Unique rodent model of distraction osteogenesis of the mandible

被引:53
|
作者
Buchman, SR
Ignelzi, MA
Radu, C
Wilensky, J
Rosenthal, AH
Tong, L
Rhee, ST
Goldstein, SA
机构
[1] Univ Michigan, Sch Med, Sect Plast Surg, Dept Surg, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Sch Med, Orthopaed Res Lab, Ann Arbor, MI 48109 USA
[3] Univ Michigan, Sch Dent, Dept Orthodont & Pediat Dent, Ann Arbor, MI USA
关键词
D O I
10.1097/00000637-200211000-00012
中图分类号
R61 [外科手术学];
学科分类号
摘要
Despite the increasing use of distraction osteogenesis (DO) of the mandible, the molecular mechanisms regulating new bone formation during DO remain poorly understood. The purposes of this study were (1) to establish a unique rodent model of DO capable of outlining parameters for new bone formation at the distraction site and (2) to determine a critical-size defect to differentiate osteogenesis resulting from distraction from conventional fracture healing at the osteotomy site. Adult Sprague-Dawley rats were fitted successfully with this newly developed distraction device. Analyses demonstrated that the device could distract the rat mandible reliably to 5.1 mm with complete union. Acute intersegmental gaps of 2 mm resulted in complete bony union in a manner consistent with fracture healing, whereas 3-mm acute gaps resulted in varying degrees of bony union. Acute intersegmental gaps of 5.1 mm invariably resulted in fibrous nonunion. In summary, the authors have developed a rodent model of DO of the mandible. Their distraction protocols resulted successfully in advancement to 5.1 mm with bony consolidation. Notable fracture healing occurred at immediate intersegmental spaces as large as 3 mm. A gap of 5.1 mm was sufficient to act as a critical-size defect, resulting consistently in fibrous nonunion. These findings validate the effectiveness of this distraction device and establish the critical-size defect of a rat mandible at more than 3 mm. This novel model of DO provides an effective method of examining fundamental mechanisms responsible for new bone formation in the craniofacial skeleton.
引用
收藏
页码:511 / 519
页数:9
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