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Osteochondritis dissecans (OCD) is a pathologic process that results in the detachment of subchondral bone and its overlying articular cartilage from the underlying bone. Several options are available to treat adult OCD, including debridement, drilling, loose body removal, microfracture, various methods of arthroscopic reduction and internal fixation (ARIF), osteochondral autografting, and allografting. Primary repair is described in this chapter.
Primary repair should be considered after a course of 6 months nonoperative treatment has failed or in the setting of an unstable lesion.
Anatomic reduction of the lesion is paramount to achieve stability.
Must stimulate healing at the base of the lesion.
Absorbable or nonabsorbable implants may be used.
It is essential to achieve appropriate visualization of the lesion and the base of the defect. An open approach may be used as needed.
A larger arthrotomy is required for access to patellofemoral lesions.
Excision of a portion of the anterior fat pad can improve visualization of the lesion and greatly facilitate insertion of cannulated implants during arthroscopic treatment.
Treatment of OCD lesions should be thought of as fracture fixation. Compression should be generated along a vector orthogonal to the fracture site to optimize healing.
In the arthroscopic treatment of medial femoral condyle lesions, particularly classic lesions that abut the intercondylar notch, it is often easiest to hinge the lesion open along its intercondylar edge.
A free fragment with minimal subchondral bone has a very low probability of healing.
Nonabsorbable implants should be removed at 2–3 months to assess for healing and to prevent screw prominence with fragment settling.
In removing headless, variable-pitch screws, a noncannulated screwdriver should be used to initiate removal. The torque required to initiate unscrewing of a well-seated screw is sufficient to cause the tip of a cannulated screwdriver to break. After the screw has been unscrewed several turns, a guidewire should be inserted and a cannulated screwdriver used to complete the removal.
Follow a strict postoperative protocol with non–weight-bearing status.
Osteochondritis dissecans (OCD) is a pathologic process that results in the detachment of subchondral bone and its overlying articular cartilage from the underlying bone. This causes destabilization and vulnerability to fragmentation and shear forces. The end result is degenerative change and often loss of function of the affected compartment. The etiology is likely multifactorial and may be related to repetitive microtrauma or an acute traumatic or ischemic incident, genetic predisposition, endocrine dysfunction, or an ossification abnormality. ,
The prevalence of OCD is estimated at 15 to 30 cases per 1000 patients annually, affecting the medial femoral condyle (lateral aspect most commonly) in 80% of patients, lateral femoral condyle in 15%, and patellofemoral in 5%. , A major distinction in OCD lesions is that between juvenile (open physes) and adult (closed physes). While juvenile OCD lesions often respond favorably to conservative management, , symptomatic lesions in adults are almost always intervened upon in effort to avoid progress toward their inevitable osteoarthritic conclusion. , , The goal of reparative procedures is to improve blood supply to the lesion, restore the integrity of the native subchondral interface, and preserve the overlying articular cartilage. Several options are available to treat adults with OCD, including debridement, drilling, loose body removal, microfracture, arthroscopic reduction and internal fixation (ARIF), and osteochondral autografting and allografting. , Multiple authors have suggested treatment algorithms to help surgeons decide when and with which method to intervene. Primary repair by rigid, compressive fixation of unstable lesions offers an attractive and effective means of treatment by preserving the native osteochondral surface.
Patients often report several months of stiffness, activity-related swelling, and poorly localized pain. They may report catching or locking symptoms, exacerbated by increased activity, due to unstable lesions or loose bodies.
Thoughtful physical examination is necessary, as certain signs may be misleading and many are nonspecific. Observe for a change in gait, specifically an antalgic gait. There may be an effusion, loss in range of motion, and quadriceps atrophy depending on severity. Because the most common location for an OCD lesion is on the medial femoral condyle by the trochlea, tenderness may be elicited with palpation over this area and can be confused for patellofemoral pain. Observe for the Wilson signthe patient will ambulate with the affected leg in relative external rotation to decrease contact of the lesion with the medial tibial eminence. A positive Wilson test (not to be confused with Wilson sign) is indicated by reproduction of pain through internal rotation of the tibia between 30 and 90 degrees of flexion and relief with subsequent external rotation. The test has low sensitivity, but if the result is initially positive in a confirmed case of OCD, it reliably becomes negative with the healing of the lesion. ,
Plain radiographs should include standard anteroposterior, flexion weight-bearing anteroposterior (notch view), lateral, and Merchant views. The notch view is useful for identifying posterior condyle lesions.
OCD lesions commonly appear as an area of osteosclerotic bone with a high-intensity line between the defect and the epiphysis ( Fig. 69.1 ).
Magnetic resonance imaging (MRI) is the most informative imaging modality, providing information on the quality of bone edema, subchondral separation, and cartilage condition, as well as lesion size, location, and depth. Meeting one of the following four criteria defined by De Smet and colleagues will provide up to 97% sensitivity and 100% specificity in predicting lesion stability ( Fig. 69.2 ) :
Thin, ill-defined, or well-demarcated line of high signal intensity, measuring 5 mm or more in length at the interface between the OCD lesion and underlying subchondral bone
Discrete rounded area of homogeneous high signal intensity, with a diameter of 5 mm or more beneath the lesion
Focal defect with an articular surface of the lesion with a width of 5 mm or more
High–signal intensity line traversing the articular cartilage and subchondral bone plate into the lesion
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