Does Inflammatory Bowel Disease Lead to Low Bone Mineral Density in the Lumbar Spine?
People with inflammatory bowel disease (IBD) are at a higher risk of both osteoporosis and osteoporosis-related fractures. However, the majority of studies that have focused on IBD and bone mineral density (BMD) are from selected referral centers. These studies do not directly delineate which aspects of IBD lead to a lower BMD in the lumbar spine and other locations in the body.
Their findings were published in the paper “The relationship between inflammatory bowel disease and bone mineral density. Results of a population-based study,” which was presented at the 2011 Annual Meeting of the American Society of Bone and Mineral Research.
For this study, the research team used 2 databases: the University of Manitoba IBD Epidemiologic Database and the Manitoba BMD Database. Both databases captured almost everyone living in Manitoba, Canada, who has IBD and who has had a clinical dual x-ray absorptiometry (DXA).
A total of 45,714 patients participated in this study. Participants were 20 years old or older. They underwent baseline testing for BMD between 1997 and 2008. It was noted that 1,230 of the participants had IBD.
BMD was measured at 4 locations: the lumbar spine (L1-L4), total hip, femoral neck, and greater trochanter.
To determine the independent effect an IBD diagnosis has on T-scores as well as on the likelihood of having an osteoporotic T-score (-2.5 or lower), multivariate linear regression and logistic regression were completed at each of the 4 BMD sites.
The researchers developed a partially adjusted model—adjusted for age, sex, and body mass index (BMI)—and a fully adjusted model. The fully adjusted model adjusted for hormone replacement therapy (HRT), osteoprotective therapy (OTX), and recent use of systemic glucocorticoid (GC).
The research team found that compared with study participants who do not have IBD, those who do have IBD were much more likely to be younger, male, and have a lower BMI.
In addition, the participants with IBD were significantly more likely to be recent users of GCs (26% vs 6%).
When adjusted for age, sex, and BMI, IBD was linked to lower T-scores at each of the 4 sites. IBD was also linked to having an osteoporotic T-score at both L1-L4 and the total hip. But IBD was associated with only a marginal reduction in T-scores at the total hip and greater trochanter when researchers further adjusted the model for exposure to GCs, HRT, and OTX.
Researchers found that in the fully adjusted model, IBD was not directly associated with a higher risk of an osteoporotic T-score at any of the 4 sites.
They concluded that although patients who have IBD are at a higher risk for a lower BMD as well as osteoporosis, this is not seen after adjusting for exposure to GCs and other medications.
These results suggest that the harmful effects of inflammatory bowel disease on bone mineral density are predominantly related to GCs rather than to IBD itself. Additional research is needed to delineate the independent effects of IBD, inflammatory activity, and IBD treatments on BMD and osteoporosis-related fracture risk in the lumbar spine and in other locations in the body.