Objective. To quantify the relationship between inflammation and angiogenesis in synovial tissue from patients with osteoarthritis (OA).Methods. Hematoxylin and eosin staining and histologic grading for inflammation were performed for 104 patients who met the American College of Rheumatology criteria for OA and had undergone total joint replacement or arthroscopy. A purposive sample of synovial specimens obtained from 70 patients was used for further analysis. Vascular endothelium, endothelial cell (EC) proliferating nuclei, macrophages, and vascular endothelial growth factor (VEGF) were detected by immunohistochemical analysis. Angiogenesis (EC proliferation, EC fractional area), macrophage fractional area, and VEGF immunoreactivity were measured using computer-assisted image analysis. Double immunofluorescence histochemical analysis was used to determine the cellular localization of VEGF. Radiographic scores for joint space narrowing and osteophyte formation in the knee were also assessed.Results. Synovial tissue samples from 32 (31%) of 104 patients with OA showed severe inflammation; thickened intimal lining and associated lymphoid aggregates were often observed. The EC fractional area, EC proliferation, and VEGF immunoreactivity all increased with increasing histologic inflammation grade and increasing macrophage fractional area. In the synovial intimal lining, VEGF immunoreactivity was localized to macrophages and increased with increasing EC fractional area and angiogenesis. No inflammation or angiogenic indices were significantly correlated with radiographic scores.

Introduction InflammationInflammation is a response of vascularised tissue to sublethal injury [1]. Inflammation can be classified according to duration as either acute or chronic. In acute inflammation, changes in small blood vessels result in fluid and granulocytic cells accumulating at the site of injury. This reaction may trigger a systemic response such as fever, leucocytosis, protein catabolism, and altered hepatic synthesis of plasma proteins such as C-reactive protein.Chronic inflammation is characterised by tissue infiltration by macrophages and lymphocytes.Inflammation may be considered a homeostatic response designed to destroy or inactivate invading pathogens, remove waste and debris, and permit restoration of normal function, either through resolution or repair. Tissue structure is normal after resolution, whereas repair leads to a functional, but morphologically altered, organ. In acute inflammation, tissue damage is followed by resolution, whereas in chronic inflammation, damage and repair continue concurrently. The initial inflammatory response is usually acute, and may or may not evolve into chronic inflammation. However, chronic inflammation is not always preceded by an acute phase. Although usually beneficial to the organism, inflammation itself may lead to tissue damage, resulting in escalation of chronic inflammation. AngiogenesisAngiogenesis is the growth of new capillary blood vessels from pre-existing vasculature [2]. It is a fundamental process required for embryogenesis, growth, tissue repair after injury, and the female reproductive cycle. It may also contribute to the pathology of conditions such as cancer, psoriasis, diabetic retinopathy, and chronic inflammatory diseases in joints or lungs. Angiogenesis is stimulated Review Angiogenesis in the pathogenesis of inflammatory joint and lung diseases AbstractThis paper reviews hypotheses