Degradation of cartilage type II collagen precedes the onset of osteoarthritis following anterior cruciate ligament rupture

Objective To determine if degradation of cartilage matrix in primary osteoarthritis (OA) or in OA secondary to rupture of the anterior cruciate ligament (ACL) is a gradual response to excessive loading or an early, initiating event in the disease process. Methods Biopsy samples were obtained from th...

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Veröffentlicht in:Arthritis and rheumatism 1999-11, Vol.42 (11), p.2390-2398
Hauptverfasser: Price, Jo S., Till, Simon H., Bickerstaff, Derek R., Bayliss, Mike T., Hollander, Anthony P.
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container_end_page 2398
container_issue 11
container_start_page 2390
container_title Arthritis and rheumatism
container_volume 42
creator Price, Jo S.
Till, Simon H.
Bickerstaff, Derek R.
Bayliss, Mike T.
Hollander, Anthony P.
description Objective To determine if degradation of cartilage matrix in primary osteoarthritis (OA) or in OA secondary to rupture of the anterior cruciate ligament (ACL) is a gradual response to excessive loading or an early, initiating event in the disease process. Methods Biopsy samples were obtained from the low–weight‐bearing articular cartilage of the intercondylar notch, in patients undergoing knee arthroscopy (ACL injury) or arthroplasty (late‐stage primary OA) or in controls. In some cases, biopsy samples were also removed from the high–weight‐bearing articular cartilage of the femoral condyles. Biopsy specimens were extracted and assayed for total and denatured type II collagen (CII) by inhibition enzyme‐linked immunosorbent assay and for proteoglycan using a colorimetric method. All patients were assessed radiographically for cartilage erosion. In addition, the cartilage of patients with ACL injury was assessed at arthroscopy, and the knee function of patients with primary OA was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Results Increased CII degradation was detected in the low– as well as the high–weight‐bearing cartilage of patients with late‐stage OA, and there was a positive correlation between the percentage denatured collagen and the WOMAC score. Most of the patients with ACL injury had no clinical signs of OA or macroscopic cartilage erosion. However, the low–weight‐bearing articular cartilage from these patients showed a significant increase in CII degradation, similar to that observed in late‐stage OA. The proteoglycan content of articular cartilage did not change significantly in patients with OA or ACL injury compared with controls. Conclusion CII degradation is an early event following ACL injury and is unlikely to be a direct result of mechanical loading, since it was observed in cartilage obtained from a low–weight‐bearing site.
doi_str_mv 10.1002/1529-0131(199911)42:11<2390::AID-ANR18>3.0.CO;2-9
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Methods Biopsy samples were obtained from the low–weight‐bearing articular cartilage of the intercondylar notch, in patients undergoing knee arthroscopy (ACL injury) or arthroplasty (late‐stage primary OA) or in controls. In some cases, biopsy samples were also removed from the high–weight‐bearing articular cartilage of the femoral condyles. Biopsy specimens were extracted and assayed for total and denatured type II collagen (CII) by inhibition enzyme‐linked immunosorbent assay and for proteoglycan using a colorimetric method. All patients were assessed radiographically for cartilage erosion. In addition, the cartilage of patients with ACL injury was assessed at arthroscopy, and the knee function of patients with primary OA was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Results Increased CII degradation was detected in the low– as well as the high–weight‐bearing cartilage of patients with late‐stage OA, and there was a positive correlation between the percentage denatured collagen and the WOMAC score. Most of the patients with ACL injury had no clinical signs of OA or macroscopic cartilage erosion. However, the low–weight‐bearing articular cartilage from these patients showed a significant increase in CII degradation, similar to that observed in late‐stage OA. The proteoglycan content of articular cartilage did not change significantly in patients with OA or ACL injury compared with controls. 