Osteochondroses Workup

Osteochondroses, by themselves, do not primarily alter laboratory parameters. However, it is imperative to rule out other disorders before an osteochondrosis is diagnosed.

A complete hemogram is mandatory. It should include the erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) level and blood chemistries, with a particular focus on serum calcium, phosphate, and alkaline phosphatase (ALP) levels. Other laboratory investigations depend on the patient’s individual case.

Studies to detect or evaluate genetic polymorphisms, trace elements (copper, zinc), urinary deoxypyridinoline excretion, ^[20]  and plasma insulinlike growth factor (IGF)-1 levels are primarily of research interest and are not indicated for screening patients.

Most osteochondroses were first described in terms of radiographic appearances, and for the most part, they continue to be characterized on this basis. Although investigations such as magnetic resonance imaging (MRI) and bone scintigraphy may help in early identification of the disease, these studies frequently are not feasible, because patients typically do not exhibit symptoms in the early stages of disease. ^[21]

Some radiographic features reflect specific entities, whereas others are shared among the osteochondroses (see the images below).

Osteochondrosis of the lesser trochanter of the left femur (Monde-Felix disease). Image shows fragmentation.

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Osteochondrosis of the base of the fifth metatarsal bone (Iselin disease). Image shows fragmentation.

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Early involvement typically results in a centrum that appears to have reduced size, increased opacity, and irregular architecture. In addition, images may depict asymmetry in the size of bony trabeculae, as well as irregular trabeculation.

With advancement, fibrillation and fissures in the cartilage enlarge, and sequestrum formation may or may not occur. The crescent sign (ie, separation of part of the bone from a parent nucleus) may be present. In weightbearing joints, the joint space may be reduced, but this finding is unusual.

Revascularization usually manifests as worsening of the radiographic picture, ^[22] with the development of osteoporosis, absorption of necrotic tissue, and deformation of epiphysis due to a loss of underlying support (ie, step defect and buttressing phenomenon).

The picture in the squeal or burnt-out phase depends on the degree of ischemic damage and its chronologic arrest. Complete and early restoration by reparative processes leaves no deformity. By comparison, late and incomplete restoration of the blood supply—compounded by additional assault and poor protection—develops into an irregular, deformed, and misshaped epiphysis. Associated findings may include collateral and subsequent changes in the metaphysis and joint.

Specific deformities that may result include the following:

• Mushroom-shaped femoral head or hip subluxation in Perthes disease
• Kyphosis with or without scoliosis in Scheuermann disease
• Tibia vara in Blount disease
• Cubitus valgus in Panner disease
• Madelung deformity in distal radial epiphyseal involvement
• Genu recurvatum and patella alta in Osgood-Schlatter disease

Joint arthrosis is usually the delayed presentation of all of the articular osteochondroses (eg, Kienböck disease and Perthes disease) that are poorly restored. Its causes are an abnormal distribution of stresses and an irregular joint surface.

MRI may be helpful in diagnosing an osteochondrosis before obvious radiographic changes become apparent. It is also useful for differentiating osteochondrotic diseases from inflammatory conditions, such as tubercular involvement and osteomyelitis.

Physeal mapping of the growth plate can be undertaken to facilitate surgical correction (eg, of Blount disease). MRI can reveal small fragments better than other imaging studies can. It can also help elucidate residual attachments to parent bone and vascularity in cases of juvenile osteochondritis dissecans, Freiberg disease, Sinding-Larsen-Johansson disease (jumper’s knee), Osgood-Schlatter syndrome, and other osteochondroses. Moreover, associated information, such as the presence and extent of underlying bone defects, can be judged on MRI.

Early MRI shows focal hyperintensities in the epiphysis or neighboring soft tissues; these are due to edema. Variable signal intensity is seen in the avascular fragment; edema is hypointense and sclerosis hyperintense on T1-weighted images. Marrow edema in the parent bone is a regular finding. Changes in signal intensity can range from peripheral irregularity of the ossific nucleus to complete replacement of the normal marrow fat (see the image below). Intra-articular effusion may also be seen.

