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Review
. 2014 Feb;6(1):20-34.
doi: 10.1177/1759720X13514669.

Targeting the synovial angiogenesis as a novel treatment approach to osteoarthritis

Affiliations
Review

Targeting the synovial angiogenesis as a novel treatment approach to osteoarthritis

Yves Henrotin et al. Ther Adv Musculoskelet Dis. 2014 Feb.

Abstract

Synovitis is a key feature in osteoarthritis and is associated with symptom severity. Synovial membrane inflammation is secondary to cartilage degradation which occurs in the early stage and is located adjacent to cartilage damage. This inflammation is characterized by the invasion and activation of macrophages and lymphocytes, the release in the joint cavity of large amounts of pro-inflammatory and procatabolic mediators, and by a local increase of synovial membrane vascularity. This latter process plays an important role in the chronicity of the inflammatory reaction by facilitating the invasion of the synovium by immune cells. Therefore, synovial membrane angiogenesis represents a key target for the treatment of osteoarthritis. This paper is a narrative review of the literature referenced in PubMed during the past 5 years. It addresses in particular three questions. What are the mechanisms involved in synovium blood vessels invasion? Are current medications effective in controlling blood vessels formation and invasion? What are the perspectives of research in this area?

Keywords: angiogenesis; arthritis; synovium; vascularization.

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Conflict of interest statement

Conflict of interest statement: Y.H. is the founder and the chairman of the board of Artialis SA and Synolyne, two spin-off companies of the University of Liège. C.L. is supported by an unrestricted educational grant from Bioiberica.

Figures

Figure 1.
Figure 1.
Schematic representation of relationships between inflammation, angiogenesis and cartilage degradation in OA. Illustration courtesy of Alessandro Baliani. Copyright © 2014. Reproduced from Yves Henrotin’s personal slide. HIF, hypoxia-induced factor; IL, interleukin; MMP, matrix metalloprotease; NF-κB, nuclear factor-κB; NO, nitric oxide; PGE2, prostaglandin E2; ROS, reactive oxygen species; TSP, thrombospondin.
Figure 2.
Figure 2.
Macroscopic appearance of N/R (A) and I (B) synovial biopsies. Immunohistochemical detection of von Willebrand’s factor in N/R (C) and I (D) synovial biopsies. N/R and I synovial biopsies were stained with anti-von Willebrand factor antibody. The presented images are representative of the obtained results. Immunohistochemical detection of VEGF in N/R (E) and I (F) synovial biopsies. N/R and I synovial biopsies were stained with anti-VEGF antibody. The presented images are representative of the obtained results. Magnification ×20. I, inflammatory; N/R, normal/reactive; VEGF, vascular endothelial growth factor; (⇒), blood vessels; (→), intima lining.

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