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MRI Web Clinic - August 2024

Osteochondral Lesions of the Trochlea


Joanna Costello, M.D.

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Clinical History: A 15-year-old pitcher presents with elbow pain.  Coronal T1-weighted (1a), Coronal fat-suppressed T2-weighted (1b), and sagittal fat-suppressed proton density weighted (1c) images and frontal radiographs are provided. What are the findings? What is your diagnosis?

Figure 1

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Figure 2

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Coronal T1-weighted image (2a) shows a circumscribed focal inverted U-shaped area of abnormal marrow signal which is isointense to skeletal muscle in the subchondral lateral trochlea (red arrow). The coronal fat-suppressed proton density image (2b) shows an inverted U-shaped area of abnormal heterogenous signal in the subchondral marrow of the lateral trochlea with a thin surrounding rim of signal hypo-intensity and a more peripheral rim of surrounding marrow edema (red arrowheads). Thinning and heterogeneity of the overlying articular cartilage is seen. The sagittal fat-suppressed proton density-weighted image (2c) shows the posteroinferior location of the trochlear subchondral marrow signal abnormality, and heterogeneity of the overlying cartilage (dotted arc). Frontal elbow radiograph (1d) shows an inverted U-shaped subchondral lucency of the lateral trochlea with a surrounding thin rim of sclerosis (arrows), the “pseudo-intercondylar notch sign.”

 

Diagnosis

Osteochondral lesion of the lateral trochlea with degeneration of the overlying cartilage.

 

Introduction

Osteochondral lesions (OCLs) of the humeral trochlea are uncommon, though they may be a source of elbow pain in the young athlete and may be encountered in a busy sports medicine practice. Timely diagnosis and appropriate treatment may improve functional outcomes and avoid potential sequelae of chronic arthralgia and premature osteoarthritis.

 

Clinical presentation

OCLs of the trochlea are focal abnormalities of the subchondral bone and overlying articular cartilage in young athletes that may progress to osteochondral separation, loose body formation, and premature degenerative joint disease.

OCLs of the elbow most commonly occur in the dominant arm of young overhead athletes (especially baseball pitchers) and in either arm of athletes participating in activities that convert the elbow into a weight-bearing joint, including gymnasts and weightlifters.  They have also been reported in adolescents participating in various other athletic activities.1,2,3,4,5,6,7,8 The vast majority of elbow osteochondral lesions affect the capitellum with much less frequent involvement of the trochlea, radial head, and olecranon fossa. Bipolar lesions of the capitellum and radial head, coexisting capitellar and trochlear abnormalities, and bilateral OCLs occasionally occur.2,5,7,9,10,11,12 Osteochondral abnormalities of the capitellum were the subject of a prior Radsource Web Clinic.13 This discussion will focus on OCLs of the trochlea, excluding acute trauma.

Trochlear OCLs have been reported to account for between 0.5 and 7% of all OCLs.1,4,6,14 The most frequently reported presenting symptom is a gradual onset of activity-related medial elbow pain, followed by crepitus, loss of range of motion, and mechanical locking.4–6,14  A 2022 systematic review of 16 studies, which included 75 elbows in 70 patients with trochlear OCLs, reported that 90% of patients were overhead athletes (most often baseball pitchers) with a mean age of 14 years (range 8-19 years), and males (n=46) being more often affected than females (n=24).4–6,14

 

Pathophysiology

As with OCLs of other joints, no universally encompassing cause for trochlear OCLs, formerly termed osteochondritis dissecans lesions, has been agreed upon. The term osteochondritis dissecans is somewhat of a misnomer, implying the presence of osteochondral inflammation. However, no inflammatory cells have been found upon histologic examination of excised osteochondral fragments or adjacent synovium. Instead, histopathologic evaluations of OCLs have shown findings consistent with necrosis of subarticular bone, subchondral fracturing, and findings related to repetitive mechanical stress upon articular cartilage with degenerative and reparative changes.2,9,15  Prevailing etiologic theories suggest repetitive microtrauma and compressive load to an area of subchondral bone with a vulnerable blood supply, resulting in ischemia of the subchondral bone.  The articular cartilage remains intact in the early stages, and nutrition is received from the synovial fluid. If articular cartilage integrity persists, the subchondral bone will eventually remodel and be replaced; however, if the integrity of the articular cartilage becomes violated or deteriorates due to insufficient structural support by the ischemic subchondral bone, an osteochondral fragment may separate from the remaining bone with loose body formation.2,4,5,7,16 This suggests that identifying early lesions with intact overlying cartilage may be beneficial, potentially increasing the likelihood of healing after a period of rest and activity modification.  Some authors have proposed that an underlying genetic predisposition or disorder of endochondral ossification may be contributory etiologic factors as bilateral lesions and familial tendencies have been described. 2,7,17,18,19

