The tissue architecture of synovial membranes in inflammatory and non-inflammatory joint diseases

Abstract
Utilizing monoclonal reagents directed towards antigens of the monocyte-macrophage lineage and Ia antigens, the tissue architecture of synovial membranes obtained from patients with non-inflammatory joint diseases and patients with rheumatoid arthritis was studied. Emphasis was placed on the localization of the type I, type II and type III synoviocytes that previously had been defined by their cell surface phenotype with regard to the expression of monocyte-macrophage lineage (Mθ) and Ia antigens as well as by their phagocytic capacity or the ability to produce glycosaminoglycans. In patients with non-inflammatory joint diseases, cells with the Mθ+ Ia+ (type I) phenotype constituted the majority of synoviocytes immediately adjacent to the joint cavity; cells with this phenotype were also scattered in the subsynovial tissue and in the perivascular regions. The fibroblastoid type III cells defined by the absence of both Mθ and Ia antigens formed the major cell population in the subsynovial tissue in this patient group. In patients with rheumatoid arthritis, the Ia++ cells were present in a characteristic double configuration forming an intensely positive layer adjacent to the intra-articular space followed by an Ia layer that again was succeeded by an intensely Ia++ layer. Large numbers of synoviocytes bearing Mθ+ Ia+ antigens were also demonstrated in the diffusely inflamed sub-synovial tissue, in the perivascular regions as well as around and within lymphoid infiltrates. The localization of type II cells defined by the presence of Ia antigens, but the absence of Mθ antigens was indicated to be primarily in the broadened layer of synoviocytes, in the perivascular regions and within lymphoid infiltrations. While endothelial cells lacked Ia and Mθ antigens in patients with non-inflammatory joint diseases, Ia+ endothelial cells were identified in some rheumatoid samples; however, the majority of endothelial cells was also Ia negative in this patient group.