Skeletal Involvement

Administration of retinoids induces bone toxicities similar to those of chronic hyper-vitaminosis A (remodeling of long bones, cortical hyperostosis, decalcification, premature epiphyseal closure, periosteal thickening, and osteoporosis). In general, synthetic retinoids produce bony changes such as diffuse idiopathic skeletal hyperos-tosis, including anterior spinal ligament calcification, osteophytes, and bony bridges, but without narrowing of the disk space. Calcification of the anterior spinal ligament with bony bridging of vertebrae has been observed with long-term, high-dose (2 mg/kg per day) isotretinoin therapy, and minimal spinal hyperostosis has been reported in 10% of patients treated with short-term, low-dose isotretinoin. Ossification of the spinal posterior longitudinal ligament is rare. Extraspinal involvement (extraspinal tendon and ligament calcification) is significantly increased in patients receiving long-term etretinate therapy at an average dose of 0.8 mg/kg per day. Premature epiphyseal closure resulting in retardation of growth has been rarely described in children with oral retinoid treatment. The incidence of decreased bone mineral density is still under investigation. No changes in bone mineralization or in markers of bone turnover have been found after short-term therapy with isotretinoin. However, osteoporosis has been identified in patients who received long-term etreti-nate therapy (Brecher and Orlow 2003, Orfanos et al. 1987, Peck and DiGiovanna 1999).

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