Study Design. A prospective, observational study.
Objective. To evaluate the effect of epidural steroid injection (ESI) on bone mineral density (BMD) in postmenopausal women.
Summary of Background Data. ESIs are used to treat the pain associated with radiculopathy. Although it is known that exogenous steroid use can disrupt skeletal architecture, it is less clear whether ESIs result in a decrease of BMD.
Methods. Twenty-eight postmenopausal women experiencing radiculopathy elected L4–L5 ESI treatment. We had a 50% dropout rate due to noncompliance with study requirements. BMD of the hip, femoral neck, and spine along with markers of bone turnover, bone specific-alkaline phosphatase and serum C-telopeptide of collagen I (CTX), was evaluated at baseline preinjection and 3 and 6 months postinjection.
Results. There was a significant decline in the hip BMD of 0.018 g/cm2 (0.028 ± 0.007, P = 0.002) at 6 months compared with baseline. We compared this decline with an age-matched control population that exhibited a decline of 0.003 g/cm2, significantly less than our study population (P = 0.007). Bone-specific alkaline phosphatase increased significantly by 2.33 U/L from 3 to 6 months (P = 0.012), but the rise of CTX was not significant.
Conclusion. A single ESI in postmenopausal women adversely affects BMD of the hip. This is in conjunction with a rise in bone remodeling activity, as evidenced by an increase in bone-specific alkaline phosphatase and CTX. In addition, when compared with an age-matched control population, our study population exhibited a greater decline in BMD. Our findings show that epidural administration of corticosteroids has a deleterious effect on bone, which should be considered when contemplating treatment options for radiculopathy. The resulting decrease in BMD, while slight, suggests that ESIs should be used with caution in those at a risk for fracture.
A group of 28 postmenopausal women with radiculopathy were observed for 6 months after epidural steroid injection at the L4–L5 level. We found greater decline in bone mineral density of the hip than that in a matched control group whereas elevated markers of bone metabolism reflected increased remodeling activity
*Division of Endocrinology, Summa Health System, Akron, OH
†Division of Endocrinology, Diabetes and Bone Mineral Metabolism
‡Department of Orthopaedic Surgery, and
§Department of Public Health Sciences, Henry Ford Health System, Detroit, MI.
Address correspondence and reprint requests to Shlomo Mandel, MD, MPH, Department of Orthopaedic Surgery, Henry Ford West Bloomfield Hospital, 6777 West Maple Rd., West Bloomfield, MI 48322; E-mail: email@example.com
Acknowledgment date: April 2, 2012. First revision date: June 11, 2012. Second revision date: August 17, 2012. Acceptance date: August 18, 2012.
The device(s)/drug(s) is/are FDA approved or approved by corresponding national agency for this indication.
The Nancy and James Grosfeld Spine Education and Research Fund were received to support this work.
One or more of the author(s) has/have received or will receive benefits for personal or professional use from a commercial party related directly or indirectly to the subject of this manuscript: e.g., honoraria, gifts, consultancies.