Intramembranous ossification mechanism for bone bridge formation at the growth plate cartilage injury site

Journal of Orthopaedic Research - Tập 22 - Trang 417-426 - 2004
Cory J Xian1, Fiona H Zhou1, Rosa C McCarty1, Bruce K Foster1
1Department of Orthopaedic Surgery, and University of Adelaide Department of Paediatrics, Women’s and Children’s Hospital, 72 King William Road, North Adelaide 5006, Australia

Tóm tắt

AbstractSalter's type III and type IV growth plate injuries often induce bone bridge formation at the injury site. To understand the cellular mechanisms, this study characterized proximal tibial transphyseal injury in rats. Histologically, bony bridge trabeculae appeared on day 7, increased on day 10, and became well‐constructed on day 14 with marrow. Prior to and during bone bridging, there was no cartilage proteoglycan metachromatic staining and no collagen‐X immunostaining at the injury site, nor was there any up‐regulation of BrdU‐labelled chondrocyte proliferation at the adjacent physeal cartilage, suggesting no new cartilage formation at the injury site. However, infiltration of vimentin‐immunopositive mesenchymal cells from metaphysis and epiphysis was apparent on day 3, with the mesenchymal population being prominent on days 7 and 10 and subsided on day 14. Among these infiltrates were osteoprogenitor precursors expressing osteoblast differentiation factor (cbf‐α1) on day 3, along with some cbf‐α1° osteoblast‐like cells lining bone trabeculae on days 7 and 10. Some mesenchymal cells and trabecula‐lining cells were also alkaline phosphatase‐immunopositive, further suggesting their osteoblast differentiation. From day 7 onwards, some trabecula‐lining cells became osteocalcin‐producing mature osteoblasts. These results suggest that bone bridge formation after growth plate injury occurs directly via intramembranous ossification through recruitment of marrow‐derived osteoprogenitor cells. © 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.

Tài liệu tham khảo

Bailey RW, 1981, Evolution of the concept of an extensible nail accommodating to normal longitudinal bone growth, Clin Orthop, 159, 157, 10.1097/00003086-198109000-00022 Brashear HR, 1959, Epiphyseal fractures: a microscopic study of the healing process in rats, J Bone Joint Surg, 41, 1055, 10.2106/00004623-195941060-00006 10.2106/00004623-199173060-00006 10.1002/bies.950060406 10.1097/01241398-199609000-00022 10.1016/S0925-4773(99)00142-2 Ford LT, 1956, A study of experimental trauma to the distal femoral epiphysis in rabbits, J Bone Joint Surg [Am], 38, 84, 10.2106/00004623-195638010-00008 Foster BK, 2000, Paediatric orthopaedics and fractures 10.1097/01241398-199403000-00018 10.1016/S8756-3282(96)00222-0 Gomes LSM, 1988, Traumatic separation of epiphyses. An experimental study in rats, Clin Orthop, 236, 286 Ianotti JP, 1990, Growth plate physiology and pathology, Orthop Clin N Am, 21, 1, 10.1016/S0030-5898(20)31561-3 10.1148/radiology.175.3.2343128 Joyce ME, 1991, Role of growth factors in fracture healing, Prog Clin Biol Res, 365, 391 10.1097/00004694-200011000-00021 10.1302/0301-620X.70B2.3346285 Ogden JA, 2000, Skeletal injury in the child, 10.1007/b97655 10.2106/00004623-196345030-00019 10.3109/10520298809107161 10.1097/00004694-200211000-00002 10.1210/edrv.21.4.0403