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Fibrodysplasia ossificans progressiva (FOP) is a rare, extremely disabling, autosomal dominant disease of the skeletal system (1 ). The disease process involves ectopic production of osseous masses in intramuscular and perimuscular connective tissue. The osseous masses form abnormally connected sections of the skeleton, causing disfiguration and inhibiting normal motor functions (1). There is evidence that microtraumas, intramuscular injections and surgical procedures might contribute to the initiation of the disease. The patients need to avoid soft-tissue injuries, contact sports, overstretching of soft tissues and muscle fatigue, biopsies, surgical removal of heterotopic bone and non-emergency surgical procedures (2). Almost all FOP patients have some congenital anomalies, including short great toes, hallux valgus, short thumbs and hypoplasia of digital phalanges (3). Recently, a recurrent mutation in activin receptor 1 A/activin-like kinase 2 (ACVRl /ALK2), a bone morphogenetic protein (BMP) type 1 receptor, was identified in all sporadic and familial cases of FOP examined, making this one of the most specific disease-causing mutations in the human genome (2).

Treatment of an Intractable Cutaneous Ulcer in the Right Lateral Malleolus in Fibrodysplasia Ossificans Progressiva