Arthritis Treatment: Is Osteoarthritis Just Wear and Tear? No, And Here's Why!

Osteoarthritis (OA) is the most common form of arthritis affecting, according to the latest statistics from the Arthritis Foundation, about 28 million Americans.

OA has been primarily felt to be a disease of hyaline articular cartilage with secondary involvement of the synovium (lining of the joint), and subchondral bone (the bone underneath the cartilage.)

The antiquated notion of OA being a "wear and tear" disease has been supplanted by the new theory that OA is a combination of a mechanical wear process as well as an inflammatory process.

This has been supported by the fact that cartilage has no blood vessels nor does it have any nerves. Yet OA causes pain. This pain is felt to be due to inflammation involving the synovium. Cellular changes in flamed synovium in OA are not that dissimilar to the findings seen in rheumatoid arthritis.

In fact, it is the synovium that appears to drive much of the inflammation seen in OA. The synovium is lined by macrophages, cells that are potent producers of inflammatory cytokines- proteins that drive inflammation. The synovium is also rich in blood vessels and nerves.

Recent evidence though also supports the notion that chondrocytes (cartilage cells) also have a role in inflammation, this despite being relatively sparse, and located far away from blood vessels and nerves.

In fact, inflammation at the chondrocyte level might have a permissive effect on the inflammation involving the synovium... a sort of "ping-pong effect."

The question then becomes, what causes the chondrocyte inflammatory response to start in the first place. There have been reports that perhaps debris from dead cells or other protein based material originating from degraded cartilage might serve as antigens (protein triggers)to induce an inflammatory response by chondrocytes. Technically, this would be an autoimmune response by cartilage. This idea of OA being an autoimmune disease was described in an excellent editorial. Read this: (Konttinen Y, Sillat T, Barreto G, Ainola M, Nordstrom DC. Arthritis Rheum. 2012. 64: 613-616).

So why is this important to treatment? It may be that OA should be viewed in the same light as other autoimmune forms of arthritis. This might drive the investigation for OA specific therapies.

In addition, it is also recognized that cartilage has a limited ability to heal itself. It may be the newer techniques of providing mesenchymal stem cells to osteoarthritis cartilage as a method for helping cartilage to recover from injury might not be such a bad idea after all. It may be the underlying inflammation involving cartilage could actually help with the repair process.

Finally, a recent study showed that perhaps neurotransmitters can modulate the metabolic activity of chondrocytes. These substances might prove to be helpful in cartilage regeneration. An excellent discussion of this intriguing idea was recently published. For more details, read this: (Opolka A, Straub RH, Pasoldt A, Grifka J, Grassel S. Arthritis Rheum. 2012; 64: 729-739)