Systemic Bone Loss Seen in Ankylosing Spondylitis

Published: Nov 7, 2013 | Updated: Nov 8, 2013
By Nancy Walsh, Staff Writer, MedPage Today

Full Story:  http://www.medpagetoday.com/Rheumatology/BackPain/42789

Action Points

  • A loss of peripheral bone mineral density accompanied the spinal changes seen in patients with ankylosing spondylitis (AS).
  • Point out that the results are consistent with a link between trabecular bone loss in the axial and peripheral skeleton in AS.

A loss of peripheral bone mineral density (BMD) accompanied the spinal changes seen in patients with ankylosing spondylitis (AS), a sophisticated imaging study showed.

High-resolution peripheral quantitative computed tomography revealed that AS patients had significantly less trabecular volumetric BMD at the ultra-distal radius (P=0.007) and at the ultra-distal tibia (P=0.033) compared with healthy controls, according to Eva Klingberg, MD, of the University of Gothenburg in Sweden, and colleagues.

In addition, there were strong correlations between trabecular BMD at the lumbar spine and distal tibia (rs = 0.712) and at the distal radius (rs = 0.762, P<0.001 for both), the researchers reported online in Arthritis Research & Therapy.

“The results thus indicated a link between trabecular bone loss in the axial and peripheral skeleton in AS,” the investigators observed.

Ankylosing spondylitis is characterized by chronic spinal inflammation, osteoporosis and fractures, the accumulation of new bony growths known as syndesmophytes within the ligaments of the spine, and vertebral fusing.

The mechanisms of these processes have remained largely unknown because of the inadequacies of conventional imaging in these patients and the difficulties associated with obtaining biopsies, but the development of high-resolution peripheral quantitative CT is now permitting the detailed visualization of bone microarchitecture.

To explore whether this new technique could help elucidate the progressive bone abnormalities of AS, Klingberg and colleagues compared the CT results from a group of 69 male Swedish patients originally enrolled in a larger study of osteoporosis with results from 68 matched healthy individuals in Olmstead County, Minn.

Patients’ mean age was 49, and mean duration of symptoms was 23 years.

Along with the low trabecular BMD seen in the lumbar spine, AS patients also showed evidence of deteriorated bone microarchitecture, with features such as thinning of the trabeculae and cortex.

The implication was that osteoporosis in AS is a generalized process that involves trabecular bone at both spine and distal sites of the skeleton.

In contrast, fractures and pathologic bone formation at the spine were localized events that primarily involved cortical bone, as was demonstrated by further imaging and analysis.

When the researchers compared high-resolution CT results for eight patients who developed vertebral fractures and 16 matched AS controls without fractures, they found that both trabecular and cortical BMD and thickness were lower in the distal radius in the fracture group.

However, the most significant differences between patients who fractured and AS nonfracture controls was in cortical thickness at the radius (P=0.003) and the tibia (P=0.016) and in cortical cross-sectional area at the radius (P=0.001) and tibia (P=0.013).

Moreover, in a multiple regression analysis, only lower cortical cross-sectional area at the tibia was associated with fracture (B = 0.063, P=0.008), with an odds ratio of 0.939 (95% CI 0.897-0.984).

Klingberg’s team then analyzed the association of the excess bone formation at the spine and BMD, and found that syndesmophytes were visible on radiographs of 39 patients.

Multiple regression analysis adjusted for age found that the presence of syndesmophytes was associated with lower lumbar trabecular BMD (B = -0.058, P<0.001), with an odds ratio of 0.943 (95% CI 0.917-0.970) as well as with higher cortical lumbar BMD (B = 0.019, P=0.016), with an odds ratio of 1.019 (95% CI 1.004-1.035).

This finding of decreased trabecular BMD but increased cortical BMD at the spine “was presumably reflecting pathologic new bone formation in the cortex of the vertebral bodies,” the researchers explained.

However, this new bone formation at the spine wasn’t associated with a similar process in peripheral bone. Rather, it was linked with decreased peripheral trabecular thickness and density.

“The findings support the concept of osteoproliferation as being a local anabolic bone response to inflammation, mechanical stress, or micro damage, but not a systemic process in AS,” they stated.

A limitation of the study was the use of an American cohort as control, but the controls were matched for various factors including age and weight, and that region of Minnesota has a high number of residents of Scandinavian heritage, the researchers pointed out.

The authors stated that they had no competing interests.

Primary source: Arthritis Research & Therapy

Source reference: Klingberg E, et al “Bone microarchitecture in ankylosing spondylitis and the association with bone mineral density, fractures, and syndesmophytes” Arthritis Res Therap 2013; DOI: 10.1186/ar4368.

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