The Journal of Bone and Joint Surgery (American) 83:S22-24 (2001)
© 2001 The Journal of Bone and Joint Surgery, Inc.
In Vitro and in Vivo Models of Cartilage Injury
Darryl D. D'Lima, MD,
Sanshiro Hashimoto, MD,
Peter C. Chen, PhD,
Martin K. Lotz, MD and
Clifford W. Colwell, Jr., MD
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.
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Introduction
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Our previous study1 demonstrated that chondrocytes undergo apoptotis
in response to mechanical injury to full-thickness cartilage explants.
To validate this response, several models of injury across species
and in vivo were examined.
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Methods
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Full-thickness cartilage explants were harvested from weight-bearing
portions of adult bovine femoral condyles, and 5-mm-diameter disks
were punched out with a dermal punch. Explants were allowed to stabilize
in Dulbecco modified Eagle medium supplemented with 10% fetal
bovine serum for forty-eight hours. Explants were then divided into
two groups: load and control. The load group underwent a single
500-msec injury load of 30% strain in radially unconfined
compression. The control group was not loaded. A 30% strain
was found to generate a more consistent injury than the previous loading
protocol1. At ninety-six hours
after injury, explants underwent histologic examination and the
number of apoptotic cells was counted with use of TUNEL (terminal
deoxynucleotidyl transferase-mediated dUTP nick-end labeling). . . . [Full Text of this Article]
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