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Methods Biopsy samples were obtained from the low–weight‐bearing articular cartilage of the intercondylar notch, in patients undergoing knee arthroscopy (ACL injury) or arthroplasty (late‐stage primary OA) or in controls. In some cases, biopsy samples were also removed from the high–weight‐bearing articular cartilage of the femoral condyles. Biopsy specimens were extracted and assayed for total and denatured type II collagen (CII) by inhibition enzyme‐linked immunosorbent assay and for proteoglycan using a colorimetric method. All patients were assessed radiographically for cartilage erosion. In addition, the cartilage of patients with ACL injury was assessed at arthroscopy, and the knee function of patients with primary OA was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Results Increased CII degradation was detected in the low– as well as the high–weight‐bearing cartilage of patients with late‐stage OA, and there was a positive correlation between the percentage denatured collagen and the WOMAC score. Most of the patients with ACL injury had no clinical signs of OA or macroscopic cartilage erosion. However, the low–weight‐bearing articular cartilage from these patients showed a significant increase in CII degradation, similar to that observed in late‐stage OA. The proteoglycan content of articular cartilage did not change significantly in patients with OA or ACL injury compared with controls. Conclusion CII degradation is an early event following ACL injury and is unlikely to be a direct result of mechanical loading, since it was observed in cartilage obtained from a low–weight‐bearing site.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Anterior Cruciate Ligament - metabolism</subject><subject>Anterior Cruciate Ligament - pathology</subject><subject>Anterior Cruciate Ligament Injuries</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Cartilage - metabolism</subject><subject>Collagen - metabolism</subject><subject>Diseases of the osteoarticular system</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - metabolism</subject><subject>Osteoarthritis - pathology</subject><subject>Osteoarthritis - physiopathology</subject><subject>Proteoglycans - analysis</subject><subject>Rupture</subject><subject>Water - metabolism</subject><issn>0004-3591</issn><issn>1529-0131</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqVkcuO0zAUhi0EYjoDr4C8QAgWKcd2nYkLQqo6XCqNqLitLdc56RilcbAdjap5eRxSAQs2rOxz9P3n9hOiGMwZAH_JJFcFMMGeM6UUYy8WfMnYay4ULJerzVWx-viZVW_EHObr7SteqHtk9ltzn8wAYFEIqdgZOY_xew65kOIhOWMgpQQhZ-TuCvfB1CY531HfUGtCcq3ZI03HHulmQ61vx7ijfUCLNUaabpD6LmIaBT4m9Fl0E1xykTaZ9reu21PTJQzOB2rDYJ1JSFu3NwfsEg1Dn4aAj8iDxrQRH5_eC_Lt3duv6w_F9fb9Zr26LuyihKpoygphUVdgFICwEmpWqmq3K0vBUCLj7FKIsgasmspCfdnwrOI8_7naCURxQZ5NdfvgfwwYkz64aDGv1aEfoi4VL6XgPIOfJtAGH2PARvfBHUw4agZ6dESP19XjdfXkiF7kHNOjI1pnR_QvR7TQoNdbzbXKNZ-cmg-7A9Z_VZwsyMDTE2CiNW0TTGdd_MOxSuauGfsyYbeuxeN_DfavuaaE-AkSSLG0</recordid><startdate>199911</startdate><enddate>199911</enddate><creator>Price, Jo S.</creator><creator>Till, Simon H.</creator><creator>Bickerstaff, Derek R.</creator><creator>Bayliss, Mike T.</creator><creator>Hollander, Anthony P.</creator><general>John Wiley &amp; Sons, Inc</general><general>Wiley</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>199911</creationdate><title>Degradation of cartilage type II collagen precedes the onset of osteoarthritis following anterior cruciate ligament rupture</title><author>Price, Jo S. ; Till, Simon H. ; Bickerstaff, Derek R. ; Bayliss, Mike T. ; Hollander, Anthony P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4608-f68e04d80a9003c50d1698bb6631e5e1217336d0e8f8c0d7f2608228c029b3ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Anterior Cruciate Ligament - metabolism</topic><topic>Anterior Cruciate Ligament - pathology</topic><topic>Anterior Cruciate Ligament Injuries</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Cartilage - metabolism</topic><topic>Collagen - metabolism</topic><topic>Diseases of the osteoarticular system</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Osteoarthritis</topic><topic>Osteoarthritis - metabolism</topic><topic>Osteoarthritis - pathology</topic><topic>Osteoarthritis - physiopathology</topic><topic>Proteoglycans - analysis</topic><topic>Rupture</topic><topic>Water - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>Price, Jo S.