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SYNOVIAL FLUID AND MEMBRANE CYTOLOGY IN INFLAMMATORY OSTEOARTHRITIS OF THE KNEE – A PREDICTOR FOR UNICOMPARTMENTAL OR TOTAL KNEE ARTHROPLASTY



Abstract

Inflammatory changes in synovial tissues occur commonly in knee osteoarthritis (OA) and are termed “inflammatory OA”. The pathogenic significance of this inflammatory OA is uncertain. It is also not known whether inflammatory changes in the synovial membrane are reflected in the synovial fluid (SF) and whether the SF contains a similar inflammatory cell infiltrate.

This study examined 34 cases of knee joint OA and cytologically and immunohistochemically characterised inflammatory cells in the synovial membrane and SF. Specimens of SF and synovial membrane were taken at the time of knee arthroplasty.

All cases of inflammatory OA synovium contained (CD68+) macrophages; several cases also contained a scattered, focally heavy (CD3+) lymphocytic infiltrate and occasional lymphoid aggregates. Inflammatory changes in OA SF reflected this cell composition with numerous CD68+ macrophages and CD3+ lymphocytes being noted in inflammatory OA cases. The SF volume was greater (> 5ml) in cases of inflammatory OA. Non-inflammatory OA knee joints contained very few inflammatory cells, which were mainly macrophages, in both the synovial membrane and SF.

Our findings indicate that inflammatory changes in the synovial membrane of OA knee joints are reflected in the SF and that the volume of SF is commonly increased in cases of inflammatory OA. Both macrophages and lymphocytes in the inflammatory infiltrate of knee joint SF may contribute to joint destruction in OA by providing mononuclear phagocyte osteoclast precursors and the production of inflammatory cytokines and growth factors that promote osteoclastogenesis.

In conclusion, the cytology of SF and synovitic membrane are similar in inflammatory OA. With knee effusions of greater than 5mls and inflammatory synovitic membrane consideration of total knee arthoplasty in the presence of single compartment disease should be considered because of the risk of further joint destruction.

Correspondence should be addressed to: BASK c/o BOA, at the Royal College of Surgeons, 35–43 Lincoln’s Inn Fields, London, WC2A 3PE, England.