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Review
. 2001;3(3):147-53.
doi: 10.1186/ar292. Epub 2001 Feb 23.

Angiogenesis in the pathogenesis of inflammatory joint and lung diseases

Affiliations
Review

Angiogenesis in the pathogenesis of inflammatory joint and lung diseases

D A Walsh et al. Arthritis Res. 2001.

Abstract

This paper reviews hypotheses about roles of angiogenesis in the pathogenesis of inflammatory disease in two organs, the synovial joint and the lung. Neovascularisation is a fundamental process for growth and tissue repair after injury. Nevertheless, it may contribute to a variety of chronic inflammatory diseases, including rheumatoid arthritis, osteoarthritis, asthma, and pulmonary fibrosis. Inflammation can promote angiogenesis, and new vessels may enhance tissue inflammation. Angiogenesis in inflammatory disease may also contribute to tissue growth, disordered tissue perfusion, abnormal ossification, and enhanced responses to normal or pathological stimuli. Angiogenesis inhibitors may reduce inflammation and may also help to restore appropriate tissue structure and function.

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Figures

Figure 1
Figure 1
Vascular plasticity in rheumatoid arthritis and osteoarthritis. (a) Vascular distribution in the normal joint. Blood vessels in the synovium (s) are highly organised, with larger vessels sparsely distributed in the sublining region, branching to form dense microvascular networks adjacent to the synovial surface and capsule (cap). An additional vascular network in the subchondral bone (b) does not normally cross into the articular cartilage (cart), which remains avascular. (b) In rheumatoid arthritis (RA), hyperplastic synovial pannus (p) attaches to and invades articular cartilage and adjacent bone. The synovial vascular network is reorganised, leading to reduced vascular densities adjacent to the joint space and increased vascular densities in the deeper synovium. Similar changes in vascular organisation occur in the synovium in osteoarthritis (OA). However, rather than destruction of bone and cartilage by pannus, vascular invasion of cartilage in the developing osteophyte (o) and at the osteochondral junction may lead to advancing endochondral ossification. Innervation of new vessels by fine, unmyelinated sensory nerves may contribute to increased pain sensation.

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