</creatorcontrib><creatorcontrib>Till, Simon H.</creatorcontrib><creatorcontrib>Bickerstaff, Derek R.</creatorcontrib><creatorcontrib>Bayliss, Mike T.</creatorcontrib><creatorcontrib>Hollander, Anthony P.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Arthritis and rheumatism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Price, Jo S.</au><au>Till, Simon H.</au><au>Bickerstaff, Derek R.</au><au>Bayliss, Mike T.</au><au>Hollander, Anthony P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Degradation of cartilage type II collagen precedes the onset of osteoarthritis following anterior cruciate ligament rupture</atitle><jtitle>Arthritis and rheumatism</jtitle><addtitle>Arthritis Rheum</addtitle><date>1999-11</date><risdate>1999</risdate><volume>42</volume><issue>11</issue><spage>2390</spage><epage>2398</epage><pages>2390-2398</pages><issn>0004-3591</issn><eissn>1529-0131</eissn><coden>ARHEAW</coden><abstract>Objective To determine if degradation of cartilage matrix in primary osteoarthritis (OA) or in OA secondary to rupture of the anterior cruciate ligament (ACL) is a gradual response to excessive loading or an early, initiating event in the disease process. Methods Biopsy samples were obtained from the low–weight‐bearing articular cartilage of the intercondylar notch, in patients undergoing knee arthroscopy (ACL injury) or arthroplasty (late‐stage primary OA) or in controls. In some cases, biopsy samples were also removed from the high–weight‐bearing articular cartilage of the femoral condyles. Biopsy specimens were extracted and assayed for total and denatured type II collagen (CII) by inhibition enzyme‐linked immunosorbent assay and for proteoglycan using a colorimetric method. All patients were assessed radiographically for cartilage erosion. In addition, the cartilage of patients with ACL injury was assessed at arthroscopy, and the knee function of patients with primary OA was assessed using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Results Increased CII degradation was detected in the low– as well as the high–weight‐bearing cartilage of patients with late‐stage OA, and there was a positive correlation between the percentage denatured collagen and the WOMAC score. Most of the patients with ACL injury had no clinical signs of OA or macroscopic cartilage erosion. However, the low–weight‐bearing articular cartilage from these patients showed a significant increase in CII degradation, similar to that observed in late‐stage OA. The proteoglycan content of articular cartilage did not change significantly in patients with OA or ACL injury compared with controls. Conclusion CII degradation is an early event following ACL injury and is unlikely to be a direct result of mechanical loading, since it was observed in cartilage obtained from a low–weight‐bearing site.</abstract><cop>New York</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>10555035</pmid><doi>10.1002/1529-0131(199911)42:11&lt;2390::AID-ANR18&gt;3.0.CO;2-9</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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subjects Adolescent
Adult
Aged
Aged, 80 and over
Anterior Cruciate Ligament - metabolism
Anterior Cruciate Ligament - pathology
Anterior Cruciate Ligament Injuries
Biological and medical sciences
Biopsy
Cartilage - metabolism
Collagen - metabolism
Diseases of the osteoarticular system
Female
Humans
Male
Medical sciences
Middle Aged
Osteoarthritis
Osteoarthritis - metabolism
Osteoarthritis - pathology
Osteoarthritis - physiopathology
Proteoglycans - analysis
Rupture
Water - metabolism
title Degradation of cartilage type II collagen precedes the onset of osteoarthritis following anterior cruciate ligament rupture
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