Intra-articular injection of rhFGF-18 improves the healing in microfracture treated chondral defects in an ovine model.

Microfracture is a common cartilage repair procedure. Strategies to improve healing post-microfracture include the use of growth factors to enhance hyaline cartilage production. This study investigates the effect of intra-articular recombinant human fibroblastic growth factor 18 (rhFHF18) on the healing of a chondral defect treated with microfracture in an ovine model. Chondral defects (8 mm diameter) were created in the medial femoral condyle of 80 sheep (n = 16/treatment group). Defects were treated with microfracture alone or microfracture + intra-articular rhFGF-18 (administered either as one or two cycles of 3× weekly injections). Outcome measures included mechanical testing, macroscopic International Cartilage Repair Society repair score, modified O'Driscoll histology score, qualitative histology, and immunohistochemistry for types I, II, and VI collagen. In treated animals, there was a statistically significant improvement in ICRS tissue repair score and tissue infill score, in the modified O'Driscoll score between control and 1 cycle of rhFGF-18 at 6 m, and in the cartilage repair score and structural characteristic score between the control and both rhFGF-18 groups at 6 m. There was no evidence of degeneration of adjacent cartilage in the rhFGF-18 treated cartilage. The increase in hyaline cartilage-like tissue formed in the microfracture + rhFGF-18 treated groups indicates that rhFGF-18 potentiates the formation of hyaline cartilage repair following microfracture.

Alterations in sclerostin protein in lesions of equine osteochondrosis.

Osteochondrosis (OC) is a common and clinically important joint disease that occurs in many species, including humans, pigs, chickens and horses. It has been described as a focal failure of endochondral ossification (EO), but no cellular/molecular mechanisms are fully described that explain the cause of this condition. Recently a Wnt signalling inhibitor, sclerostin, has been described in osteoarthritic cartilage, where it has been proposed to protect damaged cartilage from degradation. Cartilage degradation is a key event in EO, thus, abnormalities of sclerostin in growth cartilage could, potentially, lead to a failure of EO and, thus, OC. The aim of this study was to describe the distribution of sclerostin protein in normal and OC growth cartilage. Immunohistochemistry (IHC) was used to localise sclerostin protein in normal and OC growth cartilage. Growth cartilage was harvested from the distal femur of horses aged between 6 and 18 months. Cartilage was classified as normal or having lesions consistent with a diagnosis of early OC. IHC was used to identify sclerostin protein in cartilage sections. Sclerostin protein distribution was semiquantified using a grading system and shown to be upregulated throughout all three zones of cartilage in lesions of OC (IHC score 8.1 compared to IHC score of 0.88). These results indicate that sclerostin may be contributing to the development of OC lesions by inhibiting extracellular matrix remodelling or may reflect the response of damaged cartilage. Clearly, further work is required to fully characterise this observation but, with antisclerostin antibodies used to treat human osteoporosis, the possibility of development of a systemic treatment of OC remains a potential goal.