The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 78, Issue 3

Current Concepts Review | March 01, 1996

Current Concept Review - Osteochondritis Dissecans*

ROBERT C. SCHENCK, JR., M.D.†; JON MARC GOODNIGHT, M.D.†, SAN ANTONIO, TEXAS

*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. No funds were received in support of this study.

J Bone Joint Surg Am, 1996 Mar 01;78(3):439-56

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Extract

Osteochondritis dissecans is a localized injury or condition affecting an articular surface that involves separation of a segment of cartilage and subchondral bone. It is found primarily in the ankle, knee, and elbow joints. Although relatively infrequent, osteochondritis dissecans has been reported extensively in the orthopaedic literature. Various theories about its etiology have been proposed, but none has been accepted universally or has adequately explained its occurrence; however, the lesion is probably caused by factors that vary depending on the specific joint involved and on the specific site within that joint. The treatment of osteochondritis dissecans has evolved from the removal of loose bodies, first reported more than 150 years ago¹⁰⁸, to the resurfacing of defects with an osteochondral autogenous graft¹⁵⁸. The results of current treatment are still not uniformly successful.

Figures in this Article

Introduction

Osteochondritis dissecans has been confused with other abnormalities of the joint surface, and therefore the orthopaedic literature must be read with care. Other, severe conditions described in the literature have been grouped under the heading of osteochondritis dissecans; these have included osteochondral fractures^{104,110,116,123,133}, osteonecrosis, accessory centers of ossification, osteochondrosis, and hereditary epiphyseal dysplasia^{22,118,119,147}. In several clinical investigations, different terms, such as osteochondrosis dissecans¹⁰⁷ and osteochondral fragments^{51,70,81,83,122}, have been used to describe this entity. The recognition that many disorders may result in an osteochondritis dissecans-like lesion is fundamental to an understanding of this condition.

The orthopaedic literature includes descriptions of lesions of osteochondritis dissecans in the talus^5,12,28, the capitellum^19,96,156, the patella^43,127,138, the femoral head¹⁰⁷, the distal part of the tibia¹⁰, and the wrist^52,148. The male: female ratio has been reported as two to one¹⁰⁷ and as three to one^31,101, with eight (33 per cent) of twenty-four patients having bilateral involvement in one series⁵⁹. The current review will concentrate on osteochondritis dissecans at its most common sites: the knee, ankle, and elbow.

Osteochondritis dissecans affects two distinct populations of patients as differentiated by the status of the physes. Children and adolescents between the ages of five and approximately fifteen years old who have open physes have the juvenile form of the disease^22,59. Older adolescents who have closed physes and adults are classified as having the adult form. Osteochondritis dissecans is rare in patients who are less than ten or more than fifty years old⁷⁹. It is most frequently seen in young male patients, especially athletes¹. The knee is the most commonly affected joint¹⁰⁷, being involved in about 75 per cent of patients³¹.

†Department of Orthopaedics, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78284-7774.

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Figs. 1-A through 1-E: The right knee of a sixteen-year-old girl who had osteochondritis dissecans of the lateral aspect of the medial femoral condyle. Fig. 1-A: Anteroposterior radiograph showing the lesion (arrows).

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Fig. 1-B: Lateral radiograph showing the posterior position of the lesion (arrows) on the lateral aspect of the medial femoral condyle.

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Fig. 1-C: Tunnel radiograph showing a loose body (arrow).

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Fig. 1-D: Tunnel radiograph, made with the knee in greater flexion than in Fig. 1-C, showing the lesion (arrows).

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Magnetic resonance image showing the lesion (arrows).

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Anteroposterior and lateral views of the knee, showing the radiographic classification described by Cahill and Berg^23,24.

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Anteroposterior and lateral views of the knee, showing the radiographic classification described by Cahill and Berg^23,24.

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Figs. 3-A and 3-B: Radiographs of a knee that had a large osteochondritis dissecans lesion of the medial femoral condyle. Fig. 3-A: Tunnel radiograph.

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Fig. 3-B: Lateral radiograph after compression fixation with cannulated 4.0-millimeter AO screws.

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Figs. 4-A and 4-B: Anteroposterior radiographs of a patient who sustained a severe sprain of the ankle in a motor-vehicle accident. Fig. 4-A: Immediately after the injury.

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Fig. 4-B: Sixteen months after the injury, a lateral stage-III osteochondritis dissecans lesion of the talus is visible. The solid arrow indicates the base of the defect, and the arrow outlined in white points to the detached lesion.

History

Paré¹⁰⁸ is credited with being the first to describe the removal of loose bodies, presumably osteochondral fragments, from joints, in a report published in 1840. In 1870, Paget¹⁰⁶ described a pathological process that he termed quiet necrosis, which resulted in the creation of loose, necrotic osteochondral fragments from articular surfaces. König⁷⁴, in 1888, described a pathological condition that led to the formation of loose bodies (referred to as arthrophytes or corpora mobile in that era) of femoral origin that were found in hip and knee joints with no evidence of pre-existing trauma. He believed that an inflammatory reaction of both the bone and the cartilage, followed by spontaneous necrosis, was a major component of this condition, and he chose the term accordingly: osteochondritis, referring to an inflammation of the osteochondral joint surface, and dissecans, derived from the Latin dissec, which means to separate. Later investigators¹⁰¹ noted the absence of inflammatory cells in histological sections of excised osteochondral loose bodies and believed that trauma was a more important etiological factor. Nevertheless, use of the original name has persisted.

Osteochondritis dissecans, as described in the earlier literature, usually was treated either non-operatively or with an arthrotomy for removal of the loose fragment^13,149. Closed treatment is still preferred for patients who are first seen early in the disease process and for those who have open physes. As diagnostic capabilities and knowledge of osteochondral healing have progressed, additional options have become available for operative treatment of the lesions in later stages. Magnetic resonance imaging has become useful in the staging of lesions in the knee, elbow, and ankle. The advent of diagnostic and operative arthroscopy has resulted in more detailed pathological descriptions and, theoretically, in a lower rate of morbidity. Drilling of the site of the defect, fixation of the lesion to the site of separation, and placement of osteochondral grafts have been described^{4,18,57,70,82,83,87,89,129,130,141,158}. Current methods of operative treatment involve fixation of the lesion or drilling of the site of the defect with removal of loose bodies.

Osteochondritis Dissecans of the Knee

Clinical Presentation

The symptoms of osteochondritis dissecans of the knee depend on the stage of presentation. Lesions early in their course are associated with poorly defined symptoms. Pain and swelling are variable. As the lesion progresses, catching, locking, and giving-way are noted. Locking, in which motion of the knee is halted, is distinguished from catching, in which motion is partially inhibited. The symptoms are frequently intermittent and are related to activity or exertion. The presence of loose bodies is associated with more constant symptoms of catching or locking, swelling, and pain. Patients who have an advanced lesion may note a sensation of having a foreign body within the affected joint³¹.

