Lumbar Scoliosis in Postmenopausal Women Increases With Age but Is Not Associated With Osteoporosis

Janet Rubin; Rebecca J. Cleveland; Alexander Padovano; David Hu; Maya Styner; James Sanders

Disclosures

J Endo Soc. 2021;5(5) 

In This Article

Discussion

Lumbar scoliosis complicates the analysis and treatment of osteoporosis. To discover whether lumbar scoliosis is associated with osteoporosis, we performed a cross-sectional analysis in postmenopausal women. The data set detected no association between lumbar scoliosis and osteoporosis at any region of interest within or across any age group. Our analysis further showed that lumbar scoliosis increased in prevalence and severity as women aged, so that nearly 40% of women in their ninth decade had clinically significant Cobb angles as defined by a lumbar curve greater than or equal to 10°. This suggests that such a high prevalence of lumbar scoliosis will affect the diagnosis of spinal osteoporosis in aging women.

Comparing across randomly selected samples from each decade of postmenopausal women, we found an expected age-dependent loss of bone density in the hip sites, leading to an increased diagnosis of osteoporosis. Twenty-two percent of women in their 60s met the definition of osteoporosis, with a T score less than or equal to –2.5 at any of 3 surveyed sites. T scores in the hip neck progressed with increasing age, contributing to 33% of the 84 to 88 year group meeting criteria for a diagnosis of osteoporosis. Interestingly, osteoporotic T scores measured in the lumber spine region remained largely the same between all age groups, a point that our data suggest may be due to increasing prevalence of lumbar curvature. In the youngest age sampled, we found a wide spread of Cobb angles, yet only 11.5% was clinically significant. The proportion of clinically significant Cobb angles was 27.3% within 10 years, and 39.4% in the oldest cohort. Importantly, despite the correlation of age and osteoporosis, the advancing Cobb angle was not associated with T score at any site.

In the cross-sectional analysis, we assessed the lateral curvature of patients' lumbar spines by digitally measuring the Cobb angle on lumbar DXA images. Prior studies demonstrated that digital measurements of spine parameters—available on many reporting programs—are more precise than manual measurements,[20] and that Cobb angles can be reliably measured from DXA radiographs.[15,21,22] We validated this methodology by comparing Cobb angles measured from DXA scans to those measured from other imaging modalities and found that interstudy reliability was high (ICC 0.92).

Our study adds to the literature that suggests lumbar BMD values are significantly higher in patients with degenerative spinal disease.[23] While density in the lumbar vertebrae may be increased because of sclerotic remodeling of vertebral end plates, this increase does not necessarily infer less propensity to macroscopic or microscopic fracture.[24] As such, decisions regarding treatment response of spine osteoporosis are confounded by lumbar scoliosis, which interferes with the reliability of serial density scanning. We thus speculate that the failure of lumbar T scores to decrease along with hip density is at least partially due to aberrant increases in bone density associated with advancement of lumbar scoliosis. Indeed, the older a woman is, the more spine BMD may reflect age-related scoliosis. As such, T scores in the hip region represent more reliable data to predict fracture risk.

Patients with lumbar scoliosis are often excluded from clinical studies of osteoporotic treatments because sequential spine densities are unreliable and expected to be higher than actual measured areal bone density at the site of the patient's hip.[25] There is little formal guidance to overcome this challenge in clinical decision making, despite prevalent use of DXA and plain films to image the lumbar spine in osteoporosis patients.[26] Because vertebral fractures are more common in the postmenopausal population than hip fractures, obtaining an accurate assessment of this end point is critical and yet the medical literature has failed to address the knowledge gap of diagnosing compression fractures in the setting of scoliosis or answering whether these anatomically related entities are also mechanistically interrelated.

Many studies have shown that scoliosis increases with aging. As early as 1977, a large cross-sectional study showed that the prevalence of scoliosis in adults was higher than in school-aged children.[27] A review of DXA scans both from men and women found an increasing incidence of clinical scoliosis rising from 3% in individuals younger than 60 years to 21% in patients in their 80s.[21] Another large analysis of Cobb angles in older women found a 13% prevalence of clinical lumbar scoliosis, but age conferred only a small predictive effect.[22] Other studies show that Cobb angles increase in patients with scoliosis: Ten-year follow-up in adult scoliotic patients showed increased angle severity with advancing years,[21,28] with an average rate of lumbar curve progression of more than 3° per year.[29,30] Our results confirm that the prevalence of scoliosis increases with advancing age. The prevalence of scoliosis was 11.5% (21 of 182) in the youngest group and 39.4% (61 of 155) in the oldest group. Among the patients with serial DXA scans (Figure 5), Cobb angle increased an average of 0.70° for every year increase in age. Importantly, our subanalysis did not select for scoliosis or BMD, but rather for availability of serial DXA scans for analysis; as such, it would appear that many women with straight spines in their sixth decade acquire curvature as they age. Development of lumbar scoliosis mostly likely results from the combined effects of age-related degeneration of the vertebral body, facet joints, intervertebral discs, ligaments, and muscles. Intervertebral disc degeneration may lead to facet joint subluxation, which can cause remodeling of the posterior elements and result in segmental instability and scoliosis.[31] In individuals age 75 years followed for 10 years, degenerative changes, most commonly in the lumbar region, increased significantly in the subsequent 10 years,[32] consistent with the advancing scoliosis that we report here.

It is unclear whether there is a causal relationship between osteoporotic vertebral compression fractures and spine scoliosis.[33] Healey and Lane investigated the association between scoliosis and vertebral compression fractures in a group of 50 older women with biopsy-proven osteoporosis with known compression fractures.[34] Nearly half of these women had clinically significant scoliosis, but compression fractures themselves did not lead to a curve because the posterior spinal elements are not disrupted in compression fractures. Another theory is that scoliosis does predispose patients to fractures, since vertebrae within scoliotic curve are subject to eccentric loading. This is supported by the fact that most compression fractures occur at the apex of the thoracolumbar or lumbar curves.

Our study is limited by the cross-sectional design, and by the inability to separate scoliotic changes in the lumbar spine from potential lumbar fractures. Despite this, the data are clear with regard to a lack of association between lumbar scoliosis and advancing hip osteoporosis at either the FN or total proximal density sites. We also did not examine thoracic scoliosis, or compare data in men, both subjects that we hope to study in the future, and hope that modifiers of scoliosis can be addressed in prospective studies. Another limitation is that many comorbidities, influences of lifestyle, and medication history were not included in our analysis, and are likely to affect both the determination of osteoporosis and potentially the progression of scoliosis. Because ours was a retrospective study, an a priori power calculation was not performed. We did perform a post hoc power analysis for the partial correlation between lumbar scoliosis and osteoporosis while adjusting for 2 covariates—age and weight. Using an α of .05, a null correlation of 0, and our actual sample size of 300, analysis showed we had high power (> 99%) to detect even a weak partial correlation of 0.30. This supports our conclusion that an association between scoliosis and osteoporosis could not be identified.

Our analysis will help clinicians to answer their patients' questions regarding the discrepancy between spine and hip densities, etiology of their back pain, and speculation as to height loss during aging. Importantly, a majority of all fractures, including vertebral fractures, are not attributable to osteoporotic bone density,[35] and this recent study also suggested that the magnitude of association between BMD and fracture risk decreases over time. Thus, although osteoporosis is clearly associated with risk of fracture, other risks, including falls and other morbidities of aging, predominate—and when our data reveal that the prevalence of scoliosis increases. In the future, the contribution of lumbar scoliosis, which will inherently alter mechanics of the spine, both to lumbar and thoracic fracture burden in older patients, will be an important area of investigation.

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