Synovial mast cell responses during clinical improvement in early rheumatoid arthritis
- aInflammation Research Unit, Schools of Pathology and Medicine, University of New South Wales, Australia, bDepartment of Rheumatology, Prince of Wales Hospital, Sydney, Australia, cRheumatology Research Unit, Repatriation General Hospital, Daw Park, Adelaide, Australia
- Dr H P McNeil, School of Pathology, University of New South Wales, Sydney, Australia 2052.
- Accepted 15 July 1998
Abstract
OBJECTIVES To determine the synovial mast cell response in early rheumatoid arthritis (RA) during clinical improvement, and to examine for relations with clinical and histological parameters of disease activity.
METHODS Twenty two synovial samples were obtained from six patients with RA using needle arthroscopy. The mean disease duration at baseline was eight months, and two to three further samples were obtained over a mean follow up period of 15 months during which treatment initiated clinical improvement occurred. Sections were immunostained to detect MCT and MCTC mast cells and correlations were sought between clinical and histological data.
RESULTS The overall mean synovial mast cell density was 40.3 cells/mm2, with regional densities of 60.6 and 34.2 mast cells/mm2 in the superficial and deeper synovial layers respectively. The MCT subset predominated, outnumbering MCTC by 3:1. There was a significant correlation between the histological inflammation index and the MCT density, (r = 0.4, p < 0.05) but not the MCTC subset. The regional distribution and predominant subset of mast cells varied in individual patient’s synovia over time, with a trend towards restriction of the mast cell response to the superficial synovium during clinical improvement.
CONCLUSIONS The mast cell response in early RA is characterised by substantial expansion of predominantly MCTmast cells that correlates with histological indices of inflammation. During clinical improvement, this expansion tended to become more superficial. Taken together with previous studies of long duration RA, which implicate MCTC cells in synovial damage and disease progression, these results suggest that MCT and MCTC mast cells may possess distinct functions in the spectrum of inflammatory events occurring during RA.