The age of the patient at the time of presentation is the primary determinant of treatment. In children and adolescents with open physes, osteochondritis dissecans of the knee is classified as the juvenile form. The average age of the patients at the time of the diagnosis has ranged from 11.3 to 13.4 years^23,24,98. Mubarak and Carroll⁹⁸ reported on seventy-three patients who had juvenile osteochondritis dissecans, fifty-one (70 per cent) of whom were male. The average age at the time of the diagnosis was 13.4 years. After the physes had closed, the patients were classified as having the adult form of the disease. Although adult osteochondritis dissecans may arise de novo, it is usually the result of an incompletely healed and previously asymptomatic lesion from juvenile osteochondritis dissecans. The age at the time of presentation of adult osteochondritis dissecans has usually ranged from seventeen to thirty-six years²³, but it can be seen at any adult age. The symptoms are similar to those of juvenile osteochondritis dissecans and include swelling, catching, and locking of the knee.

Physical Examination

The lateral aspect of the medial femoral condyle is the most commonly affected location in the knee, with physical findings localized to this area. Weight-bearing surfaces of the medial and lateral femoral condyles are frequently involved; osteochondritis dissecans should not be considered an affliction of only the non-weight-bearing portion of the medial femoral condyle²³. The physical examination may reveal crepitus in the medial tibiofemoral compartment. A joint effusion may be associated with any condition in which there is mechanical irritation, including osteochondritis dissecans. Tenderness may be diffuse and poorly localized in the early stages of the disease, but well defined point tenderness is usually present in the later stages.

A patient who has a lesion of the medial femoral condyle may walk with the leg externally rotated in an attempt to avoid impingement of the tibial spine on the lateral aspect of the condyle. Wilson¹⁵² described a physical sign for osteochondritis dissecans of the knee. The sign is elicited by flexing the knee to 90 degrees, internally rotating the tibia, and then slowly extending the knee. A positive Wilson sign is pain at approximately 30 degrees of flexion that is relieved by external rotation of the tibia.

Imaging Studies

The medial femoral condyle is affected in 73 to 85 per cent of patients (114 of 156 in one study⁷⁹ and eighty-five of 100 in another¹), with approximately one-quarter having involvement of the weight-bearing portion of the condyle. A notch or tunnel posteroanterior radiograph is the best way to visualize a lesion in this location⁹⁴.

On radiographs, the lesion typically appears as a well circumscribed area of sclerotic subchondral bone separated from the remainder of the epiphysis by a radiolucent line (Figs. 1-A, 1-B, 1-C, 1-D through 1-E). If only anteroposterior and lateral radiographs are used, the lateral radiograph is the most helpful, as noted by Harding⁶⁵. Harding described two lines drawn on the lateral radiograph: one along the posterior femoral cortex and the other along the Blumensaat line (intercondylar notch). The arc of articular surface between these two lines is the common location of lesions of osteochondritis dissecans on the medial femoral condyle. Cahill and Berg^23,24 described a useful classification system in which the anteroposterior radiograph is divided into five segments: the notch is designated as segment 3; the medial tibiofemoral compartment is divided into segments 1 and 2; and the lateral tibiofemoral compartment is divided into two equal segments, 4 and 5. The lateral radiograph is divided into three segments on the basis of Harding's description: A, anterior to the Blumensaat line; B, between the Blumensaat line and a median drawn from the posterior femoral cortex; and C, the condylar area posterior to a line drawn along the posterior femoral cortex. A posteromedial femoral condylar lesion involving the entire weight-bearing surface would be classified as C1—2 (Figs. 2-A and 2-B).

Cahill and Berg²⁴ described the appearance of osteochondritis dissecans with use of technetium bone scintigraphy, performed every six weeks. They noted the sensitivity of such bone scans as a measure of osteoblastic activity and regional blood flow. They also noted that the degree of osseous uptake seemed to be related to the remaining potential for healing of the fragment. On the basis of the degree of uptake, they described four stages of lesions: stage I—the lesion is visible on plain radiographs, but bone scans reveal normal findings; stage II—the scan reveals increased uptake in the area of the lesion, which can also be seen on plain radiographs; stage III—in addition to the stage-II findings, there is increased isotopic uptake in the entire femoral condyle; and stage IV—all of the characteristics of stage III are present and there is also uptake in the tibial plateau opposite the lesion. These investigators used technetium imaging to plan a course of treatment. They believed that stage I indicates either a healed fragment or an unhealed lesion without osteoblastic activity. They assumed that a lesion that was stage II or higher had potential for repair as a result of the apparent osteoblastic activity, and they considered bone-grafting unnecessary for such lesions. They also thought that a symptomatic patient with a stage-I or II lesion should be allowed to return to sports activities^23,24.

Magnetic resonance imaging has recently been used in the evaluation of patients with osteochondritis dissecans^{41,75,93,102,112}. Mesgarzadeh et al.⁹³ reported that magnetic resonance imaging permits visualization of loose bodies and of the degree of displacement of the major fragment. These authors recommended use of this technique to follow the healing response and the degree of revascularization of the lesion. Dipaola et al.⁴¹ studied the relationship between the appearance on arthroscopy and that on magnetic resonance imaging of osteochondritis dissecans lesions. The findings on the magnetic resonance images correlated closely with the arthroscopic classification, but they correlated poorly with plain radiographic findings. In other words, lesions that appeared similar on plain radiographs were seen to be widely disparate on magnetic resonance imaging, suggesting that magnetic resonance imaging is more sensitive in the evaluation of these lesions. Magnetic resonance imaging also allows determination of displacement of the fragment, the fluid interfaces, and the integrity of the articular surface. Magnetic resonance imaging and computed tomography are used in preoperative planning to determine if the fragment is detached.

Kramer et al.⁷⁵ used magnetic resonance arthrography with contrast medium to determine the stage of the lesion and whether it was detached, and the imaging findings were verified in twenty-four of twenty-five knees at the time of arthroscopy. The integrity of the surface of an osteochondritis dissecans lesion can be detected with magnetic resonance imaging, but detection is improved in the presence of an effusion because of the orthographic effect of free joint fluid on T2-weighted images. These authors noted improvement in the detection of all types of lesions after intra-articular injection of gadolinium (Magnevest; Schering, Berlin, Germany). Other authors have noted the sensitivity of a fluid interface secondary to an effusion in determining the presence of a detached osteochondritis dissecans lesion^{40,41,66,100,153,160}.

Nelson et al.¹⁰², in 1990, used magnetic resonance imaging to predict the grade of the lesion in eleven of twelve patients at the time of arthroscopy. In one patient, a grade-2 lesion was thought by both radiologists to be grade 3, according to the classification system described by Clanton and DeLee³¹ (grade 1, a depressed osteochondral fracture; grade 2, an osteochondral fragment attached by an osseous bridge; grade 3, a detached, non-displaced fragment; and grade 4, a displaced fragment [loose body]).

