Osteochondritis Dissecans of the Elbow

Introduction and Epidemiology

Osteochondritis dissecans (OCD) was first described by König in 1887 as a possible explanation for the presence of loose bodies within a joint. Initially, he postulated that inflammation led to the atraumatic formation of loose bodies, hence the designation of “osteochondritis.” Although the exact cause of OCD remains elusive, we recognize it to be acquired, focal lesions of subchondral bone with varying degrees of osseous resorption, fragmentation, and sclerosis that risk possible disruption of superficial articular cartilage.

OCD lesions remain a disease of maturing joints. The overall incidence of OCD across all joints declines to 2.52 (female) and 4.41 (male) per 100,000 person-years in patients aged 20–45 years. Several authors have noted an increasing incidence of OCD in the elbow with time and decreasing age at presentation ^, and suggest that it may correlate with the increasing popularity of competitive sports among young athletes.

Of all the OCD lesions diagnosed in adolescent athletes, the elbow represents only 12% of lesions. The reported incidence of elbow OCD lesions in patients aged 6–19 years is 2.2 per 100,000, with 3.8 per 100,000 in males and 0.6 per 100,000 in females. This represents a 6.8 times greater odds ratio in males than females. Additionally, the same study found that the odds ratio was 21.7 times higher in patients aged 12–19 years when compared with those aged 6–11 years. The vast majority of elbow OCD lesions (97.5%) are found in the capitellum, with rare lesions seen on the trochlea (2.5%) and radial head ^, ( Fig. 19.1 ).

Capitellar OCD lesions are typically seen in adolescent athletes engaging in repetitive overhead activities such as baseball, gymnastics, football, javelin, or overhead weight lifting. Kida et al. describe a prevalence of 3.4% among adolescent baseball players (14.5 ± 1.5 years), as detected by ultrasound. The authors also found that players with elbow OCD had played for longer periods, started playing at an earlier age, and experienced more elbow pain. Furthermore, patients who had continued to pitch despite having elbow pain demonstrated more advanced lesions. This was additionally confirmed by Matsuura et al. who found a prevalence of 3.2% among baseball players aged 10–12 years using ultrasound.

Although no large-scale studies have been undertaken with female athletes, several reports note an elevated risk of capitellar OCD in female gymnasts. Although Kessler et al. noted a 6.8 times greater odds ratio of having elbow OCD in adolescent males as opposed to females, these findings are likely biased by sport popularity in Southern California. A similar, but much smaller, cohort out of Boston noted similar rates of OCD among male and female athletes. Interestingly, in the cohort out of Boston, female gymnasts were noted to be more likely to present at a younger physical and skeletal age and to have an injury to their nondominant arm compared to the group of largely male baseball players.

Mechanism of Injury

Although the initial description by König in 1887 suggested a central role for inflammation in the formation of osteochondral fragments, this has since been disproven by multiple histologic studies. Currently, the most widely accepted cause for OCD formation across joints is repetitive microtrauma. Within the elbow, this theory is supported by the relatively high prevalence of capitellar OCD in adolescent baseball players and gymnasts, where the elbow is subjected to repetitive valgus loading. For baseball players, the elbow is subjected to high valgus stress during the late cocking and early acceleration phases of throwing, which generates both compressive and shear forces across the radiocapitellar joint. In contrast, the stress experienced during gymnastics appears to be an axial load, 60% of which is born by the radiocapitellar joint. ^, Interestingly, female gymnasts' events result in increased axial loading and adduction moment, potentially placing them at higher risk of elbow injury than their male counterparts. ^, The variation in loading pattern between baseball and gymnastics translates into different locations for capitellar OCD between baseball players, who have more anterior lesions, and gymnasts, who have more distal lesions.

However, repetitive microtrauma may only be part of the elbow OCD story. The European Pediatric Orthopedic Society conducted a large multicenter study, which demonstrated that only 55% of patients with knee OCD regularly participated in sports or strenuous physical activity. Importantly, OCD may also result from obesity or anatomic variations. Kessler et al. found that extreme childhood obesity, as defined by body mass index >35 kg/m ² or weight 1.2× the 95th percentile, increases the risk of OCD formation across all joints by 86%. Interestingly, the highest risk joints in this study were the elbow and ankle, where extreme obesity conferred 3.1 and 3.0 times increased risk of OCD formation, respectively.

Lower extremity alignment plays a significant role in the development of OCD in the knee, with varus knees tending to develop medial femoral condyle OCD lesions and valgus knees tending to develop lateral femoral condyle OCD lesions. Anatomic considerations appear to be critical to elbow OCD development as well. First, the converse pattern appears to be true for the elbow, where patients with capitellar OCD are more likely to have a varus carrying angle than matched controls. Second, Schenck et al. demonstrated in cadaveric studies that a stiffness mismatch is present in the radiocapitellar joint, which may lead the lateral capitellum to experience a higher strain environment during valgus load. Third, healing after injury may be compromised by limited vascular supply to the distal/anterior capitellum. The immature capitellum lacks a substantial metaphyseal blood supply and instead relies on branches from the radial recurrent and interosseous recurrent arteries. ^, This leaves the capitellum vulnerable to ischemia, particularly in the setting of repetitive injury.

One potentially unifying theory involves disordered ossification of a portion of the epiphysis. ^, According to this theory, there is an unspecified insult (single or repetitive) to the epiphysis that leads to either temporary or permanent cessation of ossification in one region. The remainder of the epiphysis continues to grow and undergo endochondral ossification, leading to the development of a growing defect. Here, a complete cessation in ossification would generate a completely cartilaginous OCD, whereas a temporary stop would generate a partially ossified fragment. Although Barrie ^, did not provide any direct evidence to support this mechanism, unpublished MRI data out of the Research in Osteochondritis of the Knee (ROCK) group suggest it may be visible on MRI. Regardless, capitellar OCD formation is likely the result of a combination of factors including repetitive stresses across the radiocapitellar joint, tenuous vascular supply to the capitellum, and a mismatch in stiffness between the radial head and lateral capitellum.