Abstract
Hereditary hypophosphatemic rickets and spontaneous dental abscesses: a case report
Highlights
Vitamin D-resistant hypophosphatemic rickets, known as familial or hereditary hypophosphatemic rickets (HHR), results in renal phosphate wasting and has a global prevalence estimate of 1:20.000 [1,2]
Two causes need to be considered in renal phosphate wasting: on the one hand caused by a primary renal tubular defect, which won’t be further discussed, on the other hand as a secondary effect due to increased fibroblast growth factor 23 (FGF23) signaling, as is seen in HHR [3]
The increased FGF-23 has a dual effect in HHR
Summary
Vitamin D-resistant hypophosphatemic rickets, known as familial or hereditary hypophosphatemic rickets (HHR), results in renal phosphate wasting and has a global prevalence estimate of 1:20.000 [1,2]. Clinical signs include skeletal aberrancies: short stature, (lower limb) bone deformities and frontal bossing, as well as muscular complaints and dental anomalies. The latter results in spontaneous periapical abscesses and fistulae occurring without any history of trauma or dental decay [7]. Radiographic examinations, including a panoramic view and cone beam CT-scan, showed periapical translucencies at the upper left central incisor, the lower left canine, the lower left primary and secondary molars and the lower right secondary molar (21-33-3637-47) (Figure 2c) It displayed enlarged pulp chambers and pulp horns, nearby the dentino-enamel junction.
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