This article demonstrates the feasibility of using recombinant human bone morphogenetic protein (rhBMP-2) as a substitute for autogenous iliac crest bone for repair of congenital facial clefts in humans. In this series, 50 cleft sites were repaired in 43 patients using rhBMP-2 without the use of autogenous graft tissue. Successful osseous union was achieved in 49 of the 50 sites. In one patient, the graft failed to consolidate. Severe clefts were managed by combining distraction osteogenesis and rhBMP-2. Eliminating the need to harvest autogenous iliac crest bone resulted in substantial decrease in morbidity. The constructed alveolus performed clinically as normal bone and responded to natural tooth eruption and orthodontic movement. Histology of the tissue constructed showed normal, vital bone. Although additional investigation is warranted to determine the optimum protocol for the use of this material in alveolar cleft repair, the technique should be considered as a viable treatment option in cases in which avoiding iliac crest harvesting is desirable.

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A case involving concomitant presentation of a #7 lateral facial cleft with a complete cleft of the ipsilateral lip, alveolus, and palate is presented. The mandibular defect was Pruzansky III with a foreshortened body, absent ramus and absent masseter. Taking advantage of developmental field theory, reconstruction of the osseous defect was undertaken using the autogenous periosteum as a source of mesenchymal stem cells. Expansion of the periosteum was followed by implantation of Helistat (Integra Life Sciences, Plainsboro, NJ) collagen sponge saturated with recombinant human bone morphogenetic protein-2. Stimulation of this distraction-induced envelope by rhBMP-2 resulted in abundant production of bicortical membranous bone in situ within 12 weeks. The neoramus was subsequently suspended from the cranial base, and a temporalis muscle transfer was used to provide motor control of the jaw. Synthesis of bone in this manner is termed DISO (distraction-assisted in situ osteogenesis). The biologic rationale and clinical implications of DISO are discussed.

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