Some inconsistencies exist in the anatomic descriptors that indicate the same trochlear anatomy. For the purposes of this article, trochlear anatomy is described as follows.  From medial to lateral, the spool-shaped trochlea is comprised of a larger medial articular facet (in the literature sometimes also referred to as the medial crista), the trochlear groove (in the literature also referred to as the trochlear apex or sulcus), the smaller lateral facet (in the literature sometimes referred to as the lateral crista), the lateral trochlear ridge (the ridge along the lateral margin of the lateral facet) and the zona conoidea, the small articular surface along the lateral aspect of the lateral trochlear ridge that borders the capitellum. The zona conoidea articulates with the medial aspect of the beveled rim of the radial head that surrounds the central concave fovea of the radial head.20,21 (Figure 3.)

 

Figure 3

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Figure 3. The trochlear articular surface consists of the medial articular facet (blue), trochlear groove (yellow), lateral facet (red), lateral trochlear ridge (green), and the zona conoidea (magenta).

 

Two retrospective studies, each of which included the largest thus far reported cohorts of trochlear OCLs, each noted two predominant trochlear OCL pattern subgroups that differed in appearance, location, and proposed etiology.

In a 2019 retrospective review of 28 cases of trochlear OCL lesions, Wang et al. described the “typical” trochlear OCL subgroup, which included 25 elbows or 89% of cases. These were located on the inferior trochlear articular surface at a sagittal angle (on a leftward facing sagittal image in which 0-180 degrees is anterior) between 90-270 degrees (or between 3-9 o’clock on the leftward facing sagittal image). These were all significantly more anteriorly positioned than the “atypical” trochlear OCL subgroup. The vast majority of the “typical” lesions (n=23/25) were on the lateral facet of the trochlea centered about 3.1 +/-4.4 mm lateral to the trochlear groove, which corresponds to the medial margin of the capitellar ossification center (Figure 4). The “atypical” OCL subgroup included three elbows, or 11% of all lesions. These were posteromedially located (sagittal angle of > 270 degrees or 12-3 o’clock)(Figure 4).5  A little over half of elbows with trochlear OCLs had associated MRI abnormalities, coexistent capitellar OCLs being the most frequently identified coexistent pathology, noted in 6/28 (21%)5.

Marshall et al. also found the majority (n=10, 77%) of trochlear OCLs affect the posteroinferior aspect of the lateral facet of the trochlea, with the remaining (n=3, 23%) involving the posteromedial trochlea. The lateral lesions were circumscribed and larger (10-14mm) than the smaller (<6mm) posteromedial lesions.  Both of the above studies note that the location of the laterally positioned lesions corresponds to a zone of vulnerable vascular supply of the pediatric distal humerus that persists into adulthood, as previously illustrated in cadaveric studies by Haraldsson, Yamaguchi, and Kimball.16,22,23,24

It has been proposed that the “typical” trochlear OCLs, which most commonly involve the inferolateral trochlea, result from ischemia of subchondral bone involving the medial margin of the capitellar ossification center, resulting in failed fusion between the capitellar and trochlear ossification centers.5  Marshall et al. hypothesize that athletic activities that involve repetitive elbow extension/hyperextension may impinge upon the already tenuous blood supply to the lateral trochlea (Figure 5), which predominantly enters from the posterior arcade. Alternatively, they postulate that repetitive extension/hyperextension-related osseous abutment may increase intraosseous pressure, compromising blood supply in the watershed area. 4,5

Both retrospective studies reported that the “atypical” or posteromedial trochlear OCLs have a higher percentage of associated ligamentous abnormality, most commonly UCL sprain. It has been proposed that the posteromedial trochlear osteochondral lesions are likely the result of repetitive abutment within the posteromedial compartment, which may be exacerbated by ulnar collateral ligament insufficiency as has previously been described in throwing-related hyperextension valgus overload syndrome.4,5,25

 

Figure 4

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Figure 4. 3D images depict the locations of the “typical” (red) and the “atypical” (blue) OCL of the trochlea.

