Abstract
Chronic lengthening of immobilized, neurally intact muscle leads to the addition of sarcomeres in series. Confirmation of a similar adaptation during distraction osteogenesis is crucial for providing a rationale for a successful outcome of the intervention. When distraction osteogenesis (at less than equal to 1.4 mm/day) is done in skeletally immature animals, muscle adapts by creating a longer and functionally intact muscle. This is achieved through muscle growth, the proliferation of myogenic cells ultimately leading to serial addition of sarcomeres. When distraction osteogenesis is done in skeletally mature animals, however, the same distraction regimen leads to a lengthened muscle that has significant fibrosis and weakness, the latter possibly a result of partial denervation. Despite a modest but significant elevation of local insulinlike growth factor-1 in the lengthened muscles from adult animals, muscle growth is not adequate and leads to a loss of function. In adult animals, the distraction osteogenesisinduced increase in insulinlike growth factor-1 is insufficient to facilitate muscle growth during lengthening. Muscle can be targeted for future therapeutic use of insulinlike growth factor-1; however, such a therapy also may lead to increased fibrosis.