Bone marrow edema in the foot—MRI findings after conservative therapy

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Abstract

Bone marrow edema (BME) is a rare cause of pain in the foot. We reviewed 23 patients with unilateral idiopathic bone marrow edema located in the foot. The patients' mean age was 59.1 years (32–73). Bone marrow edema was located 12 times in the talus, four times in the cuneiform bones, four times in the metatarsal bones, two times in the calcaneus, and once in the navicular bone. Edema secondary to an activated osteoarthritis, to mechanic stress, to a chronic regional pain syndrome or to trauma were excluded. The size of BME was categorized large in nine cases (50–100% of the bone involved), in nine cases medium (25–50%) and in five cases small (<25%).

Conservative therapy consisted of infusions with the vasoactive substance iloprost and limited weight-bearing for a period of three weeks. After 3 months, in 15 patients BME showed total regression on MRI scan. In three there was subtotal regression and in three no change in the size of the BME (p<0.0001).

No correlation between the primary size of BME and outcome was seen (p=0.453). No progression to AVN occurred in our patients. In two patients BME appeared to migrate to neighbouring bones and in one patient to a femoral head.

Conclusions. Bone marrow edema syndrome is rarely seen in the foot. Progress to avascular necrosis is unlikely. Conservative therapy can be recommended.

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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