Curr Rheumatol Rep (2014) 16:441 DOI 10.1007/s11926-014-0441-8

SYSTEMIC LUPUS ERYTHEMATOSUS (M PETRI, SECTION EDITOR)

Treatment of Osteonecrosis in Systemic Lupus Erythematosus: A Review T. Andrew Ehmke & Jeffrey J. Cherian & Eddie S. Wu & Julio J. Jauregui & Samik Banerjee & Michael A. Mont

# Springer Science+Business Media New York 2014

Abstract Osteonecrosis (ON) is a devastating illness that can lead to severe joint disease in young patients. The pathogenesis of ON is largely unknown; however, there have been numerous reports associating risk factors including systemic lupus erythematosus (SLE) with the disease. The risk of ON for SLE patients is believed to be a result of both the SLE disease state itself and the concomitant use of corticosteroids. The objective of osteonecrosis treatment is typically to halt progression or delay the onset of end-stage arthritis that may require a total joint arthroplasty (TJA). Joint-preserving procedures are attempted for pre-collapse and some post-collapse lesions. After severe subchondral collapse has occurred, TJA is often necessary to relieve pain. The purpose of this article is to draw attention to recent evidence regarding several treatment options for the management of SLE-associated ON, including lesion observation, medication, joint-preserving techniques, and TJA. Keywords Osteonecrosis . Hip . Knee . Shoulder . Joint replacement . Joint preservation

Introduction Osteonecrosis (ON) is a disease that leads to bone ischemia and potential joint destruction [1]. Despite the numerous This article is part of the Topical Collection on Systemic Lupus Erythematosus T. A. Ehmke : J. J. Cherian : E. S. Wu : J. J. Jauregui : S. Banerjee : M. A. Mont (*) Rubin Institute for Advanced Orthopedics, Center for Joint Preservation and Replacement, Sinai Hospital of Baltimore, 2401 West Belvedere Avenue, Baltimore, MD 21215, USA e-mail: [email protected] M. A. Mont e-mail: [email protected]

publications, no clear consensus on etiology or pathogenesis has been reported. However, the risk of developing ON has been linked to numerous factors, including: corticosteroids, alcohol abuse, cigarette smoking, and a variety of inflammatory arthropathy including systemic lupus erythematosus (SLE). Reports have estimated the risk of ON for SLE patients to range from 3 to 44 % [2–5]. This risk is believed to be caused by both the SLE disease state itself and the concomitant use of corticosteroids. SLE is believed to increase the risk of ON through a hypercoagulable state, with one study revealing that among patients who had osteonecrosis and SLE there was a 32 % higher incidence of a variety of coagulation-property abnormalities compared with that in a control group [6]. In addition, these patients are prone to antiphospholipid syndrome, which may also be associated with osteonecrosis. Moreover, reports have revealed a higher incidence of ON among SLE patients compared with other inflammatorydisease patients on comparable doses of corticosteroids [3], which is believed to be a result of a synergistic relationship between corticosteroid use and SLE disease activity. Corticosteroids are well known as an associated factor for the development of ON, in particular for patients who have received high doses [3], have greater cumulative doses [7•], and were younger at age of first exposure [5]. Osteonecrosis most often affects the femoral head, followed by the knee and shoulder and the ankle, with reports of elbow [8], wrist [9], and foot disease [10]. Multifocal disease affecting more than three of these joints is not infrequent in SLE patients, occurring approximately 3 % of the time [11•, 12]. Staging and subsequent treatment of ON is often on the basis of the presence of subchondral bone collapse, which can be classified by the Ficat and Arlet system (See Table 1, and Fig. 1 images) [13]. The objective of osteonecrosis treatment is typically to halt progression or delay the onset of end-stage

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Table 1 Ficat and Arlet classification ≠refer to Fig. 1) Stage 1 Stage 2 Stage 3 Stage 4

Only visible on MRI Subchondral cysts and sclerosis Subchondral collapse of femoral head Advanced joint destruction

arthritis that may require a total joint arthroplasty (TJA). Although numerous classification systems have been developed to aid in determining prognosis and treatment, lesions can generally be classified as either pre-collapse or postFig. 1 Radiography images for Ficat and Arlet classification (refer to Table 1). Stage 1. Stage 2. Stage 3. Stage 4

collapse. In pre-collapse lesions, the contour of the joint surfaces is maintained. In general, joint-preserving procedures are the first line of treatment for these types of lesions. The rationale of joint-preserving procedures is to relieve intraosseus pressure, increase blood flow to the necrotic subchondral bone, and in some cases provide structural support for the underlying subchondral bone. For post-collapse lesions joint-preserving procedures have been revealed to have a higher failure rate, thus making arthroplasty often necessary. Other factors to take into account when considering joint-preserving procedures versus arthroplasty include

Curr Rheumatol Rep (2014) 16:441

patient age and activity level, lesion size and location, and associated medical comorbidities and risk factors. The purpose of this article is to draw attention to recent evidence regarding several treatment options for managing SLE-associated ON, including: 1. non-operative treatments; 2. joint-preserving techniques; and 3. total joint arthroplasty. This report will focus primarily on studies investigating ON of the hip in SLE patients. However, in many cases there is a paucity of literature on osteonecrosis in SLE specifically. In these cases, we preferentially selected studies that had SLE subgroups and emphasized their results. If no specific SLE data was available, we extrapolated data from the general ON population. In addition, when available we have described the treatment options for SLE involvement of other joints, including the shoulder and the knee. Diagnosis Diagnosis of osteonecrosis in SLE is primarily on the basis of radiography findings, after clinical findings raise suspicion. The diagnosis of ON always begins with a thorough history and physical examination, in which patients should be assessed for common risk factors associated with ON. Typically, patients who are believed to have ON present complaining of bone pain; however, this can vary depending on the patient and the joint involved. Once a patient is believed to have osteonecrosis, diagnostic imaging begins with standard antero-posterior and lateral radiographs. Plain radiographs can assess for evidence of articular-surface collapse. Patients who have no evidence of joint collapse can be further assessed with magnetic resonance imaging (MRI). This is the test of choice for diagnosing early-stage ON lesions, with reports revealing sensitivity and specificity greater than 99 % [44]. Conversely, technetium 99 bone scans are not indicated for the diagnosis of osteonecrosis because of poor sensitivity and specificity, with one study revealing that bone scanning detected only 56 % of osteonecrosis lesions detected by MRI in the setting of multifocal disease confirmed by histopathology [14]. Non-operative Management Observation Observational treatment is usually reserved for only small (

Treatment of osteonecrosis in systemic lupus erythematosus: a review.

Osteonecrosis (ON) is a devastating illness that can lead to severe joint disease in young patients. The pathogenesis of ON is largely unknown; howeve...
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