A New Theory on Hip Osteoarthritis

Hip Impingement and Arthritis, new evidence for a connection?

An X-ray showing hip arthritis.
An X-ray showing hip arthritis. ZEPHYR/Getty Images

Hip osteoarthritis (OA) is traditionally thought of as the result of wear and tear on the joints. It’s often presented as a combination of bad luck and the result of too much use and abuse on the cartilage. That may not paint the entire picture. A big component of hip OA is genetics, which we briefly reviewed in a prior article. Our understanding of the causes of OA is rapidly increasing and a number of interesting theories are now gaining traction.

 Two key areas of research in hip OA are the mechanics that may predispose a hip joint to developing arthritis, and the second is a focus on the biochemical processes that lead to cartilage degeneration and erosion. Recent research published in the Journal of Bone and Joint Surgery combines these two research focuses and presents an important step forward in our understanding of hip OA.

Before we move further let’s briefly discuss the anatomy of the hip joint, and the 10,000ft overview of the biology of arthritis. The hip joint is made of a ball, the femoral head, and a cup or socket which is referred to as the acetabulum. Both the femoral head and acetabulum are lined with cartilage. Cartilage is an amazing material which has the ability to glide with minimum friction; it is 100 times more slippery than ice.

The downside of cartilage is that once damaged it does not heal well, as a matter of fact it doesn’t heal at all and the only thing our body can do is replace it with a worse quality material called fibrocartilage.

  Osteoarthritis leads to destruction of cartilage. This is mostly due to inflammation within the effected joint. Inflammation leads to activation of small molecules that can eat away cartilage.

A few mechanical factors have been described that pre-dispose a hip joint to developing osteoarthritis. One of such factors is when the femoral head (the ball) does not have a good fit with the acetabular cup (socket).

This can happen because the femoral head is not round, or the socket is too deep. The term for this condition is femoroacetabular impingement or FAI. While FAI is widely accepted as a common cause of hip pain in the younger active patient, the link between FAI and OA is still tenuous. Recent research provides an important stepping-stone in providing a potential mechanism for how FAI can lead to hip OA.

Researchers in Japan analyzed tissue samples of patients with OA and others with FAI for expression of genes for inflammatory molecules and other molecules related to the break down of cartilage. They analyzed a total of 60 patients, 30 with FAI and 30 with OA. Their data found that cartilage in the FAI group had more gene expressed for inflammatory molecules and molecules that break down cartilage compared to patients with OA. This suggests that a high level of inflammation is present is people with FAI, and molecules that have been linked to destruction of cartilage are quite active. The researchers also found that the expression of cartilage destructive molecules was higher in patients with hips that were less round, so the larger the FAI lesion the more cartilage digesting molecules would be expressed.

Overall this is a very early step in providing a mechanism by which FAI predisposes people to developing OA. The researchers in the above study believe that the cartilage in the hip joint of a patient with FAI is injured because there is a mismatch between the shape of the ball and the socket, and repeat damage from this shape mismatch leads to inflammation and activation molecules that destroy cartilage. That theory is yet to be conclusively proven, however if it turns out to be true this would offer an exciting opportunity to develop treatments for patients with FAI before they develop OA.

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