Corticosteroids (CS) are commonly administered by intra-articular injection to control the symptoms of osteoarthritis; however, CSs also suppress articular chondrocyte matrix synthesis. Both triamcinolone and methylprednisolone acetate significantly suppressed BMPs −2 and −7, and TGF-b1 expression, suggesting a mechanism by which CSs suppress articular chondrocyte matrix synthesis and cartilage homeostasis. Osteoarthritis (OA) is a common and debilitating disease that affects approximately 30% of the US population and is also a major clinical problem in companion animals. There are many drugs available to manage the symptoms of OA. Of these, intra-articular corticosteroid (CS) administration is a common and very effective anti-arthritic therapy, and is frequently administered to equine athletes. CSs exert their potent anti-inflammatory effects by blocking phospholipase A and reducing inflammatory mediator production; however, CSs also suppress matrix-biosynthetic activity of articular chondrocytes. This activity, along with ther increased joint use that symptomatic relief allows, has been linked to ‘steroid arthropathy’; a progression of arthritis driven by compromised chondrocyte homeostatic capacity. Several lines of experimental and clinical evidence emphasise the importance of TGF-b and BMP autocrine/paracrine activity in maintaining the homeostatic status of articular chondrocytes (reviewed in Oshin and Stewart 2007). This study was carried out to address the following objectives: 1) To assess the effects of CS on expression of chondro-protective TGF-β and BMP ligands in equine articular chondrocytes, and 2) To determine if exogenous BMP ligand administration can mitigate the suppressive effects of CSs on articular chondrocyte synthesis of collagen type II (Coll II) and glycosaminoglycans (sGAG).Summary
Introduction
