Official websites use. Share sensitive information only on official, secure websites. Correspondence should be addressed to A Linglart Email: agnes. This work is licensed under a Creative Commons Attribution 3. In children, hypophosphatemic rickets HR is revealed by delayed walking, waddling gait, leg bowing, enlarged cartilages, bone pain, craniostenosis, spontaneous dental abscesses, and growth failure.
Healing rickets is the initial endpoint of treatment in children. Therapy aims at counteracting consequences of FGF23 excess, i. Corrective surgeries for residual leg bowing at the end of growth are occasionally performed. In addition to the conventional treatment, optimal care of symptomatic patients requires pharmacological and non-pharmacological management of pain and joint stiffness, through appropriated rehabilitation.
Much attention should be given to the dental and periodontal manifestations of HR. Besides vitamin D analogs and phosphate supplements that improve tooth mineralization, rigorous oral hygiene, active endodontic treatment of root abscesses and preventive protection of teeth surfaces are recommended. Current outcomes of this therapy are still not optimal, and therapies targeting the pathophysiology of the disease, i. FGF23 excess, are desirable. In this review, medical, dental, surgical, and contributions of various expertises to the treatment of HR are described, with an effort to highlight the importance of coordinated care.
Phosphate wasting ineluctably leads to hypophosphatemia and numerous consequences including mineralization defects. In children, hypophosphatemia is revealed by vitamin D-resistant rickets and results in variable degrees of delayed walking, waddling gait, leg bowing, enlarged cartilages, bone pain, craniostenosis, spontaneous dental abscesses, and growth failure.
Symptoms might be present, although to a lesser degree, in adults who underwent the conventional treatment throughout their childhood and adolescence.