 

Figure 5

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Figure 5. The medial margin of the capitellum and posteroinferior aspect of the lateral facet of the trochlea lie in a watershed area with tenuous blood supply.

 

 

Collins et al. described a small series of patients presenting with elbow pain, the majority of whom were competitive athletes, who were found to have osteochondral lesions of the posterior aspect of the lateral trochlear ridge or zona conoidea, often with some associated hypertrophic spurring along the posterior aspect of the lateral trochlear ridge. The lateral trochlear ridge articulates with the posteromedial radial head with maximal joint contact in supination. This articulation is proposed to play a significant role in joint stability but may be prone to the development of osteoarthritis.6,20

 

Imaging

AP and lateral X-rays are typically the first line of screening for an athlete with elbow pain. Radiographical detection of trochlear OCD may be challenging. Obtaining 45-degree flexion views and comparison views of the contralateral elbow may be helpful.7,26 Overlap of the ulna on the frontal projection may decrease conspicuity, and a subtle trochlear OCD lesion may be mistaken for a normal variant exaggerated trochlear notch angle on radiographs. However, no focal inferiorly directed concavity of the subchondral plate should be seen.5,27 X-rays may appear normal. Alternatively, they may demonstrate subtle focal subchondral rarefaction, focal subchondral sclerosis with or without fragmentation, or a focal semicircular inferiorly direct concavity at the articular surface, described by Pruthi et al. as the pseudo-intercondylar notch sign.4–6,14,19  Wang et al. noted that 94% of 28 trochlear OCD lesions were detectable radiographically in retrospect, with the majority demonstrating the pseudo-intercondylar notch sign. However, findings were subtle and were commonly missed.5,19  Marshall et al. found none of the smaller posteromedial trochlear lesions to be detectible radiographically. Similarly, more than half of the lateral trochlear ridge lesions were not conspicuous radiographically.4,6

In the at-risk athlete with persistent pain and negative or only subtle findings on X-rays, MRI is generally considered the most reliable study to evaluate for the presence of osteochondral lesions, associated osteochondral or soft tissue pathology, effusion, or joint bodies.  Regarding osteochondral lesions, the goal of MRI is to identify the size and location of osteochondral lesions, to assess the overlying cartilage, the stability, and, if possible, the viability of a lesion. While MRI findings associated with lesion instability have been investigated for the more common capitellar OCLs, the same has not yet been done for trochlear lesions. Some have advocated extrapolating from current knowledge regarding capitellar OCLs to guide the assessment and management of trochlear OCLs, though this has not yet been validated.14,28 Typical trochlear OCLs often demonstrate an inverted U-shaped area of uniform low to intermediate signal surrounded by peripheral hypo-intensity in the subchondral trochlear marrow on T1 weighted images (T1WI).  The area of abnormality may demonstrate normal, increased, or decreased intrinsic marrow signal on T2 weighted images (T2WI). Stable typical trochlear OCLs are sometimes more conspicuous on T1 rather than T2 weighted images.  Extrapolating from our understanding of OCLs elsewhere, signs indicative of an unstable lesion include a fluid filled osteochondral defect, a peripheral rim of T2 hyperintense signal approaching that of joint fluid surrounding the lesion, breaks in the subchondral plate, an in-situ osteochondral fragment that has shifted in position, multiple or large (>5mm) subchondral cysts deep to the lesion, a rim of peripheral enhancement following intravenous gadolinium administration or contrast intravasating into the plane between the defect and surrounding bone on an MR arthrographic images. Loose bodies may be associated with unstable lesions and have also been found in association with surgically proven stable OCLs with overlying chondral degeneration and delamination.  2,12,29

 

Figure 6

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14-year-old pitcher with worsening elbow pain when throwing for 18 months. Coronal T1-weighted image (6a) shows a small inverted U-shaped area of abnormal marrow signal of the subchondral lateral trochlea, which is isointense to skeletal muscle with a peripheral low signal rim (red arrow). Coronal fat suppressed T2-weighted image (6b) shows an inverted U-shaped area of intermediate to low signal in the same region with a thin peripheral rim of low signal and mild surrounding marrow edema (red arrow). The sagittal fat-suppressed proton density-weighted image (6c) shows the characteristic posteroinferior location of a “typical” trochlear OCL (dotted arc). The frontal elbow radiograph at the time of initial presentation (6d) shows a subtle inverted U-shaped subchondral lucency of the lateral trochlea (arrow) with a surrounding thin rim of sclerosis or the “pseudo-intercondylar notch sign.”