Etiology

Trauma

Trauma has been discussed as a possible etiological factor in the development of osteochondritis dissecans lesions of the knee^50,56,154. Direct trauma, such as a blow to the knee, obviously could create a transchondral fracture of the femoral condylar surface. However, because of the predilection of osteochondritis dissecans for the posterolateral portion of the medial femoral condyle, most investigators have proposed indirect trauma as a factor.

Fairbank⁴⁷ proposed that repetitive impingement of the tibial spine on the lateral aspect of the medial femoral condyle during internal rotation of the tibia is a causative factor in osteochondritis dissecans. This theory was later supported by Smillie¹³¹, who thought that concomitant ligamentous laxity is an associated factor. Another indirect traumatic etiology was postulated by Aichroth¹, who noted that the odd facet of the patella articulates with the classic site of osteochondritis dissecans on the medial femoral condyle when the knee is in full flexion. He thought that the lesion is caused by an ununited subchondral fracture in association with pathological patellofemoral contact. The classic osteochondral fracture of the lateral femoral condyle secondary to a patellofemoral dislocation has been described separately from these lesions and possible etiological factors. Makin⁹⁰ reported on osteochondral fractures of the lateral femoral condyle secondary to reduction of the patella. He correctly considered these to be acute transchondral fractures rather than osteochondritis dissecans lesions per se^72,77,92. Cahill²³ recently described osteochondritis dissecans as a stress fracture in 204 patients who recalled no obvious traumatic event. Mubarak and Carroll⁹⁸ noted that trauma is an unlikely cause of osteochondritis dissecans since affected sites are located at specific locations in the knee and not randomly, as would be expected with trauma. The role of indirect microtrauma as an etiological factor remains theoretical.

Ischemia

A vascular mechanism has also been proposed as an etiology of osteochondritis dissecans^27,30,44,59. This theory suggests that an abnormal subchondral bone structure allows susceptibility to a pathological fracture. Enneking⁴⁴ stated that subchondral bone has a vascular end arterial arcade, much like the bowel mesentery, with poor anastomoses to surrounding arterioles. He thought that, in osteochondritis dissecans of the knee, a diminished local blood supply results in an ischemic segment of bone, which then behaves like a sequestrum. Ingrowth of vascular and mesenchymal buds causes resorption of the necrotic bone, and granulation tissue is formed between the viable and the necrotic bone. Trauma then causes the overlying articular cartilage to fracture, and a loose osteochondral fragment is produced. Rogers and Gladstone¹²¹ also studied the vascularity of the distal part of the femur, and their data conflict with those of Enneking⁴⁴. They found that the blood supply to the condylar region of the femur is very rich, with numerous anastomoses to intramedullary cancellous bone. Therefore, they suggested that ischemia is an unlikely etiology of osteochondritis dissecans of the knee.

Osteonecrosis of the knee may produce an osteochondral lesion similar to that of osteochondritis dissecans⁴⁹. An osteochondral fracture that is secondary to osteonecrosis must be classified as a clinical entity separate from that of osteochondritis dissecans, although some early reports of osteochondritis dissecans may have included such fractures^31,149.

Chiroff and Cooke³⁰ studied the histological characteristics of six excised lesions of osteochondritis dissecans. Two specimens were loose bodies, and four were fragments that had been partially detached. They found no signs of avascular necrosis in the sections of bone, additional evidence against a vascular etiology for osteochondritis dissecans.

Defects of Ossification

Some authors have proposed that osteochondritis dissecans in young patients results from an abnormality of ossification that fails to heal^{8,9,21,78,117}. It has been theorized that, with such an abnormality, stress to the affected osteochondral segment results in partial or complete detachment. Ribbing¹¹⁷, in 1955, described a separation of the accessory ossific nucleus during childhood with subsequent partial reattachment. Subsequent episodes of trauma led to complete separation of the chondral surface and to an osteochondritis dissecans lesion. He proposed a mechanism of traumatic vascular disruption between the center of ossification and the detached osseous islets that results in avascular necrosis of the islets. He theorized that a zone of fibrocartilage and avascular fibrous tissue is thus created in the area vacated by the separated fragment. Ribbing¹¹⁷ noted that "the aetiology of osteochondrosis dissecans is complex; it is both constitutional and traumatic. An accessory bone nucleus, detached in childhood, during adolescence partly fuses into the adjacent cancellous bone and partly remains separated from the latter by islands and strands of persisting cartilage."

Caffey et al.²¹ reviewed the radiographs of children who had marginal irregularities in the epiphyseal outline of the distal part of the femur and divided the patients into three groups. Patients in group I had varying degrees of roughening of the epiphyseal surface and small areas of calcification beyond the irregular margin, those in group II had larger indentations in the epiphysis, and those in group III had the same characteristics as those in group II as well as independent islands of bone in the marginal indentation or crater. These investigators thought that the radiographs of the patients in groups II and III resembled those of patients who have osteochondritis dissecans.

Sontag and Pyle¹³⁴, however, reported that irregularity or roughening of the epiphyseal outline of the distal femoral epiphysis may be a normal variant. They were able to associate these irregularities with periods of rapid skeletal growth. Their data may constitute an argument against the theory that abnormal ossification is associated with osteochondritis dissecans, as the epiphyseal defects seen in many patients with early lesions may have been a result of normal development.

Mubarak and Carroll, in two studies^97,98, carefully examined patients who had juvenile osteochondritis dissecans of the knee. In 1979, they reported on a family in which twenty of thirty-one members had the lesion⁹⁷. Interestingly, radiographs of all of the children who were less than twelve years old showed irregularity of ossification bilaterally in at least one location. These authors thought that juvenile osteochondritis dissecans is usually the result of irregularities of ossification. They later reported on seventy-three patients who had osteochondritis dissecans of the knee, thirty-four (47 per cent) of whom had multiple lesions⁹⁸. They concluded that multiple lesions may represent a forme fruste of epiphyseal dysplasia. They found little support for the concept that either internal trauma (to the tibial spine or the cruciate ligaments) or external trauma causes the disorder.

Genetic Causes

Several studies^{54,97,136,137,150} have documented families with a predisposition for osteochondritis dissecans in various joints. Ribbing¹¹⁷ suggested that osteochondritis dissecans represents a subgroup within a larger category of epiphyseal disturbance. The diagnosis of multiple epiphyseal dysplasia should be ruled out in all patients in whom the diagnosis of osteochondritis dissecans is being considered. Multiple epiphyseal dysplasia is known to be propagated by autosomal dominant and autosomal recessive mechanisms, and some of the patients in these series may have had varying degrees of this disorder. Associations between osteochondritis dissecans and dwarfism, tibia vara, and Legg-Calvé-Perthes disease have been reported^143,150,157. As was noted earlier, Mubarak and Carroll⁹⁷ found abnormalities of ossification in one family with osteochondritis dissecans.

