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Natural History and Diagnosis of OCD

OCD lesions may or may not cause symptoms early on. They apparently first appear in the early part of adolescence, well before skeletal maturity is reached and the child's "growth plates" fuse (close). Prior to fusion of the growth plates, if the lesion remains undisturbed (i.e., does not loosen or separate), the chance for spontaneous healing by way of natural reunification of the abnormal subchondal ossicle with the parent bone is reasonably high. In patients between 10 and 13 years of age, simple rest and avoidance of stress to the knee joint over a period of time may be enough to allow such natural healing to take place. As skeletal maturity approaches, the chances for spontaneous healing diminish, and the probability that surgical treatment of some type will be needed increases

Some undetected cases of OCD remain unhealed and clinically silent (cause no symptoms) until a patient reaches their twenties and sometimes even their thirties or later. Some patients can harbor a fairly large osteochondritis dissecans lesion in their knee without realizing it until it frankly separates and literally pops loose inside their joint! Separation may occur either gradually, or all at once during a mildly stressful event such as a routine pivoting or turning maneuver. In a teenager or young adult, the sudden onset of knee locking or internal "clunking" followed by joint swelling (without having experienced the degree of knee stress usually required to tear healthy ligament or cartilage tissues) should suggest to an examining physician the possibility of a recently loosened or separated osteochondritis dissecans lesion. OCD is notoriously misdiagnosed and underdiagnosed, particularly in adolescents whose lesions have not yet separated. These patients usually experience only vague symptoms and may have no knee swelling whatsoever. Routine x-rays ordered by pediatricians may not include the special views necessary to see an osteochondritis dissecans lesion clearly, leaving it to go untreated and thus possibly loosen and separate later on. Unless an MRI scan or the appropriate x-rays are ordered, it usually takes an orthopedic surgeon to make the diagnosis. A scene that has recurred many times in my office is a 15 or 16-year-old patient (who had voiced vague complaints to skeptical parents over several years) saying, "See, there really was something wrong with my knee!" By then, however, surgery is almost always needed.

The potential adverse consequences of osteochondritis dissecans depend very much upon the size of the lesion, its location and how amenable it is to "restorative" treatment. Restorative treatment leads to healing of the lesion, with preservation of the weight-bearing joint surface. Small lesions in non-critical regions of the tibial joint surface and patella often have a fairly benign clinical course, even when the only treatment possible is removal of the loose osteochondral fragment from the joint, which leaves a defect in the articular surface. Unsuccessfully restored femoral condylar lesions are more likely to cause arthritis over time.

Large, advanced lesions of the femoral condyles that are fragmented or otherwise not amenable to restorative treatment leave substantial, crater-like defects in the main weight-bearing surface of the knee joint, with almost uniformly poor long-term results. Such a knee behaves like a ball-bearing with a large divot in its surface, essentially wearing itself out prematurely. Some varieties of femoral osteochondritis dissecans involve a fairly extensive zone of abnormal, underlying subchondral bone. These leave a deep crater if the lesion loosens and separates. Other varieties of OCD extend only superficially into the underlying subchondral bone. In all cases that do not heal spontaneously, the patient's body forms a zone of fibrous tissue between the parent bone and the OCD fragment. This fibrous interface layer is relatively inert (inactive) tissue. The few living cells within this fibrous tissue try to absorb the dead bone in the overlying OCD fragment, which thickens the fibrous tissue layer as the adjacent bone dissolves. Because fibrous tissue is soft, this makes for a loss of structural support beneath the OCD lesion (see FIGURE 3).

FIGURE 3 - This MRI image scan shows a side-view close-up of the rear portion of a femoral condyle afflicted with a large osteochondritis dissecans lesion (arrow). The black triangular structure immediately below the OCD lesion represents a cross section of the patient's normal meniscus (the so-called "knee cartilage"), with the tibia being located immediately below that. At the junction of the dark OCD lesion and the lighter-shaded normal bone of the main femoral condyle, the structurally weak, fibrous interface zone can be seen. This is where a lack of underlying joint surface support develops, allowing repetitive, pistoning micro-motion of the OCD lesion under the weight-bearing stresses of daily activity. This is similar to the way floorboards will move when you step on them if the underlying framing is weak. If you look closely at the lower, far right end of the OCD lesion, you can see a short black line. This represents an early dissection fissure developing through the articular surface cartilage covering the femoral condyle. Such fissures typically develop along the outer perimeter of OCD lesions, gradually separating them from their parent bone.

This lack of underlying support allows the cartilaginous joint surface to flex repeatedly under weight-bearing stresses, much like floorboards with weak support framing beneath them. Such repetitive, abnormal micromotion causes fatigue breakdown of the articular (surface) cartilage along the lesion's perimeter (the border interface between the OCD fragment and the surrounding, structurally stable femoral surface), culminating in an open crack or fissure demarcating some or all of the lesion. As noted previously, this is the "dissection" process that gave OCD the last part of its name.

If the ossific (bone tissue) nucleus of the OCD lesion shrinks substantially in size, the entire lesion may weaken and break apart (see FIGURE 4), thus precluding any attempt at direct surgical repair and reunification (healing by way of incorporation back into the parent bone).

FIGURE 4 - This photograph shows fragments of an OCD lesion that were removed from a young patient's knee joint. The patient's lesion went untreated until it loosened and then literally broke apart into several pieces, precluding their replacement back into the crater that was left in the femoral condyle. What you see here is the back side of the OCD fragments, with the yellowish tissue being what was left of the underlying bone and the white tissue behind the bone representing the overlying articular (joint surface) cartilage. The measurement scale shown is in centimeters. .
   
 
 
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