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While specific inhibition of COX-2 with celecoxib alone was sufficient to cause increased utilization of arachidonate by the lipoxygenase pathway, increases of LTB4 production were even greater in the presence of indomethacin, suggesting that the inhibition of both COX-1 and COX-2 provided more arachidonate substrate for metabolism by the lipoxygenase pathway.
It seems OA chondrocytes, much like activated macrophage and monocytes produce a broad spectrum of products derived from both the cyclooxygenase and lipoxygenase pathways consistent with our hypothesis.