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Synovial Membrane Cellularity and Vascularity Ann Rheum Dis: First Published As 10.1136/Ard.54.6.511 on 1 June 1995

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Synovial Membrane Cellularity and Vascularity Ann Rheum Dis: First Published As 10.1136/Ard.54.6.511 on 1 June 1995 Annals ofthe Rheumatic Diseases 1995; 54: 511-515 51 Synovial membrane cellularity and vascularity Ann Rheum Dis: first published as 10.1136/ard.54.6.511 on 1 June 1995. Downloaded from Oliver FitzGerald, Barry Bresnihan Studies of the synovial membrane in joint vascularity is seen, depending on the type of inflammation, over many years, have proven of membrane surface. mixed benefit: while it is rarely of diagnostic The cartilage-pannus junction, important in value, clues to understanding the mechanisms the development of joint erosion, has also been involved both in the initiation and main- studied carefully in normal samples. Allard tenance of the inflammatory response have et al analysed the cellular composition both of been uncovered. While the path to under- the cells adjacent to bone and of the cells standing is fraught with difficulty, progress is contained in the layer of tissue which extends slowly being made and, it is hoped, will lead over and merges with the cartilage, lining the in turn to novel and better treatment joint cavity.7 Adjacent to bone, the cells stain approaches. This review of synovial membrane predominantly with the monocyte/macrophage cellularity and vascularity will describe our marker 63D3; in contrast, those cells lining the current understanding of the pathways to joint joint cavity express the monoclonal antibody damage. 67, thought to be a marker for material surrounding type B synoviocytes.8 Normal celiularity and vascularity Normal synovial tissue is characterised by a Synovial membrane in early rheumatoid surface layer of cells, or intima, below which is arthritis a loose connective tissue which contains fibro- Most of the studies of rheumatoid arthritis blasts, macrophages, adipocytes, mast cells, (RA) synovial membrane have been performed nerve fibres, vascular endothelial cells, and on samples obtained from patients with long occasional polymorphs and lymphocytes.' The established disease, largely at arthroplasty. intima contains two or possibly three cell types. There have only been a few studies in early Type A cells are of bone marrow origin and disease, when samples are more likely to reflect conform to the ultrastructural criteria for factors important in disease initiation rather monocyte derived macrophages. They express than those contributing to chronicity. http://ard.bmj.com/ macrophage markers including CD68 and Schumacher and Kitridou described 24 CD 14 and also stain with non-specific patients with synovitis of recent onset, six of esterase.2 Type B cells are fibroblastic in type whom developed RA.9 They described variable and can be distinguished cytochemically and (< 10 cells in depth) lining cell proliferation immunochemically from fibroblasts deeper in with largely a perivascular lymphocytic the tissues. Being involved in collagen infiltration. There were prominent vascular the synthesis, they express ,B subunit of the changes, but no lymphoid follicles and only on September 27, 2021 by guest. Protected copyright. enzyme prolyl hydroxylase.3 They are distinct occasional polymorphs were observed. The in terms of their ability to express uridine intensity of the inflammation did not appear to diphosphoglucose dehydrogenase (UDPGD) correlate with the disease duration. Lindblad which is an important enzyme involved in et al also studied arthroscopic biopsies from a hyaluronan synthesis-a specialised synovial small number of RA patients with disease membrane function.3 The constitutive duration between nine months and five years.'0 expression of vascular cell adhesion molecule Again, lining layer thickening was observed, (VCAM)-1 by type B synoviocytes is also an with cells positive for both OKM1 and OKT9, important distinguishing feature not shared by suggestive ofmacrophage infiltration and acute fibroblastic cells elsewhere in the synovial proliferation. The sublining cells were largely membrane.4 The exact function of this of the helper T lymphocyte phenotype and VCAM- 1 expression remains a matter of focal aggregates of B cells were also seen. speculation, but it suggests a role in trapping More recent studies from our own group of cells within the lining layer. The third type of 11 RA patients with a mean disease duration intimal cell is dendritic in type, accounts for of 22 months have quantified the cellular Department of Rheumatology, < 1% of the total, is CD68 negative but infiltrate." Again, variable lining layer thick- St Vincent's Hospital expresses the class II related marker, RFDIL. ening was seen (mean 4 cells in depth; and University Studies on synovial vascularity date back to range 2-32). In the