In a review in 1977, Petrie¹¹¹ found no definite genetic etiology for osteochondritis dissecans. First-degree relatives of thirty-four patients who had osteochondritis dissecans were studied for the presence of the disease, and only one was found to have it. A hereditary influence in some patients who have osteochondritis dissecans has been reported by Stougaard^136,137, Gardiner⁵⁴, and others^{53,63,103,113,114,132}. However, in most patients, hereditary influence is probably slight.

Natural History and Treatment

The natural history of osteochondritis dissecans about the knee depends on the age of the patient at the time of presentation. Lesions affecting children (that is, lesions of juvenile osteochondritis dissecans in patients with open physes) frequently heal. Those that do not heal and lead the child's parents to seek medical attention result from continued activity²³. Adult forms of osteochondritis dissecans of the knee rarely heal with non-operative treatment²³. It is theorized that, in both age-groups, the articular cartilage softens as it loses the support of the subchondral layer of bone. If the disease process is not arrested, additional trauma causes separation of a bone fragment, and a crater remains. The physical separation of the segment of bone renders healing unlikely. If the lesion involves the weight-bearing surface of the joint, the incongruity of the articular surface progresses to more advanced changes consistent with degenerative joint disease.

The treatment of osteochondritis dissecans remains somewhat controversial for several reasons⁴. Because this disorder is relatively uncommon, most physicians have not had substantial clinical experience with a large number of patients. Healing of created osteochondral defects with cartilaginous tissue has been noted in experimental animal models¹²⁴, but there has been limited success in humans. The ability to induce mechanically sound hyaline cartilage to cover the surface of subchondral bone is truly a therapeutic challenge¹⁷. Furthermore, osteochondritis dissecans affects many different joints, and the lesions vary with regard to size, location, stage of progression, and mechanism of injury. These many variables of presentation make it difficult to draw meaningful conclusions from the literature. To our knowledge, no prospective, randomized clinical trials have been performed to compare various regimens of treatment for damage to the articular surface. Furthermore, there is confusion because of the presentation in the literature of juvenile and adult osteochondritis dissecans as the same condition²³.

DePalma et al.³⁹ and Mitchell and Shepard⁹⁵ described the reparative process that articular cartilage undergoes during the healing response. Defects of articular cartilage do not heal with the regeneration of normal cartilage; instead, they are filled with mesenchymal tissue, which is converted into fibrocartilage. This newly formed fibrocartilage possesses a decreased amount of proteoglycans compared with that found in hyaline cartilage. Fibrocartilage is less resilient than normal articular hyaline cartilage, and continued trauma to the joint eventually leads to degeneration of the articular surface⁷⁶.

Green and Banks⁵⁹ used a cast or brace in an attempt to prevent fragmentation of the joint surface so that healing could progress. In their series of twenty-four patients who ranged in age from four to fifteen years old (seventeen patients were less than twelve years old), they reported an excellent result (normal physical and radiographic findings and no symptoms) in seventeen of eighteen children who had been managed non-operatively with a brace or cast for an average of four months. Eight patients had a bilateral lesion about the knee.

Chiroff and Cooke³⁰ studied the histological and microradiographic characteristics of osteochondritis dissecans lesions in older adolescents and young adults. They found no completely detached lesions, and the underlying bone was viable, being covered by a bed of fibrocartilage that was undergoing endochondral ossification. Because signs of healing were present, these authors recommended non-operative management, unless the lesion was completely separated, for this subset of patients.

Crawfurd et al.³⁴ noted the importance of the location of the lesion within the joint. They studied twenty-one undetached lesions of the knee that had been left in situ and that had been determined to be stable on arthroscopy. Follow-up arthroscopy at an average of 7.5 years showed healing of thirteen lesions. Ten of the twenty-one lesions were in the common location on the lateral aspect of the medial femoral condyle and only three of these had healed, compared with ten of eleven stable lesions located elsewhere in the joint. These authors concluded that stable osteochondritis dissecans lesions in the common location in the knee often do not heal spontaneously, and they recommended that these lesions be treated with internal fixation.

Linden⁸⁰ described the natural history of osteochondritis dissecans lesions in sixty-seven joints of fifty-eight patients, who had been followed clinically and radiographically. At an average of thirty-three years, no loose fragments had been replaced and no internal fixation had been used. Children who had open physes did not have secondary degenerative changes; however, thirty-eight of forty-eight patients who had had the first manifestation of the disease after closure of the physes had gonarthrosis. Linden stated that "symptoms and roentgenographic gonarthrosis become more frequent and approach 100 per cent with time." Löfgren⁸⁵ also noted spontaneous healing of osteochondritis dissecans lesions in children.

The basic tenets of operative treatment include restoration of the congruity of the joint surfaces, enhancement of the local blood supply to the fragment or crater, rigid fixation of unstable fragments, and protected weight-bearing with motion of the joint as soon as possible postoperatively. Accepted operative indications include symptomatic loose bodies; detachment that occurs during observation or non-operative treatment; predicted physeal closure within six to twelve months; juvenile lesions that remain symptomatic despite adequate non-operative treatment; and an established non-union of a fragment, determined on the basis of bone scans, magnetic resonance imaging, and clinical judgment²².

Most children who have juvenile osteochondritis dissecans and open physes can be successfully managed non-operatively^{14,22,23,29,42,59,80,130,139,146,151}. The chance that such treatment will be successful decreases with closure of the physes. Cahill²² recommended non-operative treatment only if progression of the lesion and the clinical response of the patient could be closely monitored and if at least six to twelve months remained before closure of the physes. Cahill proposed limitation of activities until the patient was free of symptoms as well as protected weight-bearing with use of splints or crutches²². He did not believe that a cast should be used because of the deleterious effects of immobilization, an observation supported by Hughston et al.⁶⁷. Cahill²² recommended that non-operative treatment be abandoned if symptoms persist for three months and if serial bone scans show little or no increase in uptake.

Smillie^130,131 was apparently the first to recommend open drilling, replacement, and internal fixation for a loose, separated fragment in the knee joint. Internal fixation of the loose fragment has also been advocated by Anderson et al.⁴, Cahill²², Green⁵⁸, Hughston et al.⁶⁷, Lipscomb et al.⁸⁴, and Outerbridge¹⁰⁵. Many authors have discussed fixation of loose osteochondritis dissecans lesions to allow healing^26,32,82.

