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Leukocytes Cause Inflammatory Response to Traumatized Articular Cartilage in Acute Phase of Joint Injury

[+] Author Affiliations
Dejan Milentijevic, Russell F. Warren

Hospital for Special Surgery, New York, NY

David M. Green

Baylor College of Medicine, Houston, TX

Koosha Aslani

The City College of CUNY, New York, NY

Peter A. Torzilli

Hospital for Special Surgery, New York, NYThe City College of CUNY, New York, NY

Paper No. SBC2007-176402, pp. 603-604; 2 pages
doi:10.1115/SBC2007-176402
From:
  • 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

abstract

Painful and inflamed joints result from joint trauma involving disruption of the cartilage [1]. The pathogenesis of post-traumatic osteoarthritis is not well understood but is most likely multifactorial. Other factors, such as inflammation, may be a critical precursor for post-traumatic arthritis. Transient acute synovitis and inflammation following a traumatic event can persist for months and may be representative of a serious joint injury [2]. Joint effusion aspirates from patients in the acute phase of injury have a higher level of activated leukocytes and an increased rate of reactive oxygen species (ROS) production relative to autologous peripheral blood [3]. In an in vitro study, the presence of inflammatory leukocytes caused more chondrocyte death isolated from traumatized matrix region relative to impacted cartilage alone [4]. Our previous study showed that severe trauma may not be a good predictor for the development of post-traumatic arthritis since chondrocyte death and matrix loss was minimal up to seven days post-trauma [5].

Copyright © 2007 by ASME

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