ABERRANT VASCULARITY AND VON-WILLEBRAND-FACTOR DISTRIBUTION IN INFLAMED SYNOVIAL-MEMBRANE

Objective. Von Willebrand factor (VWF) is an adhesive glycoprotein pro duced and secreted constitutively by endothelial cells. vWF is release d upon endothelial stimulation and/or vascular injury, and mediates ad hesion and aggregation of platelets. Our aim was to quantify synovial vasculature and to evaluate vWF distribution in situ in synovial membr anes in various arthritides. Methods. Immunohistochemical staining of VWF in synovial membranes from patients with rheumatoid arthritis (RA) (N = 9), psoriatic (PsA) (N = 3), and reactive (ReA) (N = 4) arthriti s, and from 6 noninflammatory controls: osteoarthritis (N = 1), chondr omatosis (N = 1), meniscus lesion (N = 4). Morphometric assessments we re performed with an image analyzer. Results. In RA, mean number of bl ood vessels/mm(2) in the thickened synovium was relatively low (131 +/ - 57 vs control 257 +/- 115, p = 0.0137, ReA 346 +/- 83, p = 0.0002, P sA 434 +/- 157, p = 0.0127). In particular, the superficial layer, cor responding to the thickness of normal synovial membrane (i.e., 56 +/- 5 mu m), was sparsely vascularized (70 +/- 37 in the superficial vs 21 9 +/- 104 in the deeper layer, p = 0.0047). Synovial thickening was no t seen in ReA and PsA, In accordance with its constitutive metabolism, vWF was found in the endothelial cells, inside the blood vessels, and in the subendothelium. In addition, RA was characterized by weak endo thelial immunoreactivity and perivascular vWF. In ReA, perivascular vW F staining was visible in areas of inflammatory cell infiltrates. Conc lusion. Morphometric findings indicate decreased vascularization of th e superficial synovial membrane in RA. Second, vWF may play a role in the inflammatory/reparative responses in synovium in RA and ReA, which were characterized by vascular stimulation/injury and abnormal VWF di stribution.