Treatment of osteochondritis dissecans with simple excision of the loose or partially attached fragment in the knee has been reported to be unsuccessful by several authors^{3,22,23,58,60,67}. Green⁵⁸ noted poor results after excision but recognized the technical difficulty associated with replacement of a loose fragment. He thought that the results of replacement, if not precise, may be worse than those of excision because of residual irregularity of the articular surface; therefore, he recommended replacement of a large fragment but excision of a smaller one if it cannot be replaced anatomically. Hughston et al.⁶⁷ thought that open arthrotomy and internal fixation with Kirschner wires to fix a large fragment yielded better results than did excision and curettage of the base of the crater. Almgård and Wikstad³ also recognized the poor results of excision and recommended the routine use of arthrograms to guide treatment. They advocated limitation of activity and protected weight-bearing for patients who had intact articular cartilage. For those who had disruption of the cartilage, they recommended internal fixation of an attached fragment and extraction of loose bodies with reconstruction of the intra-articular defect. These authors did not elaborate on their technique of reconstruction of the defect³. Cahill^22,24 also noted categorically poor results with simple excision of a fragment about the knee.

Smillie¹³⁰ was one of the first to describe fixation of a separated osteochondritis dissecans lesion with use of pins. Lipscomb et al.⁸⁴ used Kirschner wires to reattach a large fragment and emphasized the importance of removal of the fibrous tissue at the base of the crater, drilling of the bed of the defect to increase vascularity, and use of bone graft to restore the congruity of the joint surfaces if necessary.

Cahill²² suggested that, since the results of excision are so poor, this procedure should be considered ineffective and every effort should be made to replace a loose fragment unless the degree of maceration prevents reattachment. With his method, the lesion is curetted down to bleeding subchondral bone, with care being taken to avoid overexcavation. The base of the crater is then drilled in an attempt to enhance vascularity, and the fragment is trimmed, replaced, and securely fixed with Kirschner wires. The Kirschner wires are later removed in a retrograde fashion to avoid disturbance of the healing osteochondral segment. Bone-grafting is used to elevate a fragment that would remain depressed when replaced.

Fixation with bone pegs^{57,70,83,128,129} involves the use of autogenous corticocancellous bone graft for internal fixation of the osteochondritis dissecans lesion to the site of the defect. Matchstick-sized strips of corticocancellous bone are obtained from the proximal part of the tibia and placed into the fragment and the site of the defect. Cancellous bone-graft material is packed as needed into the lesion to restore articular congruity. Lindholm et al.⁸³ reported good results with this method for sixteen of eighteen lesions, with eventual healing of the defect in all seventeen patients who were studied. Johnson and McLeod⁷⁰ used this technique in two patients; they noted that it provided easy access to bone-graft material and obviated the need for removal of the hardware while providing biological fixation, which may stimulate revascularization of the subchondral bone. They also noted that Kirschner wires can provide poor fixation and may be bent or broken in the postoperative period and protrude into the joint. Scott and Stevenson¹²⁸ used this technique with supplemental Kirschner-wire fixation in fifty-four patients; forty-seven were able to return to active military duty. Slough et al.¹²⁹ recently reported good results with use of bone-peg fixation in eight of ten knees (nine patients), at an average of 2.9 years.

Attention has recently been focused on the reconstruction of osteochondritis dissecans defects with use of osteochondral allogeneic and autogenous grafts. McDermott et al.⁸⁷ inserted allogeneic grafts, within twenty-four hours after they had been obtained, to reconstruct 100 osteochondral defects resulting from various conditions, including osteonecrosis, osteoarthrosis, trauma, and osteochondritis dissecans. Four of the defects were the result of osteochondritis dissecans, and the treatment was successful for only one of them. McDermott et al. concluded that this technique may be better suited for indications other than osteochondritis dissecans. Garrett⁵⁵ reported the results in twenty-four patients who had an osteochondral defect of the knee that had been treated with an osteochondral allogeneic graft; all twenty-four had improvement postoperatively. Radiographs showed osseous bridging at six to twelve weeks, and arthroscopy revealed apparent viable articular cartilage without chondromalacia⁵⁵. Yamashita et al.¹⁵⁸ used internal fixation with AO screws in the transplantation of osteochondral autogenous grafts in two patients. The grafts were taken from a non-weight-bearing portion of the medial femoral condyle. Transplantation was followed by a period of non-weight-bearing and by subsequent removal of the screws. A biopsy performed at the time of the removal of the screws showed viability of the graft.

Arthroscopy

Arthroscopy is a valuable tool in the evaluation and treatment of osteochondritis dissecans of the knee. The arthroscope provides direct visualization of the lesion, a less invasive means for operative treatment than open arthrotomy, and documentation of healing^{16,35,48,61,62}.

In an early report, Guhl⁶¹ reviewed the use of various arthroscopic procedures directed at preservation of the fragment and noted healing in eighteen (75 per cent) of twenty-four patients. Recently, Bradley and Dandy¹⁸ used an arthroscope in conjunction with drilling with Kirschner wires for fragments that were attached. They reported healing in nine of eleven patients at one year. They also reported prompt relief of pain and good results in children but found that adults managed with the same procedure had no relief of pain.

Ewing and Voto⁴⁶ used an arthroscope to aid in removal of the fragment in conjunction with drilling and abrasion of the base of the crater in twenty-nine young adults who had osteochondritis dissecans. At thirty-five months, twenty-one patients (72 per cent) had a satisfactory result as assessed subjectively and fifteen (52 per cent) had associated intra-articular abnormality. Of ten patients who had so-called second-look arthroscopy (re-examination after treatment), eight had healing with fibrocartilage.

Anderson et al.⁴ used diagnostic arthroscopy, followed by antegrade curettage (reflection or temporary removal of the fragment with curettage of the crater), local femoral bone-grafting, and pinning of large lesions of the medial femoral condyle through a medial arthrotomy to treat osteochondritis dissecans lesions in skeletally mature patients. They immobilized the knee for six weeks postoperatively and removed the pins eight to twelve weeks after healing. Sixteen of seventeen lesions healed, with two excellent, nine good, and five fair results.

Johnson et al.⁷¹ recently reported on arthroscopically assisted fixation with screws for the treatment of osteochondritis dissecans in thirty-five knees (thirty-two young adults). They used cannulated, partially threaded 4.0-millimeter AO screws and performed a second arthroscopy for removal of the screws two months postoperatively (Figs. 3-A and 3-B). They found that thirty-three lesions (94 per cent) had healed by the time of the second arthroscopy, and twenty-eight patients (88 per cent) had an excellent or good result. Three types of lesions were encountered: those in which the articular cartilage was intact, with the lesion being either stable or mobile with compression; those in which the articular cartilage had separated, with the lesion remaining either in situ or hinged; and completely loose fragments. They noted erosion of the head of the screw into the opposing tibial articular cartilage in patients who did not comply with the protocol of strict postoperative non-weight-bearing.

Thomson¹⁴¹ reported radiographic healing in sixteen of eighteen patients who had been managed with Herbert compression-screw fixation. Wombwell and Nunley¹⁵⁵ reported healing in one patient with use of this technique. Mackie et al.⁸⁹ inserted Herbert screws under arthroscopic guidance in three patients who had early-stage osteochondritis dissecans. The patients were allowed to bear weight immediately and had a decrease in symptoms at the one-year follow-up evaluation.

