Osteochondritis dissecans of the elbow: recent evolution of pathogenesis, imaging, and treatment modalities

The etiology and pathogenesis of osteochondritis dissecans (OCDs) lesions remain controversial.

This review presents the recent evolution about the healing, imaging, pathogenesis, and how to treat OCD of the capitellum in overhead athletes.

Compressive and shear forces to the growing capitellum can cause subchondral separation, leading to OCD, composed of 3 layers: articular fragment, gap, and underlying bone. Subchondral separation can cause ossification arrest (stage IA), followed by cartilage degeneration (stage IB) or delayed ossification (stage IIA), occasionally leading to osteonecrosis (stage IIB) in the articular fragment. Articular cartilage fracture and gap reseparation make the articular fragment unstable. The mean tilting angle of capitellar OCD is 57.6 degrees in throwers. Anteroposterior radiography of the elbow at 45 degrees of flexion (APR45) can increase the diagnostic reliability, showing OCD healing stages, as follows: I) radiolucency, II) delayed ossification, and III) union. Coronal computed tomography and magnetic resonance imaging with an appropriate tilting angle can also increase the reliability. MRI is most useful to show the instability, although it occasionally underestimates. Sonography contributes to detection of early OCD in adolescent throwers on the field. OCD lesions in the central aspect of the capitellum can be more unstable and may not heal. Cast immobilization has a positive effect on healing for stable lesions. Arthroscopic removal provides early return to sports, although a large osteochondral defect is associated with a poor prognosis. Fragment fixation, osteochondral autograft transplantation, and their hybrid technique have provided better results.

Further studies are needed to prevent problematic complications of capitellar OCD, such as osteoarthritis and chondrolysis.