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Why does cartilage degenerate? » cartilage degeneration



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cartilage degeneration explained

Why does cartilage degenerate?

A lot of things in life, like your skin and your intervertebral disks, start out like nice plump grapes and end up looking a bit more like a raisin.  Most of these changes seem to be due to things that we can not do anything about — the passage of time being the primary one, genetics being the other.  The cartilage in your weight bearing joints tends to give years and years of good service, but at some point it starts to wear out.  The process of natural degeneration of articular cartilage is still not perfectly understood, and while it appears that accumulated wear and tear and aging certainly play a role in how long your joints last, this is by no means the entire story.

The vast majority of joint replacement surgeries in the United States are performed for people who have developed osteoarthritis.  This is the most typical type of degenerative arthritis, and it is much more common than post-traumatic osteoarthritis (arthritis caused the residual deformity left by fractures that involve a joint), or inflammatory arthritis (arthritis caused by immune diseases that cause the joints to self-destruct), for example.  There appears to be a strong genetic component affecting when and where someone develops arthritis.  For example, many of my patients that ultimately choose to have a hip replacement will tell me that one of their parents had similar complaints or a similar surgical procedure at about the same age, or one of their siblings is currently considering having surgery as well.  In several instances I have had the relatives of a patient come into clinic so that we could obtain multi-generational X-rays of their joints and it can be quite striking how similar the patterns of arthritic change affecting the major weight bearing joints can be.

osteoarthritis affecting the hands

One of the most common questions that I get asked is whether certain activities (marathon running being the most frequently mentioned) lead to the development of osteoarthritis.  So far, the jury is still deliberating on that point.  For example, a recent paper from Penn State looked at MRI scans of 22 marathon runners and compared those scans to 15 people who were considered “sedentary.”  The researchers found that immediately after running, there was a measurable decrease in cartilage thickness that seem to suggest that the cartilage was more compressible, which isn’t surprising since the person had just been pounding away on the pavement for the last 26.2 miles.  However, the implications of this decreased thickness and increased compressibility are unknown.  Cartilage may receive a lot of nourishment from repetitive loading and unloading which forces joint fluid into the cartilage (much like the way that sponge can soak up water and then release it when it is squeezed) and this may allow the cartilage to be more resilient over time.  In my mind, the benefits of staying active far outweigh the theoretical concerns of wearing out the joints too early — as long as you run, cycle, swim, or exercise with what would be considered good body mechanics.

MRI scan of the knees before and after exercise

FUNCTIONAL CARTILAGE MRI T2 MAPPING: EVALUATING THE EFFECT OF AGE AND TRAINING ON KNEE CARTILAGE RESPONSE TO RUNNING.  Timothy J. Mosher, MS, MD, Yi Liu, MD, and Collin M. Torok, MD.  Published in Osteoarthritis Cartilage.  2010 March; 18(3) 358-364.

There are certain morphological conditions that seem result in a predisposition towards early arthritis of the hip, and this is one of the most fascinating areas of research currently in orthopedics.  The mechanism, implications, and successful treatment of CAM and PINCER impingement have not been completely worked out yet, but there is the suggestion that abnormal forces, especially shear forces across the surface of the cartilage, may be particularly detrimental.  Shear forces seem to develop when there is some sort of structural abnormality of the joint, such as instability, or in the case of CAM impingement, when there is a mismatch or an incongruity between the shape of the femoral head and the socket.  For more on femoral acetabular impingement, click here.

Once the cartilage starts to degenerate, it tends to follow a relatively predicable pattern.  When scientists follow the changes that occur at the microscopic level as the osteoarthritis progresses, there seems to be a relative loss of type of molecule called proteogylcans inside the cartilage layer, and the collagen network that lends structural support to the cartilage starts to fragment and break apart.  As the cartilage becomes less competent at handling and dissipating the loads created by weight bearing and exercise, the bone underneath the cartilage starts to thicken and enlarge.  This process is what results in bone spurs.  If you remember your introductory physics course work, you’ll remember that Force is defined as Mass * Area and the definition of Stress is defined as Force divided by Area.

Stress = Force / Area.  Increased stress is dissipated by Increasing the surface area of the joint.

The bone starts to feel a greater amount of stress because the cartilage is not dissipating the loads effectively, so in response, the bone tries to dissipate that stress by enlarging the surface area of the joint.  That is why the bone starts to thicken at the periphery by adding on “bone spurs”.  Most of my patients seem to understand this analogy: if you think of grandmother’s hands, you’ll recall that they were probably a bit knobby and the knuckles were thickened and irregular.  This process was a natural response to the loss of the normal articular cartilage in the small joints of the fingers, and as the cartilage wore out, bone spurs developed around the joints in order to try to accommodate the stress caused by gripping objects, lifting heavy pans off a hot stove, and manipulating knitting needles.

So far, attempts to get cartilage to regenerate are in their infancy.  There has been a lot of promising laboratory studies, and a few semi-successful clinical trials, but these experimental procedures have typically been used on patients who are much younger than the average patient who is considering a total hip arthroplasty.  The patient with moderate to severe osteoarthritis needs a new smooth surface to lubricate their joints, and currently the best way to achieve that goal is to replace the joint.  There are some promising joint preservation procedures in the area of the treatment of femoral acetabular impingement and our hope is that these procedures will prevent some patients with certain anatomic signatures from developing early osteoarthritis of the hip.  At this point in time, if you’ve already gotten to the point where you have pain and joint space narrowing is recognizable on the X-ray, a joint replacement procedure is probably the only way you will be able to achieve long lasting pain relief.


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