Osteochondritis dissecans (OCD) develops when a segment of bone just beneath the cartilage surface of a joint loses its blood supply, weakens, and begins to separate. The exact cause isn’t fully settled, but the most widely accepted explanation is repetitive microtrauma to the joint, with or without a single triggering injury. Several other factors, including disrupted blood flow during growth, genetics, and joint alignment, also play significant roles.
Repetitive Microtrauma: The Leading Theory
The strongest evidence points to repeated, low-level stress on a joint as the primary driver of OCD. Each impact or loading cycle is too small to cause an obvious injury, but over time these forces damage the thin layer of bone beneath the cartilage. The bone develops tiny fractures that never fully heal before the next round of stress arrives. Eventually, the damaged bone softens, cracks, and can begin to pull away from the surrounding healthy tissue, taking its cartilage cap with it.
This theory is supported by the condition’s strong link to youth sports. Young athletes who train intensely and repetitively are diagnosed far more often than their non-athletic peers. The pattern of which joints are affected also tracks closely with the specific demands of each sport, which is hard to explain by any cause other than mechanical stress.
Sports and Activities With the Highest Risk
OCD shows up in predictable locations depending on the sport. In baseball, the throwing motion creates a valgus overload, essentially a forceful inward bend at the elbow, that compresses the outer side of the joint with every pitch. Prevalence among baseball players is estimated between 1.2% and 7.4%, with pitchers at greatest risk due to the velocity and volume of throws they accumulate over years of play.
Gymnasts face a different mechanical problem. They bear weight through fully extended arms, driving force almost straight down through the elbow. This produces OCD lesions in a slightly different spot on the same bone compared to throwers, about 30 degrees further back on the capitellum. Basketball players experience similar overhead forces at the elbow, and typically develop gradual outer-elbow pain in their dominant arm.
Football and other running sports load the knees, ankles, heels, and feet. Risk factors in these sports include high training volume, joint instability, falls, dominant-leg overuse, and weakness in the quadriceps muscles. The common thread across all of these activities is sustained, repetitive force directed at the same joint surfaces over months or years.
Disrupted Blood Supply During Growth
A second major theory involves the blood supply to the bone beneath the cartilage. During childhood and adolescence, the way blood reaches this bone changes dramatically. In younger children, blood vessels run through the outer cartilage layer (the perichondrium) to feed the growing bone. As a teenager matures, this supply shuts down and is replaced by vessels coming from the bone marrow cavity inside.
During the transition between these two systems, there’s a window of vulnerability. If the new blood supply hasn’t fully established itself before the old one recedes, patches of bone can be temporarily starved of oxygen and nutrients. This is called avascular necrosis, and it causes the bone to weaken and die in small, localized areas. The theory helps explain why OCD peaks during adolescence and why certain spots on the bone, particularly the inner (medial) side of the knee’s femoral condyle, are so consistently affected.
In adults, the mechanism shifts slightly. Experts believe the adult form of OCD is more directly tied to a vascular insult, meaning a specific disruption to blood flow, rather than the developmental transition that puts adolescents at risk.
How the Damage Progresses
Regardless of what starts the process, the chain of events follows a recognizable pattern. First, blood vessels feeding the subchondral bone are disrupted. The bone in that area dies, and the cartilage sitting on top of it begins to soften. Over time, the cartilage develops tears, fissures, and erosion. As the weakened area grows, repeated shear forces from normal joint use cause the fragment of bone and cartilage to partially or fully detach.
Clinicians grade OCD in four stages. In the earliest stage, the cartilage surface is still intact but the bone underneath is soft. In stage two, the cartilage starts to crack but the fragment remains mostly anchored. Stage three means the fragment has fully disconnected from surrounding bone but hasn’t moved out of position. By stage four, the fragment breaks free entirely and becomes a loose body floating inside the joint. These loose bodies can catch between the joint surfaces, causing sudden locking, sharp pain, and further cartilage damage.
Genetic Predisposition
Most OCD cases are not inherited, but a familial form does exist. This version is caused by a mutation in the ACAN gene, which provides instructions for building a key protein in cartilage. When this gene is altered, the protein it produces can’t attach properly to the other structural components of cartilage. The result is cartilage that’s disorganized and weak from the start, making it far more susceptible to the stresses that trigger OCD.
Familial OCD follows an autosomal dominant inheritance pattern, meaning a child needs only one copy of the altered gene (from one parent) to develop the condition. People with this genetic form tend to develop OCD in multiple joints rather than just one, and they often have family members with the same problem. Outside of this specific mutation, broader genetic factors likely influence cartilage strength, bone density, and vascular development in ways that raise or lower an individual’s risk.
Joint Alignment and Structural Risk Factors
The geometry of your joints matters. Abnormal leg alignment, particularly genu varum (bowleggedness), has been proposed as a contributing factor because it concentrates force unevenly across the knee’s cartilage surfaces. On the opposite end, valgus alignment (knock-knees) along with a discoid meniscus (an unusually shaped meniscal cartilage) are established risk factors for OCD on the outer side of the knee’s femoral condyle.
These structural differences don’t cause OCD on their own, but they change where and how force is distributed within a joint. Combined with repetitive activity, malalignment can create a focal point of chronic overload that tips the balance toward tissue breakdown.
Who Gets OCD Most Often
OCD of the knee is most common in adolescents, with those aged 12 to 19 carrying 3.3 times the risk compared to children aged 6 to 11. The overall incidence in the 6-to-19 age range is about 9.5 per 100,000, but the gap between sexes is striking: males are affected at a rate of 15.4 per 100,000 compared to 3.3 per 100,000 for females. That translates to nearly four times the risk for boys and young men.
The reasons for this disparity aren’t entirely clear, but likely reflect a combination of higher participation rates in high-impact sports, greater body mass loading the joints during growth, and possible differences in the timing of skeletal maturation.
Where OCD Develops in the Body
The knee is the most common site, and within the knee, the classic location is the back-center portion of the medial femoral condyle, the rounded knob of bone on the inner side of the thigh bone. This spot accounts for 64% to 85% of knee OCD cases. The lateral condyle (outer side) is involved in 15% to 33% of cases, while the kneecap and the groove it rides in are rarely affected.
In the elbow, OCD almost exclusively hits the capitellum, the small, rounded surface on the outer side of the lower arm bone, accounting for 97.5% of elbow cases. In the ankle, the talus bone is the target, with about 72% of lesions appearing on the inner-back portion and 22% on the outer-front. These consistent locations reflect the spots where mechanical stress is highest in each joint, further supporting the microtrauma theory.
Juvenile vs. Adult OCD
The distinction between juvenile and adult OCD is important because the underlying biology differs, and so do the outcomes. In juveniles, the growth plates are still open, meaning the skeleton is still maturing. This active growth environment gives the body a stronger capacity to repair damaged bone and cartilage. Many juvenile cases, if caught early and the joint is rested, heal on their own without surgery.
Adult OCD, where the growth plates have closed, tends to behave more aggressively. The bone’s regenerative capacity is lower, the blood supply is less adaptable, and the condition is more often attributed to a direct vascular insult rather than the developmental vulnerability of adolescence. Adult lesions are more likely to progress to fragment detachment and more likely to require surgical intervention.