 

Figure 7

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16-year-old male complained of severe right elbow pain and popping for 9 months, worse when lifting weights. He also complained of mild crepitus with range of motion of contralateral left elbow. Frontal radiographs of the right (7a) and left (7b) elbow show bilateral “pseudo-intercondylar notch signs” (red arrows) consistent with bilateral trochlear OCLs. MRI of the right elbow was performed. Coronal T1-weighted image (7c) shows an inverted U-shaped area of intermediate signal in the subchondral marrow of the lateral trochlea with a peripheral low signal rim (red arrow). Corresponding coronal fat-suppressed T2-weighted image (7d) demonstrates variable intermediate and hyperintense signal within the osteochondral lesion, surrounded by a rim of dark signal and a more peripheral thin rim of marrow edema (red arrow). Chondral heterogeneity (arrowheads) compatible with degeneration is seen on the coronal fat-suppressed T2-weighted image (7d) and sagittal fat suppressed proton density-weighted image (7e). At arthroscopy chondral degeneration and a small full thickness fissure was noted over the lesion and portions of the lesion were thought to be unstable. The OCL was treated with arthroscopic cartilage debridement, antegrade and retrograde drilling.

 

Figure 8

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15-year-old male pitcher complained of several month history of elbow pain, worse with throwing. MR arthrogram was performed. The coronal fat-suppressed T1-weighted image (8a), coronal fat-suppressed proton density-weighted image (8b), and sagittal T2-weighted image (8c) reveal a small osteochondral defect of the lateral trochlea with intra-articular contrast and fluid equivalent signal extending into the OCL crater defect (arrows, 8a,b and c), mild peripheral hyperintensity on fat-suppressed T1-weighted image (arrowhead, 8a) and coronal fat- suppressed T2- weighted image (8b) suggestive of peripheral gadolinium imbibition and marrow edema. Imaging features indicated an unstable typical trochlear OCL, which was confirmed surgically.

 

Figure 9

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22-year-old male pitcher complained of medial elbow pain with throwing. He had a history of a prior grade 2 UCL sprain treated with PRP. A sagittal fat-suppressed proton density-weighted image (9a) and axial fat-suppressed T2-weighted image (9b) show a small focus of chondral heterogeneity of the posteromedial trochlea (arrow on 9a) with an underlying small subchondral cyst and mild adjacent marrow edema (arrowheads on 9a and 9b). The appearance is characteristic of an “atypical” trochlear OCL as is thought to be due to posteromedial impingement and valgus extension overload. Also seen were findings of a chronic UCL sprain (not shown).

 

Figure 10

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57-year-old male with elbow pain and suspected biceps tear. MRI showed a chronic complete biceps tear with 4.5 cm retraction (not shown). Coronal T1-weighted image (10a) and coronal fat-suppressed proton density-weighted image (10b) show a small OCL of the lateral trochlear ridge and zona conoidea (arrows) with overlying chondral heterogeneity, focal disruption of the subchondral plate along the medial margin of the lesion (arrowheads), possible very small in- situ partially detached osteochondral body and mild surrounding marrow edema.

 

Differential Diagnosis

On radiographs, the trochlear ossification center usually appears between the ages of 8-10 years in boys and between the ages of 7-11 years in girls.  Fusion of the trochlear ossification center with the capitellum usually occurs at about or after the 12th year in boys and the 10th year in girls.  Fusion of the trochlear and capitellar ossification centers with the distal humeral metaphysis usually occurs between the 13th and 16th years in boys and between the 12th and 14th years in girls. Initially, the trochlear ossification center may appear multicentric and irregularly shaped, which should not be mistaken for pathology.24,28,30

A small discrete focus of T2 hyperintensity may occur within the center of the cartilaginous pediatric trochlear epiphysis just before the appearance of the ossification center, representing the normal pre-ossification center. This does not extend to the cartilaginous surface and is a transient physiologic finding that may be seen before trochlear ossification in an age group significantly younger than the typical occurrence of trochlear OCD lesions at a mean age of 6.6 years.31

The primary differential diagnostic consideration in the setting of a “typical” trochlear osteochondral lesion is trochlear osteonecrosis (type A) with associated fishtail deformity.

