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Temporal patterns of stromelysin‐1, tissue inhibitor, and proteoglycan fragments in human knee joint fluid after injury to the cruciate ligament or meniscus
Author(s) -
Stefan Lohmander L.,
Roos Harald,
Dahlberg Leif,
Hoerrner Lori A.,
Lark Michael W.
Publication year - 1994
Publication title -
journal of orthopaedic research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.041
H-Index - 155
eISSN - 1554-527X
pISSN - 0736-0266
DOI - 10.1002/jor.1100120104
Subject(s) - synovial fluid , anterior cruciate ligament , meniscus , osteoarthritis , medicine , synovitis , cruciate ligament , knee joint , ligament , acl injury , proteoglycan , matrix metalloproteinase , anatomy , cartilage , arthritis , surgery , pathology , physics , alternative medicine , incidence (geometry) , optics
Stromelysin‐1, tissue inhibitor of metalloproteinases‐1 (TIMP‐1), and proteoglycan fragments were quantified in knee synovial fluid samples in a cross‐sectional study of patients who had injury to the anterior cruciate ligament or the meniscus. The average concentrations of stromelysin‐1 and TIMP‐1 increased 25‐fold and 10‐fold within the first day after the trauma, respectively, and the concentration of proteoglycan fragments increased 4‐fold. From approximately 1‐6 months after injury, the levels of these markers were higher after injury to the cruciate ligament than after injury to the meniscus. From 6 months to 18 years after trauma, however, the levels of stromelysin‐1 and TIMP‐1 in patients who had an injury to the ligament were the same as the levels in patients who had a meniscal lesion. but the levels were increased compared with those for a reference group of healthy volunteers. The molar balance of stromelysin‐1 to TIMP‐1 in synovial fluid in both groups of injured joints changed from a balance representing an excess of free inhibitor in the normal joint to one representing an excess of free enzyme in the injured joint. The increased release of these markers to joint fluid both early and late after trauma may be caused by a change in the loading patterns in the knee with an injured ligament or meniscus or by synovitis induced by bleeding. The increased release may be associated with the frequent development of posttraumatic osteoarthritis in patients with these injuries.