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Objective. To evaluate in vivo expression of chemokine receptors in cartilage tissue samples from healthy and diseased joints. Methods. Presence and distribution of several chemokine receptors in cartilage samples from patients with osteoarthritis (OA) or inflammatory arthritis (IA) and from multi-organ donors were assessed by immunohistochemistry. The expression of messenger RNA (mRNA) for chemokine receptors was also analysed by reverse transcriptase-polymerase chain reaction (RT-PCR). Results. Normal and OA-affected cartilage showed a moderate to high expression of chemokine receptors, while staining of IA samples ranged from low to absent. Differences between OA and IA samples were present for all receptors but CCR2 and CXCR4. Moreover, mRNAs for CCR1, CCR5 and CXCR1 were found both in normal and pathological chondrocytes, suggesting that chemokine receptor down-modulation seen in IA samples could be a post-transcriptional event. Conclusion. Data on normal and pathological chondrocytes underline the role of chemokines in cartilage homeostasis and suggest an imbalance towards catabolic processes in inflammatory conditions.

uman osteoarthritis (OA) is a heterogeneous andmultifactorialdiseasewithmultiplepathogeneticmech-anism implicated in its development and progression. Carti-lage degradation and loss are the major features of OA; de-generative changes include fibrillation, chondrocyteproliferation into cell clusters, and matrix disruption. Al-though biomechanical factors are strongly implicated, it isunclear which stimuli regulate the hyperactive phenotype ofOAchondrocytes,includingtheirabilitytoexpresscartilage-degradingproteinases(1).Recentstudieshaveimplicatedtheupregulation of several matrix-degrading metalloproteinases(MMPs)inOAcartilageandhavesuggestedthatchondrocyteproduction of MMPs in OA cartilage reflects local synthesisthat varies with the extent of cartilage degeneration. Thedemonstration of chondrocytes producing interleukin-1and tumor necrosis factor Theseverityofcartilagelesionshasbeenassessedusinganwithin the superficial zones ofOA cartilage supports the concept that cytokine-MMP asso-ciations contribute to a highly catabolic state, chondrocyteapoptosis, and the resultant progressive degeneration of ar-ticular cartilage (2-6).