Scientific Article   |    
Cartilage Injury Induces Chondrocyte Apoptosis
Darryl D. D'Lima, MD; Sanshiro Hashimoto, MD; Peter C. Chen, PhD; Martin K. Lotz, MD; Clifford W. ColwellJr., MD
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Darryl D. D’Lima, MD
Peter C. Chen, PhD
Clifford W. Colwell Jr., MD
Division of Orthopaedic Surgery, Scripps Clinic, MS126, 11025 North Torrey Pines Road, Suite 140, La Jolla, CA 92037. E-mail address for D.D. D’Lima: ddlima@scripps.edu. E-mail address for C.W. Colwell Jr.: colwell@scripps.edu

Sanshiro Hashimoto, MD
Martin K. Lotz, MD
Division of Arthritis Research, The Scripps Research Institute, MEM 161, 10550 North Torrey Pines Road, La Jolla, CA 92037

In support of their research or preparation of this manuscript, one or more of the authors received grants or outside funding from Orthopaedic Research and Education Foundation Grant 98-052, National Institutes of Health Grant AG07996, the ALSAM Foundation, and the Skaggs Institute for Research. None of the authors received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

J Bone Joint Surg Am, 2001 Oct 01;83(2 suppl 1):S19-21
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Cartilage injury is one of the more important factors leading to secondary osteoarthritis. Previous histologic studies have demonstrated loss of chondrocyte viability after mechanical injury. More recently, it has been shown that chondrocytes undergo apoptosis in response to wounding or injurious compression1,2. An in vitro model was therefore developed to determine the effect of mechanical injury on chondrocyte viability and matrix degradation and whether cell death occurs as apoptosis or necrosis.
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