Dipaola et al.⁴¹ used a number of arthroscopic techniques to treat osteochondritis dissecans. Magnetic resonance imaging was helpful for the prediction of a detached lesion at the time of the operation.

On the basis of our review of the literature, we support the following treatment plan. The age of the patient is of primary importance in clinical decisions. Children who have a symptomatic lesion should be managed initially with limitation of activity until they no longer have symptoms. Protected weight-bearing is advised to allow healing of the subchondral bone and to prevent further displacement or degeneration of the fragment. Because it is difficult to restrict the activity of a child, a knee immobilizer, splint, or cast may be needed. Close clinical observation with serial radiographs is also important. Serial magnetic resonance images may also be useful for following healing. Operative intervention is warranted if loose bodies are present, if symptoms persist for six to twelve months, or if healing is unlikely as determined by radiographic indices, especially if skeletal maturity is imminent. Arthroscopy allows direct visualization of the defect, and drilling of intact lesions with soft articular cartilage promotes revascularization. Children who have a completely separated, displaced fragment should be managed in a manner similar to that used for adults.

A more intensive operative approach should be used in adults if healing after non-operative treatment is unlikely. Guhl⁶² provided useful guidelines for the arthroscopic treatment of osteochondritis dissecans of the knee. He suggested that lesions with intact articular cartilage can be drilled in a retrograde fashion under arthroscopic guidance. Separated lesions should be treated with curettage and drilling of the base of the crater followed by replacement of the fragment^61,62. Stable fixation with compression screws, bone pegs, or biodegradable pins is essential for osseous healing, and bone-grafting may be needed to restore the congruity of the articular surfaces. Excision should be reserved for small fragments or for lesions that cannot be reconstructed. Strict postoperative non-weight-bearing is necessary until healing has been documented, but early, active range-of-motion exercises are encouraged.

Young patients who have a completely detached, loose fragment and advanced degenerative joint disease present a difficult and challenging therapeutic dilemma¹³⁵. The treatment decisions are even more difficult when the lesion involves a major portion of the weight-bearing surface. The use of allografts to reconstruct intra-articular defects appears promising, but this technique is unproved. Osteochondral autogenous grafts have been associated with a good rate of success, but experience with this procedure is limited. Older patients who have an advanced lesion may be candidates for a total knee arthroplasty or a tibial osteotomy.

Osteochondritis Dissecans of the Ankle

Clinical Presentation

Osteochondritis dissecans of the ankle is characterized by catching with walking or with active motion of the ankle in an adult. The age of patients at the time of presentation is variable, but most patients are first seen in early adulthood. In the series of Berndt and Harty¹², the patients' ages at the time of presentation ranged from ten to seventy years; however, fifteen (63 per cent) of the twenty-four patients were initially seen between the ages of fifteen and thirty-five years. Twenty-two patients (92 per cent) had a clear history of previous trauma. Swelling is frequent. As noted by Canale and Belding²⁸, presenting symptoms may be ill defined and may be consistent with a sprain. A previous injury to the ankle is common, with most patients describing the injury as a sprain. Pain can be variable and is related to the stage of the lesion at the time of presentation.

The lesions are found in either the posteromedial or the anterolateral aspect of the talus. Posteromedial lesions are frequently asymptomatic, and the patient may have no history of trauma. Bauer et al.¹⁰ noted almost no symptoms after long-term follow-up of osteochondritis dissecans lesions of the ankle in thirty patients. In that series, twenty-seven (87 per cent) of the thirty-one joints had a medial lesion. Rödén et al.¹²⁰ reported that medial talar lesions were not secondary to trauma, were associated with fewer symptoms and little or no osteoarthrosis, and healed spontaneously. In contrast, lateral lesions are frequently symptomatic and result from trauma^{2,25,86,91,159}.

Physical Examination

Physical examination may reveal crepitus or a joint effusion along with either diffuse or well defined tenderness, depending on the stage and site of the lesion. Tenderness along the tibiotalar joint line is usually present either anterolaterally or posteromedially. There may be diffuse swelling of the joint with evidence of an effusion and reactive synovitis. Pain with compression of the tibiotalar joint and crepitus with dorsiflexion or plantar flexion are frequently present.

Imaging Studies

Berndt and Harty¹² developed the radiographic classification system that is most widely used for osteochondritis dissecans of the talus. With their system, a stage-I lesion is a small area of compression of subchondral bone; a stage-II lesion, a partially detached osteochondral fragment (a flap); a stage-III lesion—the most common—a completely detached fragment that remains in the underlying crater bed; and a stage-IV lesion, a completely detached fragment with complete displacement from the crater (a loose body).

Radiographs show a well circumscribed area of sclerotic subchondral bone separated from the remainder of the epiphysis by a radiolucent line. Radiolucency of the talar chondral surface is also seen. Computed tomography is helpful for ruling out conditions similar to osteochondritis dissecans, such as small lytic or cystic lesions or osteonecrosis¹⁶³. Although plain radiographs are usually sufficient to make the diagnosis, computed tomography can be beneficial, in preoperative planning, for accurately determining the size and location of the lesion. Magnetic resonance imaging is also useful for identifying the location of the suspected lesion. Dipaola et al.⁴¹ correlated the findings on magnetic resonance imaging without contrast medium with the stage of the lesion as determined arthroscopically. These authors found magnetic resonance imaging to be extremely useful for distinguishing a stage-II from a stage-III lesion on the basis of a fluid interface. Yulish et al.¹⁶⁰ found magnetic resonance imaging without contrast medium to be accurate on the basis of operative findings at arthroscopy or arthrotomy. Of eight patients who were managed operatively, five had disruption of the articular cartilage overlying the talar defect; magnetic resonance imaging had detected the disruption preoperatively in four of the five. De Smet et al.⁴⁰ also documented the usefulness and value of magnetic resonance imaging of the ankle without the use of contrast agents for predicting the integrity of the cartilage surface of osteochondritis dissecans lesions. Partially detached lesions were diagnosed by the presence of an irregular signal zone at the interface between the fragment and the bone of the talus on T2-weighted images. The four unattached fragments were completely surrounded by fluid.

Etiology

Trauma

The etiology of osteochondritis dissecans lesions of the ankle is somewhat clearer than that of lesions of the knee or elbow, although it is not without controversy. Trauma causing tibiotalar subluxation results in impingement of the talus on the tibia or fibula^{36,37,99,125,161}. In a study of the mechanism of injury, Berndt and Harty¹² described these osteochondral abnormalities as transchondral fractures that had failed to unite or heal (Figs. 4-A and 4-B). In cadavera, they found that anterolateral talar lesions were caused by impaction of the talus on the fibula in inversion with the ankle positioned in dorsiflexion. Posteromedial lesions occurred secondary to inversion with the ankle plantar flexed so that the talus impacted and twisted on the posterior aspect of the tibial plafond¹².

