Bone marrow edema in the foot—MRI findings after conservative therapy
Introduction
Bone marrow edema (BME) can be found as a primarily ischemic disease, mainly of the femoral head, with a lower incidence in other localizations. Only a few cases of BME in the foot have been published in the literature [1], [2], [3], [4], [5], [6], [7], [8]. Different treatment options have been reported, mainly for the femoral head and the knee. These include symptomatic non-operative treatment (reduction of weight bearing, analgesic and anti-inflammatory medication, physical therapy) and surgical treatment such as decompression (alone or in combination with electromagnetic stimulation or bone grafting). Several authors have reported a relationship between transient bone marrow edema to avascular necrosis [9], [10], but the incidence of progress from bone marrow edema to avascular necrosis is still unclear. There is still controversy as to whether ischemic bone marrow edema syndrome (BMES) reflects a distinct self-limiting disease, a kind of reflex sympathetic dystrophy [11], [12], or a diffuse but reversible early phase of avascular necrosis [9], [13]. Although there is consensus about different vascular factors contributing to bone marrow edema syndrome and avascular necrosis, the exact pathogenesis remains unclear. Current theories include thromboemboli, obstruction of arteriolar inflow or venous outflow, injury to the vessel wall caused by vasculitis, altered lipid metabolism and decreased fibrinolysis [14], [15], [16].
The aim of this prospective MRI study was to assess the course of bone marrow edema after conservative therapy with the vasoactive drug iloprost and partial weight-bearing.
Section snippets
Materials and methods
Twenty three patients (15 female, eight male) with MRI-verified bone marrow edema of the foot were investigated. Patients with avascular necrosis and osteochondritis dissecans with a demarcated bone area as well as patients with BME secondary to osteoarthritis, mechanic stress or trauma and patients with algodystrophy were excluded. The patients' mean age was 59.1 years (range 32–73). For all patients, major alcohol abuse or corticosteroid medication was excluded. Weight bearing anteroposterior
Results
Three months after therapy, plain radiographs of all patients, except for the three with initial degenerative changes were assessed as normal. No sign of progress such as sclerosis or lucencies, subchondral fracture, collapse or further narrowing of the joint space was detected.
No MRI showed signs of progress to avascular necrosis, such as demarcation, ‘double-line sign’ or collapse. On MRI, bone marrow edema resolved completely within 3 months in 15 patients (Fig. 1), the other eight patients
Discussion
Bone marrow edema syndrome was first described in 1959 by Curtiss and Kincaid [19] as a clinical syndrome characterized by hip pain, decreased bone density on plain radiographs, and spontaneous regression of symptoms in women during the last trimester of pregnancy. Subsequent reports have referred to the syndrome as transient osteoporosis, transitory demineralization and, as diagnosed by MRI, bone marrow edema syndrome [20]. The clinical course is characterized by abrupt or gradual onset of
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Idiopathic Transient Osteoporosis of the Talus: A Cause for Unexplained Foot and Ankle Pain
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