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FRI0314 Aetiology of experimentally induced osteoarthritis of the knee; biomechanical or biochemical factors?
  1. K. Wiegant1,2,
  2. M. Beekhuizen2,
  3. S.C. Mastbergen1,
  4. A.D. Barten-van Rijbroek1,
  5. L.B. Creemers2,
  6. D.B. Saris2,
  7. F.P. Lafeber1
  1. 1Rheumatology & Clinical Immunology
  2. 2Orthopaedics, University Medical Center Utrecht, Utrecht, Netherlands

Abstract

Background At the moment, osteoarthritis (OA) is seen as a multifactorial disease, caused by a combination of i.a. genetics, overloading, obesity and trauma in the past. Disturbance of joint homeostasis, due to several risk factors, can also cause OA1. In the present study we investigated the role of biomechanical loading and biochemical joint homeostasis in the development of osteoarthritis, in an experimental caprine model of joint damage.

Objectives Is the development of experimentally induced OA more due to changed biomechanics or is it due to a changed joint homeostasis?

Methods In nine skeletally mature female milk goats, cartilage damage was introduced in the right stifle joint according to the Groove model2. Grooves were made with a K-wire with a bend tip, only on the medial femoral condyle and maximally 0.5mm deep; preventing the subchondral plate from damage. The left stifle joint served as a control. After 20 weeks the goats were sacrificed and the cartilage and synovial tissue was analyzed on macroscopical, histological (both OARSI goat score) and biochemical (proteoglycan (PG) turnover) OA characteristics.

Results Macroscopic analysis showed a significant increase in the OARSI goat cartilage score for both the femoral and tibial experimental medial compartment compared to control (femur and tibia; +225% p<0.001 and +42.9% p<0.04 respectively). No effect on the ungrooved lateral compartment was seen. The histological analysis of the cartilage corroborated these results. A significant increase in the OARSI score for the experimental medial compartment (+225% p<0.001 and +81,7% p<0.006, respectively for femur and tibia) was seen. Biochemical analysis showed a decreased PG content in the medial experimental compartment compared to control (femur -12.1% p=0.038 and tibia -7.3% p=0.031). There was a slight increase in synovial inflammation in the experimental joint (p<0.003). For all previous mentioned analyses, no changes in the experimental lateral compartment or the control joint were found.

Conclusions The present study shows clearly that the development of joint damage is much more dependent on the biomechanical component, since all detectable damage is in the medial compartment. Although joint homeostasis is disturbed, indicated by moderate synovial inflammation, this did not lead to generalised OA in this time period.

  1. Abramson et al. Arthritis Res Ther. 2009.

  2. Mastbergen et al. Osteoarthritis and Cartilage 2006.

Disclosure of Interest None Declared

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