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Our 14-year-old son had surgery for osteochondritis dissecans after months of being on crutches and inactive. Unfortunately, the operation didn't work. We were so hopeful for him but it looks like the end of his snowboarding adventures. Any idea why the surgery didn't help? Other kids seem to bounce back, no problem.
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Osteochondritis dissecans (OCD) is a painful knee condition that affects teens and young adults who are usually still growing. That means the growth plates around the joints have not closed completely yet. Damage to the joint cartilage and first layer of bone (called subchondral bone) occurs causing knee pain with activity.
Until now, it's been unclear just what happens to cause this condition. Rest from activity and walking with crutches (nonweight-bearing status) is the first-line of treatment. Surgery may be needed to fix or hold any pieces or fragments of cartilage/subchondral bone that may have broken off. Japanese surgeons conducted a study recently that might help explain why treatment doesn't always result in the response hoped for.
They removed a plug of cartilage and bone from the center of an osteochondritis dissecans (OCD) lesion in 12 patients and then examined the samples under a microscope. When they took a closer look at the plugs of bone, they found a cleft (division) in the specimens.
The cleft divided the plug into two parts (upper fragment and lower base piece).
The surface of the base portion was covered with a fibrous cartilage tissue. Underneath that were active bone cells trying to repair the damage. The bottom of the upper fragment was also covered in the same kind of dense fibrocartilage. The top of the fragment had normal articular cartilage like you would see covering the surface of any joint. But underneath were dead or dying bone cells. Some specimens didn't have any bone tissue left (alive or dead) -- just cartilage cells.
The results of this study suggest a series of steps in the breakdown of cartilage and bone. First, repetitive stress from activity appears to cause a fracture of the subchondral bone. The subchondral bone has a limited supply of blood normally. This feature combined with trauma to the subchondral areas (from continued movement) results in osteonecrosis (death of bone). The necrosis affects the trabeculae, a scaffold or framework of bone cells in the subchondral layer.
The body's natural response to any cell death is to remove or resorb those dead cells. That's when the fibrous tissue is formed in an attempt to repair the damage. Deeper areas remodel to form cartilage or bone. Bone formation is more likely when there's no separation or only a partial separation of the subchondral bone. A full division seems to cut off the body's ability to mend the area with the necessary bone.
What this study showed was why certain treatment techniques do or don't work. For example, patients with cartilage and trabecular bone can recover with nonoperative care. The presence of trabecular bone makes it possible to restore the natural layer of cartilage with the underlying subchondral bone. Without this trabecular bridge, fragments that are made up of just cartilage may not reunite with bone even after surgery. Those types of injuries seem to only be able to make more fibrous cartilage, which isn't enough to repair the damage and restore the cartilage to subchondral interface.
Your son may have had cartilage fragments that had separated from the bone but with no bone cells remaining. Just reattaching the fragments isn't enough to create optimal recovery. Without the necessary framework or scaffold, new bone cells couldn't bridge the gap. Sometimes there is no obvious reason for treatment failure for this condition. Talk with your surgeon about this result. There may be some specific explanation for your son's failure to respond. Another treatment technique may be needed.
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