This talk reviews the pathophysiology, clinical findings, imaging findings and treatment options of epiphyseal osteonecrosis, bone infarcts and various types of osteohondroses with emphasis on magnetic resonance imaging (MRI). Specifically, osteonecrosis of the femoral head, humeral head, talar dome, lunate and proximal scaphoid pole will be discussed. Steinberg modified FICAT classification of the femoral head osteonecrosis and Lichtman staging of Kienbock Disease will be presented in tables. Following osteochondroses will be addressed: Legg-Calvé-Perthes disease, osteochondritis dissecans (OCD), osteochondrosis of the capitellum (Panner disease), Blount disease (tibia vara) Osgood-Schlatter disease, Sinding-Larsen-Johansson disease (jumper’s knee), Freiberg infraction, Köhler disease and Scheuermann’s disease.
Learning Objectives
Review the pathophysiology, clinical findings, imaging findings and treatment of epiphyseal osteonecrosis and bone infarcts with emphasis on magnetic resonance imaging (MRI)
Review the pathophysiology, clinical findings, imaging findings and treatment of osteochondroses including Legg–Calvé-Perthes, osteochondritis dissecans, Blount, Panner, Osgood-Schlatter, Sinding-Larsen-Johansson and Kohler diseases and Freiberg infraction with emphasis on MRI
Osteonecrosis
Osteonecrosis (ON) results from an ischemic insult to bone with subsequent death of the hematopoetic, osteoblasts, osteoclasts and fat cells. The stages of ON include ischemia, revascularization, repair, deformity and secondary osteoarthritis (OA). In the revascularization phase, necrotic bone is intrinsically weaker and susceptible to subchondral fracture. The term ON is used for infarction of the subchondral bone, while bone infarcts is the term used for the metaphyseal or diaphyseal locations. Clinical presentation is variable including insidious or abrupt onset of pain or lack of symptoms. The most common cause is trauma followed by corticosteroid therapy. Additional common etiologies include alcoholism, sickle cell disease, hemoglobinopathies and idiopathic. Less common etiologies include lupus, pancreatitis, radiation, Gaucher disease and Caisson disease (decompression syndrome). Common locations for ON include the femoral head, humeral head and femoral condyles, and after trauma the proximal pole of the scaphoid and talar dome. The most common complication is secondary osteoarthritis (OA). Bone infarcts are usually asymptomatic and multiple. Malignant transformation of bone infarcts is rare, mostly to a pleomorphic undifferentiated high grade sarcoma. Femoral head ON is more common in men than women and is bilateral in approximately 50% of cases. Early femoral head ON may present as bone marrow edema (BME) which is rarely seen. Later stages are characterized by a linear serpiginous geographic lesion (peripheral double line sign) which consists of a reactive interface with the inner dark line corresponding to necrotic bone and the outer hyperintense line corresponding to granulation tissue. With greater than 50% femoral head involvement, weight-bearing surface collapse is more likely.
Steinberg (Modified FICAT) Classification of femoral head ON will be presented.
Thirty percent of scaphoid waist fractures and 80-100% of proximal pole fractures are complicated with ON. Clinical examination is insufficient to depict scaphoid fracture complications due to a lack of specific clinical signs. Scaphoid non-union advanced collapse (SNAC) wrist comprises the presence of OA which usually occurs 5-10 years after injury resulting in significant functional impairment. Mummified fat in early ON may display “normal” high signal intensity with false negative findings on the T1W MRI sequences without fat saturation. Otherwise, early ON shows lower signal of the necrotic bone with respect to the surrounding normal bones on T1W sequences with variable signal on fluid sensitive sequences. Homogeneous enhancement on the post contrast sequences suggests viable bone marrow, inhomogeneous enhancement suggests the coexistence of ON and viable tissue, and the absence of enhancement suggests ON. False negative cases may relate to fibrous tissue ingrowth. The utility of dynamic contrast-enhanced MRI is debatable.
ON of the lunate (Keinböck disease) is associated with trauma and ulnar negative variance. It has a male predominance with a peak age of 20-40 years old. Patients present with dorsal wrist pain and decreased grip strength. Contrast enhanced MRI is the preferred approach for assessing the viability of lunate bone marrow.
Lichtman Staging of Kienbock Disease will be presented.
Osteochondroses
Osteochondroses include a variety of diseases involving the epiphyses or apophyses in children with fragmentation and increased sclerosis. Some osteochondroses may be due to ischemia, while others are thought to be related to repetitive microtrauma. The majority of osteochondroses are associated with an eponym.
Legg-Calvé-Perthes disease Idiopathic ON of the femoral head, in children usually between 4-8 years old, B >> G
Osteochondritis dissecans (OCD) Usually affects adolescents, active in sports, likely due to repetitive microtrauma and is the result of a subchondral fracture. Common locations: knee, talar dome and capitellum. Fluid undermining the cartilage or bone indicates unstable fragment
Osteochondrosis of the capitellum (Panner disease) Likely due to repetitive trauma. It occurs in younger patients in the 1st decade
Blount disease (tibia vara) Affects the posteromedial portion of the proximal tibial physis, infantile and adolescent forms
Osgood-Schlatter disease Affects the tibial tuberosity in children ages 8-15
Sinding-Larsen-Johansson disease (jumper’s knee) Affects the distal patellar pole in children ages 8-15
Freiberg infraction Subchondral collapse of the second > lesser metatarsal heads, classically seen in teenage girls
Köhler disease Affects toddlers with fragmentation of the tarsal navicular (sometimes a normal variant)
Scheuermann’s disease Osteochondrosis of the vertebral body ring apophyses resulting in a kyphosis, peak age 8-12, no gender predilection
Current literature suggests possible utility of dynamic contrast-enhanced MRI in the evaluation of femoral head ON and Legg-Calve-Perthes disease.
Treatment options
ON femoral head: early stages- core decompression, late stages- hip replacement Bone infarct: No treatment is necessary. ON proximal scaphoid pole: In cases of poor blood supply as shown on MRI and/or in absence of punctate bleeding at surgery, a vascularized bone graft is preferred. Scaphoid nonunions with OA require salvage procedures (limited carpal or total wrist arthrodesis, proximal row carpectomy, scaphoid excision, or arthroplasty). Keinbock disease: Bracing, radial shortening osteotomy and revascularization procedures for earlier stages, with salvage procedures for later stages (proximal row carpectomy or partial or total wrist fusion). Osteochondroses typically spontaneously heal. Conservative treatment is initially performed.
Legg-Calvé-Perthes: Bracing with an abducted hip, physical therapy, core decompression, femoral varus derotation osteotomy or innominate osteotomy. If > 50% of the femoral head is involved, surgery will be more likely indicated. Osteochondritis dissecans: Conservative therapy for a stable fragment. Surgery may be performed for an unstable fragment or for loose bodies. Scheuermann’s disease: Bracing and physical therapy. Surgery if kyphosis > 75°.
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