Dental manifestations of patient with Vitamin D-resistant rickets

Abstract

Patients with Vitamin D-resistant rickets have abnormal tooth morphology such as thin globular dentin and enlarged pulp horns that extend into the dentino-enamel junction. Invasion of the pulp by microorganisms and toxins is inevitable. The increased fibrotic content of the pulp, together with a reduced number of odontoblasts, decreases the response to pulp infection. The most important oral findings are characterized by spontaneous gingival and dental abscesses occuring without history of trauma or caries. Radiographic examinations revealed large pulp chambers, short roots, poorly defined lamina dura and hypoplastic alveolar ridge. These dental abscesses are common and therefore the extraction and pulpectomy are the treatment of choice. The purpose of this article is to report a case of Vitamin D-resistant rickets in a 5 year-old boy, describing the dental findings and the treatment to be performed in these cases.

Dental Management of Hypophosphatemic Vitamin D Resistant Rickets

“…Low levels of vitamin D can trigger the body to release hormones that lead to the eventual loss of calcium and phosphate from bones, which leads to insufficient bone mineralization. Vitamin D Resistant Rickets (VDRR) is also known as X-linked hypophosphatemia with a prevalence of 1:20.000 people (1)(2)(3)(4). It is characterized by a calcium and phosphate metabolism disorder affecting mineralized tissues, bone and teeth (1,5).…”

“…It is characterized by a calcium and phosphate metabolism disorder affecting mineralized tissues, bone and teeth (1,5). VDRR was first documented by Albright et al (6) (1937) and mineralization defects of hard tissues in these cases are derived from renal transepithelial transport disturbance resulting in decreased tubular reabsorption of phosphate and hypophosphatemia (1,4,7). Physical findings are growth failure, bowing of the legs, short stature and walking disturbances (4,7,8).…”

“…Dental findings of this condition are enlarged pulp chambers, pulp horns which spread outside the dentino-enamel junction, enamel and dentine defects, poorly defined lamina-dura, short roots and hypoplastic alveolar ridge (4,(9)(10)(11).…”

“…The combination of all these factors contribute to recurrent dental abscesses in VDRR cases. Bacteria and their toxins which come from the oral cavity to the pulp cause pulpitis, pulp necrosis, periapical recurrent abscess or periapical complications without dental caries (1,2,4,5,7,(9)(10)(11)(12)(13)(14).…”

“…However, permanent dentition development can be improved by medical therapy after birth. Therefore, mineralized tissue defects are more common in primary dentition than permanent dentition (3,4,16).…”