Abstract
Knee osteoarthritis (OA) is a condition mainly characterized by cartilage degradation. Currently, no effective treatment exists to slow down the progression of OA-related cartilage damage. Selective COX-2 inhibitors may, next to their pain killing properties, act chondroprotective in vivo. To determine whether the route of administration is important for the efficacy of the chondroprotective properties of selective COX-2 inhibitors, a systematic review was performed according to the PRISMA guidelines. Studies investigating OA-related cartilage damage of selective COX-2 inhibitors in vivo were included. Nine of the fourteen preclinical studies demonstrated chondroprotective effects of selective COX-2 inhibitors using systemic administration. Five clinical studies were included and, although in general non-randomized, failed to demonstrate chondroprotective actions of oral selective COX-2 inhibitors. All of the four preclinical studies using bolus intra-articular injections demonstrated chondroprotective actions, while one of the three preclinical studies using a slow release system demonstrated chondroprotective actions. Despite the limited evidence in clinical studies that have used the oral administration route, there seems to be a preclinical basis for considering selective COX-2 inhibitors as disease modifying osteoarthritis drugs when used intra-articularly. Intra-articularly injected selective COX-2 inhibitors may hold the potential to provide chondroprotective effects in vivo in clinical studies.
Highlights
Knee osteoarthritis (OA) is a condition that leads to pain and is mainly characterized by cartilage degradation [1]
We identified preclinical and clinical studies investigating chondroprotective actions of selective COX-2 inhibitors either via systemic administration or via intra-articular delivery
To date there is conflicting evidence regarding the ability of selective COX-2 inhibitors to be used as disease modifying osteoarthritis drug (DMOAD)
Summary
Knee osteoarthritis (OA) is a condition that leads to pain and is mainly characterized by cartilage degradation [1]. NSAIDs provide pain relief by blocking cyclooxygenase (COX)-dependent prostanoid synthesis. Selective COX-2 inhibitors have been developed to target the inflammatory COX-2 while circumventing inhibition of the COX-1 isoform. While selective COX-2 inhibitors may provide an effective means for pain relief, targeting the inflammatory COX-2 may be a promising approach to inhibit cartilage degradation and thereby slow down knee OA progression [3]. This hypothesis is supported by the accumulating evidence showing that inflammation precedes OA disease progression [3,4]
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