sublining, 10 of the 11 College, Dublin 1743, when Hunter described the plexus of patients had a diffuse mononuclear infiltrate 0 FitzGerald vessels which supplied the synovial membrane comprising predominantly CD 14 macro- B Bresnihan and which he called the circulus articuli phages and CD5 T lymphocytes, with roughly Correspondence to: vasculosus. A more recent detailed study of equal numbers of CD4 and CD8 cells. Small Dr 0 FitzGerald, Department of normal synovial membrane has highlighted the numbers of B cells and plasma cells were also Rheumatology, high frequency of capillaries, with a peak seen. Thus lining layer thickening, vascular St Vincent's Hospital, Elm Park, density just below the lining layer between 6 proliferation and a diffuse sublining infiltrate Dublin 4, Ireland. and 11 ,um deep.6 Considerable variation in made up of macrophages, T lymphocytes, 512 FitzGerald, Bresnihan more CD4 than CD8, and a small number of with a shorter duration of disease, it may be B cells, appear to be typical features of the that E-selectin expression is more upregulated involved synovial membrane in early RA. in early disease, ICAM-1 then correlating with Ann Rheum Dis: first published as 10.1136/ard.54.6.511 on 1 June 1995. Downloaded from The examination of synovial membrane the intensity of the inflammatory response. obtained from clinically uninvolved joints is another approach to exploring changes early in the disease. The clinically uninvolved joint is Synovial membrane in established RA histologically involved, though there is less Most studies of RA synovial membrane have lining layer hyperplasia and fewer mononuclear been performed on samples obtained at joint cells infiltrate the sublining compared with the arthroplasty. While the immunohistological involved joint.'2 In a further study, a vascular findings in established disease are not dis- proliferation index and a high endothelial similar from those seen earlier on, the mono- venule (HEV)-index were calculated both in nuclear infiltrate is focal in about 70%, the clinically involved and clinically uninvolved compared with about 10% ofbiopsy samples.20 RA samples, in addition to postmortem Duke et al described four different patterns of controls.'3 Of interest, vascular proliferation infiltrate: scattered/diffuse, perivascular, lym- was not a feature of the uninvolved joint, and phoid follicles and germinal centres.2' HEV-type vessels, readily seen in actively Kurosaka and Ziff went on to study the infil- inflamed joints, were also not observed. This trates in more detail, and described lympho- suggests that vascular changes, which may cyte rich areas where most cells stained positive determine the rate of mononuclear trafficking, for OKT4, and more peripheral transitional are important in the clinical expression of joint areas containing plasma cells, macrophages, inflammation in early RA. and both OKT4 positive and OKT8 positive lymphocytes.22 More recently, Yanni et al analysed lymphoid infiltrates of different sizes Adhesion molecule expression in RA and found that the composition of each aggre- The receptor-ligand pairs important in the gate depended on the total number of mono- control of mononuclear trafficking into the nuclear cells it contained:23 large aggregates synovial membrane have been the subject of a contained a substantial number of B cells and number of recent studies.'1'6 The important cells bearing the CD45RA phenotype; in adhesion molecules expressed on the endo- contrast, small aggregates contained few B cells thelium include E-selectin, which plays a and relatively larger numbers ofT cells bearing role in the initial margination and rolling of CD8 and CD45RO. leucocytes, and both intracellular adhesion Lining layer thickening is also a prominent molecule-i (ICAM-1) and VCAM-1, which feature of established RA. Considerable are involved in leucocyte adhesion and controversy exists as to whether this thickening penetration through the endothelial junctions. is a result of macrophage recruitment or of http://ard.bmj.com/ Studies ofRA synovial membrane by our group synoviocyte proliferation. In favour of recruit- and others have shown E-selectin expression to ment, mitotic cells are rarely seen, and staining be vessel specific, the majority of vessels for the proliferation marker Ki-67 is not staining positive, particularly in the superficial observed in RA synovial membrane.24 In synovial membrane.'7 ICAM-1 expression addition, lining layer cells express a wide range is not vessel specific, cells in the lining and of macrophage antigens, and after lethal within the mononuclear infiltrates also irradiation and heterologous bone marrow on September 27, 2021 by guest. Protected copyright. staining positive. Perhaps surprisingly, vascular transplantation, the synovial macrophages are VCAM- 1 expression is either minimal or replaced by cells of bone marrow donor absent, depending
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