From the Journals

Trabecular bone loss may contribute to axial spondyloarthritis progression



Trabecular bone loss in patients with axial spondyloarthritis is associated with spinal progression in the form of more syndesmophytes, new research suggests.

A paper published in Seminars in Arthritis and Rheumatism reports the outcomes of a prospective observational cohort study in 245 patients with axial spondyloarthritis that sought to identify possible predictors of spinal radiographic progression of the disease.

Joon-Yong Jung, MD, PhD, and colleagues from the Catholic University of Korea, Seoul, South Korea, wrote that inflammation of the vertebrae is the first stage of progression of axial spondyloarthritis. One hypothesis is that this inflammation is associated with trabecular bone loss, which then leads to spinal instability, which in turns causes biomechanical stress on the area and the formation of new bone as syndesmophytes.

To evaluate the possible relationship between trabecular bone loss and syndesmophytes, researchers used dual-energy x-ray absorptiometry imaging of the lumbar spine, which can assess the microarchitecture of trabecular bone, as well as radiographs of the cervical and lumbar spine at 2 and 4 years of follow-up to assess the presence of syndesmophytes.

At baseline, 40% of patients had syndesmophytes, and the mean number of syndesmophytes was 3.3. A total of 11% of patients at baseline had mild trabecular bone loss, defined as trabecular bone score values between 1.230 and 1.310, and 10% had severe trabecular bone loss, with a score of 1.230 or less.

While on average patients had an increase of 1.41 syndesmophytes every 2 years during the study, patients with severe trabecular bone loss at baseline formed 1.26 more syndesmophytes every 2 years than did patients with normal trabecular bone loss score. After adjusting for variables such as disease activity and clinical factors, the authors found that both mild and severe trabecular bone loss were independently associated with progression of structural damage in the cervical and lumbar spine.

Patients with mild trabecular bone loss had a 120% greater odds of new syndesmophyte formation over the next 2 years, compared with those with normal trabecular bone loss scores, while those with severe loss had a 280% greater odds.

“The more severe the trabecular bone loss, the stronger the effect on the progression of the spine,” the authors wrote. Other factors associated with new syndesmophyte formation included higher C-reactive protein levels, longer symptom duration, smoking, and high NSAID index.

The study also pointed to an association between trabecular bone loss and modified Stoke Ankylosing Spondylitis Spinal Score. Patients with severe trabecular bone loss showed an average increase of 0.37 in their modified Stoke Ankylosing Spondylitis Spinal Score over 2 years, compared with patients with normal trabecular bone loss score at baseline, even after adjusting for confounders.

The authors commented that inflammation is hypothesized to lead to structural damage in two ways. “Inflammation-induced bone loss in the spine results in instability, another type of biomechanical stress, which then triggers a biomechanical response in an attempt to increase stability,” they wrote. Or inflammation leads to the formation of granulated repair tissue which then triggers new bone formation.

Whatever the mechanism, the authors said finding that trabecular bone loss is associated with disease progression suggests a possible use for the trabecular bone score as a practical and noninvasive means to predict spinal progression in patients with axial spondyloarthritis.

The study received no funding, and the authors said they had no conflicts of interest to declare.

SOURCE: Jung J-Y et al. Semin Arthritis Rheum. 2020;50(5):827-33.

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