In vivo cyclic compression causes cartilage degeneration and subchondral bone changes in mouse tibiae.

In vivo cyclic compression causes cartilage degeneration and subchondral bone changes in mouse tibiae.
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DOI:
10.1002/art.37906
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发表时间:
2013-06
影响因子:
--
通讯作者:
van der Meulen, Marjolein C. H.
van der Meulen, Marjolein C. H.
中科院分区:
其他
文献类型:
--
作者:
Ko, Frank C.;Dragomir, Cecilia;Plumb, Darren A.;Goldring, Steven R.;Wright, Timothy M.;Goldring, Mary B.;van der Meulen, Marjolein C. H.

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Alterations in the mechanical loading environment in joints may have both beneficial and detrimental effects on articular cartilage and subchondral bone and subsequently influence the development of osteoarthritis (OA). We used an in vivo tibial loading model to investigate the adaptive responses of cartilage and bone to mechanical loading and to assess the influence of load level and duration. We applied cyclic compression of 4.5 and 9.0N peak loads to the left tibia via the knee joint of adult (26-week-old) C57Bl/6 male mice for 1, 2, and 6 weeks. Only 9.0N loading was utilized in young (10-week-old) mice. The changes in articular cartilage and subchondral bone were analyzed by histology and microcomputed tomography. Loading promoted cartilage damage in both age groups, with increased damage severity dependent upon the duration of loading. Metaphyseal bone mass increased in the young mice, but not in the adult mice, whereas epiphyseal cancellous bone mass decreased with loading in both young and adult mice. Articular cartilage thickness decreased, and subchondral cortical bone thickness increased in the posterior tibial plateau in both age groups. Both age groups developed periarticular osteophytes at the tibial plateau in response to the 9.0N load, but no osteophyte formation occurred in adult mice subjected to 4.5N peak loading. This non-invasive loading model permits dissection of temporal and topographical changes in cartilage and bone and will enable investigation of the efficacy of treatment interventions targeting joint biomechanics or biological events that promote OA onset and progression.
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