title: Steady progression of osteoarthritic features in the canine groove model.
abstract: OBJECTIVE
  Recently we described a canine model of osteoarthritis (OA), the groove model with features of OA at 10 weeks after induction, identical to those seen in the canine anterior cruciate ligament transection (ACLT) model. This new model depends on cartilage damage accompanied by transient intensified loading of the affected joint. The present study evaluates this groove model at 20 and 40 weeks after induction, to assess whether the osteoarthritic features progress in time.
  
  
  METHODS
  Grooves were made in the femoral condyles of one knee without damaging the subchondral bone. After surgery the dogs were forced to load the experimental joint 3 days per week (4 hours/day) for 20 weeks by fixing the contralateral control limb to the trunk. After 20 weeks and 40 weeks (the last 20 weeks normal loading) joints were analysed for biochemical and histological features of OA.
  
  
  RESULTS
  All biochemical cartilage parameters were indicative of OA and all these parameters suggested a slow progression of degeneration over time from 20 to 40 weeks after induction, statistically significant for synthesis and content of proteoglycans as well as Mankin grade. Synovial inflammation, which was mild, diminished slightly in time.
  
  
  CONCLUSIONS
  The degenerative joint damage in the canine groove model is slowly progressive over time in the first year. The cartilage degeneration is induced by a one-time trauma and is not primarily mediated by synovial inflammation, which gives this model unique characteristics compared to presently available models for studying early osteoarthritic features in vivo. In the groove model the effect of treatment of cartilage damage is not counteracted by permanent joint instability or hampered by inflammation. Therefore, the model might be more sensitive to detect effects of therapy, aimed at cartilage protection and repair.
authors.affiliation: Department of Rheumatology & Clinical Immunology, University Medical Center Utrecht, 3508 GA Utrecht, The Netherlands. A.C.A.Marijnissen@azu.nl
authors.forename: A C A
authors.initials: AC
authors.lastname: Marijnissen
authors.forename: P M
authors.initials: PM
authors.lastname: van Roermund
authors.forename: N
authors.initials: N
authors.lastname: Verzijl
authors.forename: J M
authors.initials: JM
authors.lastname: Tekoppele
authors.forename: J W J
authors.initials: JW
authors.lastname: Bijlsma
authors.forename: F P J G
authors.initials: FP
authors.lastname: Lafeber
mesh_terms: D000818:Animals; D002358:Cartilage, Articular / Q000293:injuries* / Q000378:metabolism / Q000473:pathology; D004195:Disease Models, Animal; D004285:Dogs; D005260:Female; D007596:Joints; D010003:Osteoarthritis / Q000378:metabolism / Q000473:pathology*; D011509:Proteoglycans / Q000378:metabolism; D013583:Synovial Membrane / Q000473:pathology*; D013997:Time Factors
chemical_list: D011509:Proteoglycans