No abstract

Interleukin-1,, interleukin-2, tumour necrosis factor a, and the interferons, alfa and gamma, were measured concurrently in synovial fluid samples from 68 patients with rheumatic diseases. Mean interleukin-1r concentrations (130.3 (SD 22) pg/mI) were higher in synovial fluids from patients with rheumatoid arthritis (RA) than in those from patients with osteoarthritis (27-8 (4.5) pg/ml), while measurements in synovial fluids from patients with seronegative spondarthritis were intermediate (72-7 (32) pg/ml). Interleukin-2 and tumour necrosis factor a concentrations were lower in the inflammatory arthropathies (RA: 4-5 (0.6) U/mI, 0.39 (0.04) ng/ml; seronegative spondarthritis: 3-1 (0.3) U/ml, 0-33 (0-03) ng/ml respectively) than those in patients with osteoarthritis (5-2 (0.6) U/mI; 0.05 (0.04) ng/ml). Interleukin-2 and tumour necrosis factor a concentrations correlated in all groups (r=0-7), as did the interferons alfa and gamma (r=0-7). There was no relation between interleukin-l6 and either interleukin-2 or tumour necrosis factor a, or between the interferons and any other cytokine. Several distinct cytokine patterns were noted. Synovial fluids from two non-arthritic subjects were also examined: interleukin-l,B concentrations were low, but concentrations of the other cytokines were higher than those seen in most arthritic fluids.

Variations in chondrocyte TNF-R expression occur in OA cartilage in vivo. TNFalpha at concentrations produced by OA synovium in vitro, can degrade cartilage matrix. In most OA supernatants sTNF-R concentrations were insufficient to abrogate the effects of TNFalpha. Thus conditions exist in some OA knees for TNFalpha to contribute to focal loss of cartilage.

Objective. To determine whether bone cells alter cartilage metabolism.Methods. Bone cell cultures were established using explants obtained from the hip and knee joints of 9 patients with osteoarthritis (OA) and 6 subjects without arthritis (nonarthritic "A]). NA human cartilage biopsy samples were incubated in the presence or absence of bone-derived cells, and the effects on glycosaminoglycan (GAG) release from cartilage were measured.Results. Bone cell cultures secreted osteocalcin (OC) and did not contain cells expressing leukocyte common antigen. None of the 8 cultures established from NA bone, compared with 17 of 32 from OA bone, significantly altered GAG release from cartilage (P = 0.006). In knees with medial joint damage, 38% of the cultures derived from the medial side of the joint increased GAG release from cartilage. In contrast, 77% of the cultures derived from the lateral side of the joint had an effect on GAG, with 38% increasing and 38% decreasing GAG release. Seven cytokines were measured in OA bone cell supernatants. No significant difference was apparent in the concentration of any one cytokine when supernatants were compared according to their effects on GAG release.Conclusion. Bone cells from OA patients can influence cartilage metabolism. This might explain why increased subchondral bone activity can predict cartilage loss.

Bone cells from OA patients can influence cartilage metabolism. This might explain why increased subchondral bone activity can predict cartilage loss.