Though rare, trochlear osteonecrosis is a known potential delayed complication of pediatric distal humeral trauma, including supracondylar, medial or lateral condylar, T- condylar distal humeral fractures, and distal humeral physeal injuries.  It has been reported in the setting of high-energy displaced fractures, low-energy minimally displaced injuries, and even in association with a simple elbow sprain.32,33 Iatrogenic causes of trochlear osteonecrosis include an open medial approach to the elbow, traumatic or operative posterior soft tissue stripping, posterior distal humeral fixation instrumentation, or misdirected pin passes.32,34,35,36  This has been attributed to the fact that the blood supply to the immature trochlea is susceptible to injury related to the superficial course of portions of the posterior dominant lateral trochlear epiphyseal end arterioles and medial end arterioles that lack anastomoses with each other or with metaphyseal vessels and as such result in vascular watershed areas between the medial and lateral condyles as well as the supracondylar region.16,22–24,34,36,37 The precise incidence of trochlear osteonecrosis is not known, as early on, it may go unrecognized, and mild cases may be subclinical. However, the incidence has been estimated at less than 0.5% of all fractures treated operatively. 34  In a review of 15 patients with fishtail deformity, the average time from initial injury to presentation with fishtail deformity was 4.9 years, the mean age at presentation was ten years, and most patients presented with pain and mechanical symptoms including loss of range of motion and locking. 34   The delay between initial injury and diagnosis may be explained by minimal initial symptomatology and the possibility that clinical findings may be masked by or attributed to a recent fracture. Early radiographic detection may also be limited because the trochlea does not typically ossify until 7-13 years and because of the variable appearance of the trochlear ossification center.36

Two patterns of trochlear osteonecrosis have been described: Type A, in which only the lateral trochlear ossification center is involved, and Type B, in which the entire trochlea and sometimes the distal medial humeral metaphysis are affected.

Type A osteonecrosis results in a “fishtail” deformity of the distal humerus, a term first coined by Wilson in 1955 to describe a central deficiency of the distal humeral epiphysis flanked by the more normally developed medial trochlear epiphysis and capitellum. This deformity results in an inverted V-shaped distal humeral contour that resembles a fish’s tailfin.34,35,38 Premature fusion of the physeal plate has also been proposed as the etiology for fishtail deformity. However, most recent literature favors osteonecrosis as the cause of the abnormality.39  Both patterns of trochlear osteonecrosis may lead to osteochondral abnormalities with premature osteoarthritis and joint bodies over time. The severity of functional loss seems to parallel the extent of the necrotic defect.34,36 Delayed onset ulnar neuropathy may occur in some individuals with trochlear osteonecrosis. 34,36  Type A osteonecrosis, particularly wide fishtail deformities, may develop proximal ulnar migration and radial head escape or lateral column instability but do not typically develop angular deformities.

Type B osteonecrosis results in diffuse hypoplasia or absence of the entire trochlea and sometimes the distal medial humeral metaphysis, usually with a cubitus varus deformity, which may progress with age and be associated with instability and accelerated osteoarthritis.

Because osteonecrosis results from the initial vascular injury, no treatment for the necrosis exists. Conservative therapies aimed at improving functional limitations and surgical procedures such as arthroscopic debridement, capsulotomy, and arthroplasty to address advanced arthrosis, contractures, and loose bodies, as well as physeal ablations or osteotomies to prevent progressive osseous deformities have been employed.34,36

While parallels exist between the location and etiology of most “typical” trochlear osteochondral lesions and fishtail deformity (type A osteonecrosis) in that both conditions may result in deformity of the lateral trochlea in a zone of vascular vulnerability, these are thought to represent separate entities.  Unlike trochlear osteochondral lesions, most individuals with trochlear osteonecrosis have a history of a prior elbow fracture. Trochlear osteochondral defects, in contrast to trochlear osteonecrosis, do not progress to trochlear dissolution, fishtail, or angular deformities. The imaging appearance differs in that most “typical” trochlear osteochondral defects appear radiographically as a focal inverted U-shaped radiolucent defect of the subchondral bone of the lateral trochlea, previously described as a “pseudo-intercondylar notch sign.”19 MRI often shows a corresponding focal inverted U-shaped area of signal alteration in the subchondral bone and possibly the articular cartilage of the affected area, surrounded by the normally developed adjacent trochlear and capitellar epiphyses.

