Thirteen myelodysplastic children with 19 chronic physeal fractures were treated. All were treated with prolonged immobilization (average, 5.8 months; range, 3-18 months) in either braces or casts; four of the fractures required operative fixation to facilitate healing. All were healed at 4.8-years follow-up but, in four of the fractures, the growth plate closed prematurely. Three of the children underwent magnetic resonance imaging (MRI) of the injured physes, and one underwent physeal biopsy as part of her operative epiphysiodesis. Histologic analysis revealed three distinct zones of physeal pathoanatomy: a normal zone of proliferation; a thickened, disorganized zone of hypertrophy; and a vascularized zone of fibrous tissue adjacent to the metaphysis. On MRI, there was thickening of the physis and irregularity of the zone of provisional calcification. The physeal cartilage and the juxtametaphyseal fibrovascular tissue enhanced with gadolinium. These findings corroborate earlier mechanistic proposals for physeal injury in myelodysplasia: chronic stress or trauma to the poorly sensate limb produces micromotion at the zone of hypertrophy, yielding a widened, disorganized physis, and leading to fracture, displacement, and delayed union.
From the Departments of *Orthopaedic Surgery and §Radiology, Children's Hospital, Boston, Massachusetts; †Capital Region Orthopaedics and Sports Medicine, Jefferson City, Missouri; and ‡Department of Orthopaedic Surgery, State University of New York at Buffalo, Buffalo, New York, U.S.A.
Study conducted at Children's Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.
Address correspondence and reprint requests to Dr. W. B. Rodgers, Capital Region Orthopaedics and Sports Medicine, 1500 Southwest Blvd., Jefferson City, MO 65109, U.S.A.