Canale and Belding²⁸, in a clinical study of medial and lateral lesions of the talus, concurred that lateral talar lesions are traumatic in origin and most likely result from injury of the talus against the fibular articular surface. However, they noted that nine of fourteen medial lesions were not associated with trauma. Furthermore, the medial lesions were different morphologically from the anterolateral lesions; the medial lesions were dome-shaped, whereas the lateral lesions had a wafer-like shape. The lateral and medial lesions were identical on histological examination; both had a viable hyaline surface and a necrotic osseous section. These authors concluded that all lateral lesions are traumatic in origin, wafer-shaped, and associated with more persistent symptoms and degenerative changes than are medial lesions. Canale and Belding thought that lateral lesions are true transchondral fractures, which are traumatic in origin. Medial talar lesions can be related to trauma but, in their series, they may have been the result of another factor.

Athanasiou et al.⁶ evaluated the compressive stiffness of portions of the articular surfaces of the tibiotalar joint. They found significant differences in stiffness in the posteromedial talar articulations in fourteen cadaveric specimens (p < 0.05). These investigators hypothesized that a mismatch of stiffnesses of the articulating surfaces results in a posteromedial lesion because of repetitive microtrauma.

Natural History and Treatment

Canale and Belding²⁸ applied the classification system of Berndt and Harty¹² and recommended conservative treatment, with protected weight-bearing, of all stage-I and II talar lesions. They believed that stage-III lateral lesions are best treated operatively, whereas stage-III medial lesions can initially be treated with immobilization of the limb in a cast or brace and non-weight-bearing for six months. Operative débridement and curettage is indicated for stage-III lateral and all stage-IV lesions. However, they found that anterolateral lesions were more symptomatic and were associated with a greater degree of degenerative changes of the ankle than were medial ones.

Flick and Gould⁵¹ studied the results of arthroscopy in the treatment of osteochondritis dissecans of the talus. They noted the ease of arthroscopic access to lateral talar lesions through the standard anterolateral portal. Posteromedial lesions presented a greater technical challenge, and these authors described a technique of grooving of the anteromedial corner of the tibia to allow better exposure. Successful arthroscopic treatment has also been reported by others^7,45,109,115. Baker et al.⁷ reported generally good results in ten ankles, eight of which had a posteromedial lesion. Ewing⁴⁵ recently described his technique of excision of the fragment followed by arthroscopic curettage of the base of the crater with use of an abrasion shaver; however, he did not report the results in that paper.

Angermann and Jensen⁵ described their operative experience with a medial malleolar osteotomy for exposure and curettage of a medial talar lesion in sixteen patients. These authors noted deterioration of the results over time, with onset of pain and degenerative changes in the joint. Bryant and Siegel²⁰ described the drilling of talar lesions with use of a meniscal repair cannula to allow accurate and safe placement of the pins. Arthroscopy is very useful; however, depending on the presentation of the lesion, arthrotomy may be needed to perform the procedure thoroughly.

Osteochondritis Dissecans of the Elbow

Clinical Presentation

Osteochondritis dissecans of the elbow is characterized by pain, swelling, and limitation of motion, usually in adolescence through early adulthood. An uncommon clinical entity, it occurs as a result of overuse injuries, especially throwing activities. Bennett et al.¹¹ described changes of the capitellum and loose bodies in the elbows of professional baseball players. Little League athletes have a propensity for these lesions, caused by throwing activities; the combination of valgus compression overuse and an immature articular surface results in capitellar lesions^19,69,88,145. It is important to note that changes of the capitellum are seen in two clinical groups. Rarefaction and fragmentation of the entire ossific nucleus of the capitellum occurs in children between the ages of four and eight years old. This process, known as Panner disease, is an osteochondrosis similar in pathophysiology to Legg-Calvé-Perthes disease; it involves the entire capitellum, is usually self-limiting, and resolves with rest. Reconstitution of the capitellum occurs without late sequelae or limitations. Osteochondritis dissecans of the elbow, in contrast, occurs in adolescents and young adults between the ages of twelve and twenty-one years old, with sequelae of functional abnormalities and changes of the surfaces of the elbow joint.

Pappas¹⁰⁷ divided osteochondritis dissecans of the elbow into three categories on the basis of the age of the patient. Category I includes patients less than thirteen years old; category II, those between thirteen years old and adulthood; and category III, adults. Similar to previous investigators who have treated osteochondritis dissecans of the knee, Pappas found that younger age-groups have better results with non-operative treatment. He also noted worse results in association with a more advanced stage of the lesion.

Patients who have an osteochondritis dissecans lesion of the elbow describe an insidious onset of poorly localized, diffuse joint pain. Stiffness and swelling are variably reported. Approximately 20 per cent of patients (three of twenty-one in one study¹⁹ and five of fourteen in another⁸⁸) have a history of a single traumatic event^{1,15,27,36-38,58,80,128,142,161}. The mechanism of injury is usually overuse, with repeated microtrauma being the most common factor^19,88. In patients who have more advanced irregularity of the articular surface, more dramatic symptoms, such as catching, clicking, giving-way, and grinding, may be reported. If loose bodies are present, true locking of the joint may occur. Symptoms are usually intermittent and occur with exertion or throwing activities.

Imaging Studies

Plain anteroposterior and lateral radiographs are often sufficient to supplement a physical examination when a diagnosis of osteochondritis dissecans of the elbow is being made. The radiographs reveal the characteristic rarefaction or radiolucency of the lateral or central portion of the capitellum. Loose bodies are seen in advanced stages. Hypertrophy of the radial head is seen in conjunction with capitellar lesions in the later stages. Lesions of the capitellum occur irrespective of skeletal maturity. If the entire capitellum is involved in a child between the ages of four and eight years old, Panner disease (osteochondrosis) should be suspected.

Magnetic resonance imaging is extremely useful for evaluating the presence and stage of the lesion. Murphy¹⁰⁰ described the use of magnetic resonance imaging in three patients who had osteochondritis dissecans of the elbow. Detachment of the fragment was noted on the basis of intervening fluid seen on T2-weighted images. The operative findings showed that the stage of the lesion had been correctly predicted with magnetic resonance imaging.

Etiology

Trauma

Trauma has been proposed as an etiology of osteochondritis dissecans by many investigators^{19,69,88,96,145,156}, and few would disagree that repetitive microtrauma plays an important role in lesions of the elbow. Most authors^{19,88,144-146} have noted these lesions in athletes who throw, and they have attributed the etiology to valgus overload on the radiocapitellar joint.

