Repair of a critical size defect in the rat mandible using allogenic type I collagen

Mandibular fractures, resulting from either trauma or reconstructive surger y, can be challenging craniofacial problems. The morbidity of failed fractu re healing is significant and may require bone grafting. Donor site morbidi ty and finite amounts of autogenous bone are major drawbacks of autogenous bone grafting. Similarly, the use of allografts and xenografts may be assoc iated with an increased risk of rejection, infection, and nonunion. To circ umvent the limitations of bone grafting, research efforts have focused on f ormulating a suitable bone substitute. The purpose of our study was to eval uate the efficacy of type I collagen implants in repairing critical sized m andibular defects in rats. Twelve male Sprague-Dawley rats (200-300g) were divided equally into control and experimental groups. Full thickness, round , four millimeter in diameter defects were created in the ramus of the righ t mandible of all rats using an electrical burr at low speed. The defects w ere irrigated of all bone chips, and either filled with a precisely fitted disk of allogenic collagen type I gel (experimental animals) or left empty (control animals). Animals were killed 6 weeks after surgery and healing of the bone defects was assessed in a blinded fashion using radiologic and hi stologic analysis. Radiologic analysis of the control group revealed a clea r circular right mandibular defect in all animals, whereas the collagen dis k implant group revealed an indistinct to nonexistent right mandibular defe ct in all animals. Densitometric analysis revealed a significant difference between these groups (*P = 0.01). Similarly, gross analysis of control man dibles revealed a 4mm round, soft-tissue filled defect, while implanted def ects demonstrated gross bone spanning the defect. Finally, histologic analy sis of all control mandibles revealed clearly demarcated bony edges at the defect border with connective tissue spanning the defect. In contrast, hist ological analysis of all implanted mandibles revealed indistinct bony edges at the defect border with a thin layer of osteoblasts and viable bone span ning the defects. We have demonstrated the ability of type I collagen to pr omote healing of a membranous bony defect that would not otherwise heal at 6 weeks. The suitability of type I collagen as a carrier matrix provides am ple opportunity for tissue-engineered approaches to further facilitate bony defect healing. Promoting bone formation through tissue engineering matric es offers great promise for skeletal healing and reconstruction.