Conversely, type A trochlear osteonecrosis usually results in a more diffusely misshapen and underdeveloped lateral trochlea with an inverted V-shaped central defect or fishtail deformity.  Radiographically, the affected ossification center may appear small, sclerotic, fragmented, or absent.4 MRI may show regional marrow and chondral signal hypo-intensity on t1 weighted images, with hypo-intensity or hyperintensity on T2WI in the affected portions of the trochlear epiphysis. 4,19,32,40 The articular cartilage surface is typically intact initially. However, with time and articular incongruence related to the epiphyseal deformity, secondary osteochondral abnormalities and findings of arthrosis are often seen.32

 

Figure 11

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14-year-old male complained of several month history of elbow pain. He had a history of a remote elbow injury as a young child, details not certain. Coronal T1-weighted image (11a) and coronal fat-suppressed T2-weighted image (11b) show diffuse marrow signal abnormality which is predominantly hypointense on both T1- and T2 -weighted images involving the trochlea (dotted red) with trochlear hypoplasia. Corresponding frontal radiograph of the elbow (11c) shows a sclerotic hypoplastic fragmented trochlear ossification center (dotted yellow). The findings are consistent with osteonecrosis of the trochlear ossification center.

 

Figure 12

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15-year-old male with elbow pain. Frontal elbow radiograph (12a) shows “fishtail deformity” of the distal humerus (dotted red) with osteoarthritis. The lateral radiograph (12b) demonstrates osteoarthritis with a large loose body in the coronoid fossa (arrow) and volar subluxation of the radial head relative to the capitellum. MR arthrographic fat-suppressed coronal T1-weighted (12c) and coronal fat-suppressed T2-weighted images show the fishtail deformity of the distal humerus (dotted red) with severe chondral loss at the ulnotrochlear joint and a large loose body in the coronoid fossa (arrow). The sagittal T2 -weighted image shows a misshapen hypoplastic trochlea (arrowheads), ulnotrochlear osteoarthritis and a large loose body in the coronoid fossa (arrow). The fishtail deformity is characterized by an inverted V-shaped deformity of the distal central humerus on a background of a diffusely misshapen and hypoplastic trochlea. Conversely, a "typical" trochlear OCL appears as a focal inverted U-shaped osteochondral defect (pseudo-intercondylar notch sign) on a background of a normally developed adjacent trochlea and capitellum.

 

Hegemann’s disease, which has been considered a form of osteochondrosis versus spontaneous or idiopathic osteonecrosis of the humeral trochlea, is a very rare condition that has been reported in preadolescent or adolescent individuals at an average age range of 7.8 years, younger than those typically presenting with OCL, and similar to Panner’s disease of the capitellum.40, 41,42  The precise etiology remains unclear, though the previously described vulnerable trochlear vascular supply and trauma,  chronic repetitive microtrauma, and unrecognized trauma have been proposed. Some have theorized that Hegemann’s may represent a mild and self-limited form of the distal humeral ischemia spectrum that, in more advanced cases, leads to fishtail and cubitus varus deformity.42  Patients may present with swelling, limited range of motion, and rarely pain. In contrast to the focal subchondral abnormality noted with OCL, the trochlear ossification center is diffusely involved, with radiographs demonstrating diffuse rarefaction or lucency, which may progress to sclerosis, irregularity, fragmentation, and collapse, with or without subsequent regeneration.40–42  

Because Hegemann’s disease is very rare, the available knowledge regarding the condition has largely been gleaned from multiple case reports. These usually did not include initial and follow up MRI evaluation and frequently utilized inconsistent outcome measurements and follow periods. Given this, conclusive data regarding the disease prognosis is lacking. Though initially Hegemann’s disease was thought to be an innocuous condition, a systematic review found that no complete recovery was seen in four of six cases for which follow-up was performed.42

Other potential differential considerations in the radiographic diagnosis of trochlear osteochondral lesions might include chondroblastoma, osteoid osteoma, or synovial chondromatosis, though usually presenting clinical features, and MRI will help to differentiate these entities.

