In OA cartilage pathology, which enzyme activity is increased?

In OA cartilage pathology, which enzyme activity is increased?

• A. Increased activity of lysosomal hydrolases
• B. Increased activity of matrix metalloproteinases and ADAMTS enzymes
• C. Increased activity of alkaline phosphatase
• D. Decreased activity of collagenases

Answer: (B)

In osteoarthritis, cartilage destruction is driven by an upregulation of catabolic enzymes that break down the extracellular matrix. The most important players are matrix metalloproteinases and ADAMTS proteases. MMPs, such as MMP-1, MMP-3, and especially MMP-13, attack the collagenous framework of type II collagen in cartilage, weakening the fibrous scaffold. ADAMTS enzymes, particularly ADAMTS-4 and ADAMTS-5, target aggrecan, the major proteoglycan that provides compressive resistance. When these enzymes are increased, the matrix is degraded more quickly than it can be rebuilt, leading to cartilage thinning, fissuring, and loss of integrity. Briefly, lysosomal hydrolases are not the primary drivers of extracellular matrix destruction in OA cartilage, alkaline phosphatase relates more to bone mineralization and turnover rather than cartilage degradation, and decreased collagenase activity would oppose the actual cartilage breakdown seen in OA.

In osteoarthritis, cartilage destruction is driven by an upregulation of catabolic enzymes that break down the extracellular matrix. The most important players are matrix metalloproteinases and ADAMTS proteases. MMPs, such as MMP-1, MMP-3, and especially MMP-13, attack the collagenous framework of type II collagen in cartilage, weakening the fibrous scaffold. ADAMTS enzymes, particularly ADAMTS-4 and ADAMTS-5, target aggrecan, the major proteoglycan that provides compressive resistance. When these enzymes are increased, the matrix is degraded more quickly than it can be rebuilt, leading to cartilage thinning, fissuring, and loss of integrity.

Briefly, lysosomal hydrolases are not the primary drivers of extracellular matrix destruction in OA cartilage, alkaline phosphatase relates more to bone mineralization and turnover rather than cartilage degradation, and decreased collagenase activity would oppose the actual cartilage breakdown seen in OA.