization have concluded that serum Vitamin D concentration even in utero can affect enamel and can be clinically evident in later age. The optimum level of Vitamin D could be beneficial to prevent enamel defects and early childhood caries.

Other reported dental changes due to deficiency of Vitamin D such as delayed tooth eruption, absence of secondary dentin formation leading to teeth with enlarged pulp chamber, and high pulp horns also need further study and attention in future.

Along with periodic evaluation and Vitamin D supplements for all age groups, fortification of food would be beneficial as a population-based approach. This would definitely help to prevent young children from dental defects due to Vitamin D and would improve the dental health of the population.

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Conflicts of interest

There are no conflicts of interest.


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