 

 

Treatment and Outcomes

Because trochlear osteochondral lesions are rare, treatment protocols have not yet been well established, though some have proposed extrapolating from treatment guidelines for capitellar OCD lesions. 9,14 Elbow radiographs are usually the initial screening exam for those with elbow pain, though they may underestimate pathology.  MRI is utilized to assess the soft tissues and osteochondral structures and may provide important information regarding the size, location, suspected stability of the lesion, integrity of the overlying cartilage, presence or absence of loose bodies, and marrow signal abnormality suspicious for necrosis. For those patients without mechanical symptoms and those thought to have a stable lesion without articular incongruity or a joint body, some authors recommend rest and activity modification until pain-free and for up to 3-6 months with a gradual return to sport.4 A brief period of immobilization in an unlocked hinge brace may be offered to provide symptomatic relief for those presenting with acute symptoms. Gentle physical therapy, without axial loading or strengthening, is initiated early to regain motion for those with flexion or extension contractures.5  Arthroscopic intervention is indicated in those who have failed initial conservative management, in those with mechanical symptoms, unstable lesions, and loose bodies, and in those with coexistent ligamentous or osteochondral pathology for which surgery is indicated. Given the adjacent olecranon and coronoid processes, surgical access to the trochlea is more challenging than for the capitellum, which may contribute to a higher threshold for surgical intervention for trochlear as opposed to capitellar OCLs.5

A 2022 systematic review of trochlear OCLs included 16 studies and 75 elbows with trochlear OCD lesions, 77% of which were lateral and 23% medial. They found that 86% of these elbows were treated nonoperatively, and surgical management was provided in 14%. The surgery was arthroscopic in 13 elbows and open in 12 elbows. Arthroscopic procedures most frequently involved microfracture and debridement, followed by loose body removal and synovectomy. Open surgeries most frequently included drilling or microfracture and debridement. Retrograde nailing, olecranon osteotomy and OCD fixation, osteochondral transplantation, grafting from the olecranon, and anterior capsular release were less frequently performed. The percentage of lateral lesions requiring operative treatment was 43%, and the percentage of medial lesions requiring surgery was 44%.  Although follow-up data for both the nonoperative and operative groups was incomplete and inconsistent, available data suggested that 91% of those in the nonoperative group had resolution of pain, and 95% of those in the operative group had resolution of pain post-operatively.  When data regarding return to play was available and where applicable, all those in both the nonoperative and operative groups were reported to have returned to previous activities.4–6,9,14

 

Summary

  1. Trochlear OCLs are very uncommon, but the diagnosis should be considered in an adolescent with medial elbow pain, crepitus, or limited range of motion in at-risk (throwing or tumbling) athletes.
  2. Radiographs are used for initial screening but are relatively insensitive for small lesions.
  3. MRI should report the lesion size and location, the presence or absence of a loose body, and any coexistent osteochondral or ligamentous abnormality. Lesion stability may be estimated extrapolating from knowledge regarding MRI findings of stability for OCLs of other joints, however the accuracy of MRI for assessing the stability of trochlear OCLs has not yet been well evaluated.
  4. There are two main subgroups of trochlear OCLs:
    1. Typical – larger (than atypical OCLs), more inferiorly positioned, the majority occur laterally in the zone of vulnerable trochlear vascular supply.
    2. Atypical – smaller, posteromedial, may have associated ligamentous sprains, thought to be due to posteromedial impingement and valgus extension overload.
  5. Early detection and rest/activity modification may improve outcomes. Surgery is advised for suspected unstable lesions, joint body, and or failure to improve with rest.
  6. Differential diagnosis- The leading differential consideration for typical trochlear OCLs is fishtail deformity (type A trochlear osteonecrosis), which is usually associated with a history of childhood fracture and usually demonstrates an inverted V-shaped central distal humeral defect surrounded by a diffusely misshapen and underdeveloped trochlea.

A special thanks to Dr. David Rubin for providing multiple cases for this Web Clinic and to Dr. Michael Stadnick for providing multiple illustrations.

 

References

  1. Kessler JI, Jacobs JC, Cannamela PC, Weiss JM, Shea KG. Demographics and Epidemiology of Osteochondritis Dissecans of the Elbow Among Children and Adolescents. Orthop J Sports Med. 2018;6(12). doi:10.1177/2325967118815846 ↩
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