title: Early evolving joint degeneration by cartilage trauma is primarily mechanically controlled.
abstract: BACKGROUND
  Mechanical and inflammatory processes add to osteoarthritis (OA). To what extent both processes contribute during the onset of OA after a cartilage trauma is unknown. This study evaluates whether local cartilage damage leads to focally confined or more generalized cartilage damage with synovial inflammation in the early development of joint tissue degeneration.
  
  
  METHODS
  In nine goats, cartilage damage was surgically induced on the weight bearing area of exclusively the medial femoral condyle of the right knee joint. The other tibio-femoral compartments, lateral femoral condyle and lateral medial tibial plateau, were left untouched. The contralateral left knee joint of each animal served as an intra-animal control. Twenty weeks post-surgery changes in cartilage matrix integrity in each of the four compartments, medial and lateral synovial tissue inflammation, and synovial fluid IL-1β and TNFα were evaluated.
  
  
  RESULTS
  In the experimental medial femoral plateau, significant macroscopic, histologic, and biochemical cartilage damage was observed versus the contralateral control compartments. Also the articulating cartilage of the experimental medial tibial plateau was significantly more damaged. Whereas, no differences were seen between the lateral compartments of experimental and contralateral control joints. Synovial tissue inflammation was mild and only macroscopically (not histologically) significantly increased in the experimental medial compartments. Synovial fluid IL-1β level was not different between experimental and contralateral control joints, and TNFα was overall beneath the detection limit.
  
  
  CONCLUSIONS
  Local cartilage damage is a trigger for development of OA, which in early onset seems primarily mechanically driven. Early treatment of traumatic cartilage damage should take this mechanical component into consideration.
authors.affiliation: Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: k.wiegant@umcutrecht.nl.
authors.forename: K
authors.initials: K
authors.lastname: Wiegant
authors.affiliation: Department of Orthopedics, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: m.beekhuizen@umcutrecht.nl.
authors.forename: M
authors.initials: M
authors.lastname: Beekhuizen
authors.affiliation: Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: s.mastbergen@umcutrecht.nl.
authors.forename: S C
authors.initials: SC
authors.lastname: Mastbergen
authors.affiliation: Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: n.o.kuchuk@umcutrecht.nl.
authors.forename: N O
authors.initials: NO
authors.lastname: Kuchuk
authors.affiliation: Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: a.barten@umcutrecht.nl.
authors.forename: A D
authors.initials: AD
authors.lastname: Barten-van Rijbroek
authors.affiliation: Department of Orthopedics, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: r.j.h.custers@umcutrecht.nl.
authors.forename: R J H
authors.initials: RJ
authors.lastname: Custers
authors.affiliation: Department of Orthopedics, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: d.saris@umcutrecht.nl.
authors.forename: D B F
authors.initials: DB
authors.lastname: Saris
authors.affiliation: Department of Orthopedics, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: l.b.creemers@umcutrecht.nl.
authors.forename: L B
authors.initials: LB
authors.lastname: Creemers
authors.affiliation: Rheumatology & Clinical Immunology, University Medical Center Utrecht, Utrecht, The Netherlands. Electronic address: f.lafeber@umcutrecht.nl.
authors.forename: F P J G
authors.initials: FP
authors.lastname: Lafeber
mesh_terms: D000818:Animals; D002357:Cartilage Diseases / Q000473:pathology*; D002358:Cartilage, Articular / Q000293:injuries / Q000473:pathology*; D004195:Disease Models, Animal; D005260:Female; D006025:Glycosaminoglycans / Q000032:analysis; D006041:Goats; D053583:Interleukin-1beta / Q000032:analysis; D007719:Knee Joint / Q000473:pathology*; D020370:Osteoarthritis, Knee / Q000209:etiology / Q000473:pathology*; D011509:Proteoglycans / Q000032:analysis; D013314:Stress, Mechanical; D013582:Synovial Fluid / Q000737:chemistry; D013583:Synovial Membrane / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D006025:Glycosaminoglycans; D053583:Interleukin-1beta; D011509:Proteoglycans; D014409:Tumor Necrosis Factor-alpha
keywords: Cartilage damage; Inflammation; Mechanical; Osteoarthritis; Pathogenesis