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Arthritis Research & Therapy

Open Access

Adenoviral transfer of murine OncostatinM induces inflammation and bone apposition in joints of IL-1, IL-6 and TNF-α deficient mice

  • ASK de Hooge1,
  • FAJ van de Loo1,
  • M Bennink1,
  • CD Richards2,
  • OJ Arntz1 and
  • WB van den Berg1
Arthritis Research & Therapy20024(Suppl 1):57

Received: 15 January 2002

Published: 4 February 2002


Rheumatoid ArthritisRheumatoid Arthritis PatientAdenoviral VectorEpiphyseal CartilageBone Apposition

The IL-6 family member OncostatinM (OSM) is expressed in the joints of rheumatoid arthritis patients. Murine OSM was expressed in the joints of naive wild-type mice by an adenoviral vector (AdmuOSM). This induced inflammation. Gene expression for IL-1, IL-6 and TNF-α were greatly enhanced in the inflamed synovium. To determine the role of these cytokines in the AdmuOSM induced inflammation, we injected this vector in IL-1, IL-6 or TNF-α knockout (ko) mice. Both IL-1 and TNF-α ko mice showed reduced acute inflammation. Inflammation at day 14, however, was not reduced compared to wild-type mice. AdmuOSM induced inflammation in IL-6 ko mice did not differ from wild-type inflammation. In all the mice examined, cartilage proteoglycan depletion occurred. Depletion of proteoglycans not only occurred in the articular, but also in the epiphyseal cartilage. Early during the inflammation, the periosteum became activated and new bone apposition took place along the femur and tibia. These results suggest an important and independent role for OSM in joint pathology. Furthermore, they show that overexpression leads to damage to the epiphysis and bone apposition.

Authors’ Affiliations

Rheumatology Research Laboratory, Nijmegen, The Netherlands
McMaster University, Hamilton, Canada


© BioMed Central Ltd 2002