Osteochondritis Dissecans (OCD) is a joint disorder where a segment of bone and its overlying cartilage separates from the end of the bone. This process occurs in the subchondral bone, the layer of bone tissue just beneath the joint cartilage. The separation is often triggered by a localized disruption of blood flow, which causes the bone tissue in that specific area to die. The resulting fragment, composed of dead bone and attached cartilage, can then loosen and potentially detach into the joint space.
The Mechanical Process of Bone Separation
The immediate mechanism driving the formation of an OCD lesion is an interplay between physical stress and compromised circulation. Repetitive physical loading of a joint causes tiny, repeated injuries, known as microtrauma, to the bone surface. This stress damages the delicate network of blood vessels that supply the subchondral bone.
Disruption of these blood vessels leads to a localized loss of blood supply (ischemia), causing the death of the bone tissue (avascular necrosis). The dead bone tissue loses its mechanical strength and begins to absorb, creating a weak point susceptible to separation. As the underlying bone weakens, the intact articular cartilage above it may develop cracks and fissures.
The stability of the OCD lesion depends on the integrity of this overlying cartilage and its connection to the parent bone. A lesion is stable if the cartilage remains continuous and the fragment is held in place. With continued joint use, the fragment can progress to an unstable state where the connection is compromised.
Synovial fluid, the natural lubricant of the joint, can seep into the space between the fragment and the surrounding bone, further dissolving the connection. In the most advanced stage, the fragment fully detaches, becoming a “loose body” within the joint, which can cause symptoms like locking or catching during movement.
Activity and Anatomical Risk Factors
External and structural factors significantly increase a person’s susceptibility to the microtrauma that initiates OCD. High-level participation in specialized athletic activities is a well-established risk factor due to the excessive, repetitive strain placed on specific joints. Sports involving constant throwing, jumping, or pivoting, such as baseball, gymnastics, soccer, and basketball, frequently subject the joint surfaces to high compressive and shear forces.
Adolescents and young adults experiencing rapid growth are particularly vulnerable because their growth plates remain open. During this period, the bone structure is still maturing, and the interface between the growing bone and the joint cartilage is mechanically weaker.
Furthermore, pre-existing anatomical variations can alter the distribution of force across the joint surface. Issues like a difference in leg length or subtle joint malalignment can cause uneven loading, forcing a small area of the joint to absorb disproportionately high amounts of stress. This abnormal biomechanics lowers the threshold for repetitive microtrauma, accelerating the process of vascular disruption and bone death in that focal area.
Exploring Systemic and Genetic Contributions
While mechanical factors explain the immediate damage, internal biological characteristics may predispose an individual to developing OCD. A genetic predisposition is suggested because OCD sometimes runs in families, and identical lesions have been reported in monozygotic twins. Inherited traits related to bone structure or the vascular supply within the joint may play a role.
Researchers have identified specific genetic mutations, such as those involving the ACAN gene, which provides instructions for aggrecan, a component of cartilage. Mutations in this gene can result in disorganized and weakened cartilage, lowering the tissue’s ability to withstand normal stresses.
Endocrine and hormonal factors, particularly during periods of rapid growth, are also potential contributors. Systemic issues that affect bone density or the body’s ability to repair micro-damage influence the development and healing of the lesions.