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Review
. 2021 Oct;11(10):e526.
doi: 10.1002/ctm2.526.

Glucocorticoid-induced osteonecrosis in systemic lupus erythematosus patients

Kaichi Kaneko  1 , Hao Chen  1   2 , Matthew Kaufman  1   3 , Isaak Sverdlov  1   4 , Emily M Stein  5   6 , Kyung-Hyun Park-Min  1   7   8
Affiliations
Review

Glucocorticoid-induced osteonecrosis in systemic lupus erythematosus patients

Kaichi Kaneko et al. Clin Transl Med. 2021 Oct.

Abstract

Osteonecrosis (ON) is a complex and multifactorial complication of systemic lupus erythematosus (SLE). ON is a devastating condition that causes severe pain and compromises the quality of life. The prevalence of ON in SLE patients is variable, ranging from 1.7% to 52%. However, the pathophysiology and risk factors for ON in patients with SLE have not yet been fully determined. Several mechanisms for SLE patients' propensity to develop ON have been proposed. Glucocorticoid is a widely used therapeutic option for SLE patients and high-dose glucocorticoid therapy in SLE patients is strongly associated with the development of ON. Although the hips and knees are the most commonly affected areas, it may be present at multiple anatomical locations. Clinically, ON often remains undetected until patients feel discomfort and pain at specific sites at which point the process of bone death is already advanced. However, strategies for prevention and options for treatment are limited. Here, we review the epidemiology, risk factors, diagnosis, and treatment options for glucocorticoid-induced ON, with a specific focus on patients with SLE.

Keywords: glucocorticoid; osteonecrosis; systemic lupus erythematosus.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Pathophysiology of glucocorticoid‐induced osteonecrosis (ON) in systemic lupus erythematous (SLE) patients. The pathogenesis of GC‐induced ON in SLE patients remains unclear. Glucocorticoids (GCs) are steroid hormones that can modulate many aspects of cell biology; different GC‐mediated mechanisms, including hypercoagulability, inhibition of angiogenesis, fat cell hypertrophy, and apoptosis of bone cells, have been postulated for the onset of ON. It has also been suggested that GCs may cause ischemic ON through edema‐mediated increases in intraosseous pressure and decreased blood flow. Apoptosis of osteoblasts/osteocytes can be accelerated by ischemia. Although the various pathophysiology of SLE can contribute to the pathogenesis of ON, the contribution of individual SLE‐related factors to the development of ON has yet to be fully elucidated.
FIGURE 2
FIGURE 2
Risk factors of glucocorticoid‐induced osteonecrosis. Many studies have shown that high‐dose GCs are a major risk factor for the onset of ON in systemic lupus erythematous (SLE) patients (red*). The association of the route and duration of GC therapy with the development of ON is still controversial. Risk factors for ON are not limited to GC therapy. Various clinical factors, laboratory factors, and medications have been suggested to be correlated to the onset of ON. Many clinical manifestations of SLE patients has also been shown to impact the incidence of ON in some reports, while others have not exhibited any association with ON
FIGURE 3
FIGURE 3
The treatment of glucocorticoid‐induced osteonecrosis. The treatment of GC‐induced ON consists of two approaches: non‐operative management and surgical management. Pharmacological treatments such as bisphosphonates, statins, and anticoagulants have been used. There are surgical interventions for more advanced stages of ON such as core decompression with or without bone grafting, rotational osteotomy, and hip replacement. Although there are no accepted treatments to cure osteonecrosis, the progression to collapse and joint replacement may be prevented if ON is diagnosed early
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