Origin, diagnosis, and treatment of the dental manifestations of vitamin D-resistant rickets: review of the literature and report of case.

Previous discussions center on early diagnosis, initial treatment, and follow-up therapy for the patient with vitamin D-resistant rickets. Both the medical and dental aspects of treatment for these patients has a long-range effect on the normal developmental patterns. Although treatment is begun at an early age, some rachitic skeletal effects such as minor bowing of the legs and bossing of the skull will invariably be noticed. In patients with controlled rickets the alveolar processes undergo normal development, with apparent normal dental eruption. The poor development and calcification of the alveolus seen in the untreated patient leads to loss of the lamina dura and periodontal ligament of the teeth. Patients with resistant rickets possess a functional dentition, although not without inherent defects. Various degrees of fracture and attrition of enamel can be seen, and hypoplasia of dentin is nearly a universal result. Defects extending to the dentinoenamel junction have been shown in repeated cases. Cementum, because of its close relationship with dentin calcification, also appears abnormal. Pulp tissue may undergo abberations of physiology in resistant rickets, although further work in this respect is needed. With respect to the possible dental pathoses seen in this disease, the dental history of the patient with resistant rickets discussed in this report showed that several of the deciduous teeth, possibly the mandibular left second premolar and right first molar, and definitely the maxillary right second premolar and canine and the mandibular left canine had all undergone pulpal degeneration of apparently unknown causation. In the maxillary right second premolar and the mandibular left canine, enamel fractures were clinically and radiographically apparent. However, the maxillary right canine originally had an acute abscess with no defects other than normal, minimal wear facets. No causative factor for its necrosis could be found. Overt enamel fractures in the maxillary right second premolar and the mandibular left canine may have led to microexposures of the pulp with subsequent bacterial pulpal contamination. Suppuration present in several of the pulps when first entered during endodontic treatment, as well as chronic fistulas in several areas, support the conclusion that contamination by some means does indeed occur.