Cell death after cartilage impact occurs around matrix cracks

Jack L. Lewis, Laurel B. Deloria, Michelle Oyen-Tiesma, Roby C. Thompson, Marna Ericson, Theodore R. Oegema

Research output: Contribution to journalArticlepeer-review

92 Scopus citations


The damage from rapid high energy impacts to cartilage may contribute to the development of osteoarthritis (OA). Understanding how and when cells are damaged during and after the impact may provide insight into how these lesions progress. Mature bovine articular cartilage on the intact patella was impacted with a flat impacter to 53 MPa in 250 ms. Cell viability was determined by culturing the cartilage with nitroblue tetrazolium for 18 h or for 4 days in medium containing 5% serum before labeling (5-day sample) and compared to adjacent, non-impacted tissue as viable cells per area. There was a decrease in viable cell density only in specimens with macroscopic cracks and the loss was localized primarily near matrix cracks, which were in the upper 25% of the tissue. This was confirmed using confocal microscopy with a fluorescent live/dead assay, using 5′-chloromethylfluorescein diacetate and propidium iodide. Cell viability in the impacted regions distant from visible cracks was no different than the non-impacted control. At 5 days, viable cell density decreased in the surface layer in both the control and impacted tissue, but there was no additional impact-related change. In summary, cell death after the impaction of cartilage on bone occurred around impact induced cracks, but not in impacted areas without cracks. If true in vivo, early stabilization of the damaged area may prevent late sequelae that lead to OA.

Original languageEnglish (US)
Pages (from-to)881-887
Number of pages7
JournalJournal of Orthopaedic Research
Issue number5
StatePublished - 2003

Bibliographical note

Funding Information:
This work was supported by grants from the National Institutes of Arthritis, Musculoskeletal and Skin Diseases (AR41975), the Cathryn Mills-Davis Endowment and a National Science Foundation graduate fellowship to M. Oyen-Tiesma. The authors would like to thank Jerry Sedgewick and the staff of the Biomedical Image Processing Laboratory for their help with the computer-based image analysis, and Bruce Lindgren of the Biometrics Consulting service for advice on statistical analyses. The authors would also like to thank Toni Meglitsch, Sandra Johnson, Mary Slagle, Fred Wentorf, and Dr. Doug Adams for their time and assistance.


  • Cartilage
  • Cell viability
  • Crack
  • Impact
  • Surface


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