Different synovial vasculogenic profiles of primary, rapidly destructive and osteonecrosis-induced hip osteoarthritis. An immunohistochemistry study.

Abstract

To present a hypothesis regarding the pathways of angiogenesis in primary versus secondary hip osteoarthritis (OA). In synovial tissue samples provided by 57 consecutive patients who underwent hip arthroplasty, immunohistochemical examinations were performed using the following angiogenesis-related antibodies: VEGF-A, COX-2, maspin and the endothelial cells markers CD31 and CD105. The cases were divided into three categories: classic primary hip OA (group A; n = 16), rapidly destructive hip OA (group B; n = 24) and hip OA secondary to avascular osteonecrosis of the femoral head (group C; n = 17). The endothelial area (EA) was digitally quantified for both CD31 and CD105. The large mature vessels with CD105-positive activated endothelium predominated in group C, which also showed the highest CD105 median EA value (7.31 ± 4.01, compared to 4.76 ± 3.73 for group A and 6.69 ± 3.53 for group B). In groups A and B, synovial cell hyperplasia and the predominance of small immature vessels were characteristic. CD105, VEGF-A and COX-2 were focally seen in the synovial membrane, without maspin positivity. The severity of hip OA can be related to angiogenesis pathways that are not maspin-mediated. In primary hip OA, angiogenesis may be induced by a combined mechanism: hypoxia-related VEGF-dependent vasculogenesis and endothelial differentiation of the activated pluripotent cells, which are released from the hyperplastic synovial cells layer. An endothelial mesenchymal transition is assumed to be involved in the fibrotic process.