Advertisement for orthosearch.org.uk
Results 1 - 2 of 2
Results per page:
Applied filters
Content I can access

Include Proceedings
Dates
Year From

Year To
Orthopaedic Proceedings
Vol. 94-B, Issue SUPP_III | Pages 49 - 49
1 Feb 2012
Wimsey S Lien C Sharma S Brennan P Harper G Gorecki D
Full Access

Introduction

Osteoarthritis (OA) has historically been thought of as a degenerative joint disease, but inflammation and angiogenesis are increasingly being recognised as contributing to the pathogenesis, symptoms and progression of OA. b-dystroglycan (b-DG) is a pivotal element of the transmembrane adhesion molecule involved in cell-extracellular matrix adhesion and angiogenesis. Matrix metalloproteinases (MMPs) are the main enzymes responsible for cartilage extracellular matrix breakdown and are also implicated in both angiogenesis and b-DG degradation in a number of malignancies. We aimed to investigate the expression and localisation of b-DG and MMP-3, -9, and -13 within cartilage, synovium and synovial fluid and establish their roles in the pathogenesis of OA.

Methods

Following ethical committee approval, cartilage, synovium and synovial fluid were obtained from the hip joints of 5 osteoarthritic (patients undergoing total hip replacement) and 5 control hip joints (patients undergoing hemiarthroplasty for femoral neck fracture). The samples were analysed for b-DG expression using Western Blotting and for the distribution of b-DG, MMP-3, -9, and -13 using immunohistochemistry on paraffin embedded tissue.


Orthopaedic Proceedings
Vol. 90-B, Issue SUPP_II | Pages 373 - 373
1 Jul 2008
Wimsey S Lien C Sharma S Brennan P Roach H Harper G Gorecki D
Full Access

Introduction: Osteoarthritis has historically been thought of as a degenerative joint disease, but inflam-mation and angiogenesis are increasingly being recognised as contributing to the pathogenesis, symptoms and progression of osteoarthritis. Beta-dystroglycan is a pivotal element of the transmembrane adhesion molecule involved in cell-extracellular matrix adhesion and angiogenesis. Matrix metalloproteinases are the main enzymes responsible for cartilage extracellular matrix breakdown and are also implicated in both angiogen-esis and beta-dystroglycan degradation in a number of malignancies. We aimed to investigate the expression and localisation of beta-dystroglycan and matrix metal-loproteinase 3, 9, and 13 within cartilage, synovium and synovial fluid and establish their roles in the pathogenesis of osteoarthritis.

Methods: Following ethical committee approval, cartilage, synovium and synovial fluid were obtained from the hip joints of 5 osteoarthritic (patients undergoing total hip replacement) and 5 control hip joints (patients undergoing hemiarthroplasty for femoral neck fracture). The samples were analysed for beta-dystroglycan expression using Western Blotting and for the distribution of beta-dystroglycan, matrix metalloproteinase 3, 9, and 13 using immunohistochemistry on paraffin embedded tissue.

Results: Whilst no significant expression of beta-dystro-glycan was found in cartilage or synovial fluid, beta-dys-troglycan was expressed in the smooth muscle of both normal and osteoarthritic synovial blood vessels. Moreover, beta-dystroglycan was expressed in endothelium of blood vessels of osteoarthritic synovium, but not in the normal endothelium. In the endothelium of osteo-arthritic synovial blood vessels, beta-dystroglycan co-localised with matrix metalloproteinase 3 and 9. Discussion: Our results demonstrate that beta-dystro-glycan does not act as a cell adhesion molecule binding chondrocytes to the extracellular matrix. However, specific immunolocalisation of beta-dystroglycan within endothelium of inflamed osteoarthritic blood vessels suggests that beta-dystroglycan may play a role in angiogenesis associated with osteoarthritis. Its co-localisation with matrix metalloproteinase 3 and 9, previously reported to also have pro-angiogenic roles, may be linked. Further research is required to understand these roles more fully.