Tullos et al.^144,145 described the biomechanics of the throwing motion and noted the abnormal valgus stress placed on the elbow, especially during the acceleration and follow-through phases of pitching. They suggested that osteochondritic changes in the capitellum are secondary to compressive forces between the radial head and the capitellum as a result of tensile stresses exerted on the medial aspect of the elbow during throwing. Jobe and Nuber⁶⁹ postulated a similar mechanism of injury. Brown et al.¹⁹ evaluated eighteen patients who had osteochondritis dissecans of the elbow and stated that all of the lesions were related to repeated episodes either of throwing or of participation in racquet sports. They concluded that the "constant impingement by the radial head against the capitellum is in part responsible for the ultimate breakdown of the surface of the capitellum and the irregularity and hypertrophy of the radial head." Mitsunaga et al.⁹⁶ found that thirty-eight (67 per cent) of fifty-seven patients who had osteochondritis dissecans of the capitellum were involved in competitive sports, mostly baseball, and postulated the high stresses placed on the elbow during pitching as the etiology. Brown et al.¹⁹ noted that three patients (athletes involved in throwing activities) of twenty-one had a history of acute injury to the area; these three patients had first been seen with a non-united capitellar osteochondral fracture six months after the initial injury.

Proponents of the theory of a traumatic etiology have postulated that the subchondral bone is weakened by cyclic loading as a result of repetitive microtrauma or, less commonly, by a direct traumatic event¹⁴⁰. In a treatise on articular trauma, Tallqvist¹⁴⁰ noted that the injury eventually results in fatigue failure of the subchondral osseous elements. If the fatigue fracture fails to heal, resorption of bone at the site of the fracture leads to early separation of a fragment from its underlying bed. The separated segment of bone becomes avascular. The overlying articular cartilage is subjected to shear stresses and breaks down because osseous structural support has been lost. This breakdown of cartilage leads to fragmentation and partial or complete separation of the osteochondral fragment and to formation of a loose body. The cartilage is nourished by diffusion from the synovial fluid and remains viable, but the attached bone fragment is avascular, having lost its blood supply. Histological sections of a fragment caused by microtrauma should therefore reveal viable articular cartilage and a variably sized segment of necrotic subchondral bone. Schenck et al.¹²⁶ found a mechanical disparity of compressive stiffness between the radial head and the capitellum in cadaveric elbows. They theorized that a stiffer radial head articulating with a softer capitellum produces greater strain at the capitellar surface during compressive stresses in the radiocapitellar joint and can result in an osteochondritis dissecans lesion.

Ischemia

Haraldsson⁶⁴ noted that the predominant blood supply to the capitellum is from vessels entering the chondroepiphysis posteriorly. These vessels penetrate the non-ossified cartilage and traverse it to the developing ossific nucleus. In a child, this is a relatively long arterial course. There is no communication with vessels in the metaphysis or the chondroepiphysis. Thus, these are end vessels, and the blood supply to the lateral aspect of the distal part of the humerus is tenuous. This tenuousness supports a possible ischemic etiology of osteochondritis dissecans of the capitellum.

Natural History and Treatment

The natural history of osteochondritis dissecans of the capitellum is poorly understood. Although the late presentation of capitellar fragmentation and associated loose bodies has been well described^19,88, the arthrophysiology in the early stages of injury and healing remains unclear. In most clinical reports^19,88,156, the end-stage treatment of osteochondritis dissecans of the elbow with removal of loose bodies has been described.

McManama et al.⁸⁸ reported the results of treatment of osteochondritis dissecans involving the capitellum in fourteen adolescents. An excellent or a good result was noted in thirteen patients after a loose but attached capitellar chondral fragment had been shaved down to bleeding bone. Through a lateral arthrotomy, small defects were excised and multiple drill-holes were made with Kirschner wires to promote revascularization. Bone-grafting was not performed, and no attempt was made to preserve loose, attached fragments. These authors found arthrography to be of little value, and they cautioned against use of procedures such as local bone-grafting, internal fixation, and excision of the lateral condyle in the treatment of capitellar osteochondritis dissecans.

Woodward and Bianco¹⁵⁶ reported on forty-two male patients who had been managed for osteochondritis dissecans of the elbow between 1935 and 1970. Of twenty-two elbows for which radiographs were made, all had involvement of the capitellum. These authors' indication for operative treatment was the presence of a loose body. Curettage or drilling of the capitellar defect did not provide a better result than did removal of the loose body alone. Limitation of extension (less than 20 degrees) was a consistent finding at the long-term follow-up evaluation, yet the patients described little functional limitation.

Brown et al.¹⁹ reported on twenty-one patients who had osteochondritis dissecans of the elbow. Three patients had had an acute traumatic injury; in the remaining eighteen, the lesion was the result of overuse, with a throwing-type mechanism of injury. Radiographic findings of capitellar radiolucency were common. Removal of a loose body was the most frequently performed procedure. Functional limitations were common, and extension of the elbow was routinely limited.

In summary, most authors have noted osteochondritis dissecans of the elbow in athletes who are involved in throwing activities, as a result of repetitive overuse (microtrauma). Treatment usually involves débridement of loose bodies. The capitellar bed or crater should be curetted to remove any remaining loose fragments and then should be drilled with a Kirschner wire to stimulate vascular ingrowth. Degenerative changes and limitations of motion are to be expected in these patients.

Summary

The treatment of osteochondritis dissecans has remained controversial since it was initially described more than a century ago¹⁰¹. The etiology is still unclear, but it seems to be multifactorial and related to trauma in specific and susceptible locations. Two different populations of patients, children and adults, are affected, and the result of treatment is largely determined by the status of the physes. Children who have a lesion of the knee usually do well irrespective of the method of treatment, and those who have a persistently symptomatic lesion generally respond well to operative arthroscopy if limitation of activity and protected weight-bearing have failed. A lesion of the knee in an older patient is unlikely to heal with non-operative treatment; therefore, treatment should include techniques that promote revascularization of the subchondral bone and restoration of the congruity of the articular surfaces by replacement of the fragment with or without bone-grafting. An advanced lesion of the knee with associated degenerative joint disease in a young patient continues to be a difficult challenge, but osteotomy or the use of osteochondral autogenous grafts may be helpful. Total joint arthroplasty may be the only alternative for a refractory lesion in an older patient. Osteochondritis dissecans of the ankle is unique in that there are two different sites of presentation, posteromedial and anterolateral. Anterolateral lesions of the ankle are true osteochondral fractures that result from trauma. Lesions of the elbow are the result of overuse injuries and most commonly involve the capitellum. Lesions of both the ankle and the elbow are usually treated with débridement and subchondral curettage or drilling.

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Topics

arthroscopy ; knee joint ; osteochondritis ; osteochondritis dissecans ; wounds and injuries

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ROBERT C. SCHENCK, JR., JON MARC GOODNIGHT; Current Concept Review - Osteochondritis Dissecans*. The Journal of Bone & Joint Surgery. 1996 Mar;78(3):439-56.

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