Full Content is available to subscribers

Subscribe/Learn More  >

The Role of IL-1 in Meniscal Tissue Breakdown Following Simulated Partial Meniscectomy

[+] Author Affiliations
B. Zielinska, T. Gupta, T. L. Haut Donahue

Michigan Technological University, Houghton, MI

Paper No. SBC2007-176009, pp. 799-800; 2 pages
  • ASME 2007 Summer Bioengineering Conference
  • ASME 2007 Summer Bioengineering Conference
  • Keystone, Colorado, USA, June 20–24, 2007
  • Conference Sponsors: Bioengineering Division
  • ISBN: 0-7918-4798-5
  • Copyright © 2007 by ASME


In a healthy meniscus, the compressive strains are approximately 2–10%. [1] When 30% or more of the tissue is removed during partial meniscectomy, strains increase to approximately 18%. [1] We have previously shown that dynamic compressive strains of 20% to meniscal explants results in an increase in proteoglycan (PG) breakdown, nitric oxide (NO) production, metalloproteinases 1, 3, and 13 (MMP-1, MMP-3, and MMP-13) compared to 0, 5, and 10% compressive strain. [2,3,4] The objective of this study was to determine if interruption of the IL-1 pathway would alter this biochemical response to dynamic mechanical compression.

Copyright © 2007 by ASME



Interactive Graphics


Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal

Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging and repositioning the boxes below.

Related eBook Content
Topic Collections

Sorry! You do not have access to this content. For assistance or to subscribe, please contact us:

  • TELEPHONE: 1-800-843-2763 (Toll-free in the USA)
  • EMAIL: asmedigitalcollection@asme.org
Sign In