MRI in the same patient as in image above shows altered marrow signal intensity in the apophysis of the fifth metatarsal base. This finding is suggestive of Iselin disease.

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Revascularization leads to replacement of the necrotic focus with fatty marrow. Loose bodies and residual deformities are common in osteochondritis dissecans but rare in osteochondroses. In Scheuermann kyphosis, Schmorl nodes can demonstrate low or high signal intensity on T2-weighted MRIs in association with neighboring marrow edema. Disk herniations and diskogenic sclerosis are also observed.

Likewise, in Köhler disease or Freiberg infraction, frequent findings include deformity, fragmentation, fractures, collapse, and edema. Perthes disease may result in acetabular labral tears and metaphyseal cysts, in addition to the aforementioned features.

Bone scintigraphy has been shown to be highly sensitive and specific in detecting avascularity. Whether it is better than MRI for this particular application is still the subject of considerable controversy.

Scintigraphic changes in Perthes disease have been extensively studied; however, scintigraphic changes in other osteochondroses continue to be neglected, probably because these conditions are relatively uncommon. In Perthes disease, the preferred study is pinhole imaging with both anteroposterior and lateral views obtained by using a technetium-99m tracer (see the images below).

Perthes disease. Anteroposterior view of the pelvis and both hips. Image shows pathology involving the right hip joint. Also depicted is flattening, fragmentation, and sequestrum formation affecting the capital epiphysis of the femur, with metaphyseal cyst formation and osteopenia. Of note, no subluxation of the hip joint is observed.

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Perthes disease. Lateral view of the same patient as in image above shows flattening of the epiphysis, as well as sclerosis with deformation of the femoral head.

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In the initial stages of ischemia, even before any radiographic changes are seen in a symptomatic patient, bone scans show a striking absence of tracer uptake. This absence may be noted either focally or in the entire epiphysis. Uptake in the physis and acetabular rim is normal.

These findings represent growth disturbance in the epiphysis when metabolic activity, and obviously blood flow, are low, before the beginning of a reparative response from the surrounding physis or metaphysis. In this way, bone scanning can help in making an early diagnosis months before radiographic changes become obvious.

As a reparative response is mounted in the form of revascularization from neighboring uninvolved epiphyses and metaphyses, activity at the margin of the hypoactive necrotic focus increases, and the focus itself gradually decreases in size. Also observed is increased activity in the neighboring physis and metaphysis; this finding represents an osteoblastic response.

A normal distribution of the tracer in the entire epiphysis, as compared with the opposite side, heralds complete healing. In rare cases, degenerative changes can account for the increased activity.

Bone scans may be useful in assessing acetabular containment of the head, sclerosis, subchondral fractures, intra-articular effusions, and fragmentation of the chondral surface. Disappearance of previous activity (eg, from the lateral column in Perthes disease) indicates collapse or infarct. This is a poor prognostic marker. Schmorl nodes show increased tracer uptake in the acute phase and normal or increased activity in late phases.

Surface microscopy may facilitate differentiation of osteochondrosis from osteochondritis. A study by Rothschild and Lambert found that osteochondrosis was associated with smooth borders and a gradient from the edge to the defect base, whereas osteochondritis and subchondral impaction fractures were associated with subsidence of the affected area of the articular surface with irregular edges. ^[23]  In addition, multiple channels penetrated the base of osteochondrosis and smoothly perforated.

In general, all stages of the disease process have been described as involving the following histologic features:

• Necrosis of the bone and cartilage
• Revascularization
• Formation of granulation tissue
• Osteoclastic resorption of necrotic trabeculae
• Formation of mature and lamellar bone

The features listed above are not specific to any particular entity and generally resemble those of ischemic necrosis.

The collagen-to-proteoglycan ratio is reduced, as demonstrated by means of electron micrographic studies.