Objective. To determine whether a vertebral corner that demonstrates an active corner inflammatory lesion (CIL) on magnetic resonance imaging (MRI) in patients with ankylosing spondylitis (AS) is more likely to evolve into a de novo syndesmophyte visible on plain radiography than is a vertebral corner that demonstrates no active inflammation on MRI.Methods. MRI scans and plain radiographs were obtained for 29 patients recruited into randomized placebo-controlled trials of anti-tumor necrosis factor ␣ (anti-TNF␣) therapy. MRI was conducted at baseline, 12 or 24 weeks (n ‫؍‬ 29), and 2 years (n ‫؍‬ 22), while radiography was conducted at baseline and 2 years. A persistent CIL was defined as a CIL that was found on all available scans. A resolved CIL was defined as having completely disappeared on either the second or third scan. A validation cohort consisted of 41 AS patients followed up prospectively. Anonymized MRIs were assessed independently by 3 readers who were blinded with regard to radiographic findings.Results. New syndesmophytes developed significantly more frequently in vertebral corners with inflammation (20%) than in those without inflammation (5.1%) seen on baseline MRI (P < 0.008 for all reader pairs). They also developed more frequently in vertebral corners where inflammation had resolved than in those where inflammation persisted after anti-TNF treatment. This was confirmed in the analysis of the prospective cohort, in which significantly more vertebral corners with inflammation (14.3%) compared with those without inflammation (2.9%) seen on baseline MRI developed new syndesmophytes (P < 0.003 for all reader pairs).Conclusion. Our findings indicate that a syndesmophyte is more likely to develop from a prior inflammatory lesion, supporting a relationship between inflammation and ankylosis.

Objective. Focal fat infiltration is frequently visible on magnetic resonance imaging (MRI) of the spine in patients with ankylosing spondylitis (AS) and likely reflects postinflammatory tissue metaplasia. To support the concept of coupling between inflammation and new bone formation, we tested the hypothesis that focal fat infiltration at a vertebral corner is more likely to evolve into a de novo syndesmophyte.Methods. MRI scans were obtained at baseline and radiographs were obtained at baseline and 2 years in 100 AS patients from 2 cohorts: a clinical trial cohort (n ‫؍‬ 38) and an observational cohort (n ‫؍‬ 62). In the clinical trial cohort, patients were randomized to receive anti-tumor necrosis factor (anti-TNF) therapy or placebo for 12-24 weeks and then open-label treatment for 2 years. In the observational cohort, patients received either standard therapy (n ‫؍‬ 36) or anti-TNF therapy (n ‫؍‬ 26) for 2 years. Vertebral corner inflammation and fat infiltration were assessed independently by pairs of readers who were blinded with regard to the radiographic findings.Results. New syndesmophytes developed significantly more frequently in vertebral corners with fat in both the clinical trial (10.2%) and the observational (6.5%) cohort as compared to those without either Conclusion. Our data lend support to the hypothesis that inflammatory lesions evolve into new bone through a process of tissue metaplasia that includes fat infiltration.A hallmark of ankylosing spondylitis (AS) is the development of new bone in the spine, which typically leads to ankylosis across the disc spaces. Bone proliferation typically starts at the vertebral rim and grows in the direction of the anulus fibrosus, parallel to the vertebral axis. Ossification may extend across the vertical length of the anulus and becomes visible on radiographs as a syndesmophyte.Until recently, it was hypothesized that ankylosis occurred in response to inflammation and following a reparative process that included cartilage metaplasia. However, data from animal models of spondylarthritis (SpA), principally ankylosing enthesitis, directly challenged this hypothesis by demonstrating that anti-tumor necrosis factor ␣ (anti-TNF␣) therapy did not prevent the development of ankylosis (1). An alternative hypothesis was then proposed whereby pathogenetic factors such as altered gene expression, biomechanical factors, and bacteria trigger the concomitant expression of inflammation and new bone formation, which then proceed

The new SPARCC MRI SSS method can detect structural changes in the SIJ with acceptable reliability over a 1-2-year timeframe, and should be further validated in patients with SpA.

Objective. Fat metaplasia in bone marrow on T1-weighted magnetic resonance imaging (MRI) scans may develop after resolution of inflammation in patients with ankylosing spondylitis (AS) and may predict new bone formation in the spine. Similar tissue, termed backfill, may also fill areas of excavated bone in the sacroiliac (SI) joints and may reflect resolution of inflammation and tissue repair at sites of erosions. The purpose of this study was to test our hypothesis that SI joint ankylosis develops following repair of erosions and that tissue characterized by fat metaplasia is a key intermediary step in this pathway.Methods. We used the Spondyloarthritis Research Consortium of Canada (SPARCC) SI structural lesion score (SSS) method to assess fat metaplasia, erosions, backfill, and ankylosis on MRIs of the SI joints in 147 patients with AS monitored for 2 years. Univariate and multivariate regression analyses focused first on identifying significant MRI predictors of new backfill and fat metaplasia. We then assessed the role of backfill and fat metaplasia in the development of new ankylosis. All analyses were adjusted for demographic features, treatment, and baseline and 2-year change in SSS values for parameters of inflammation and MRI structural lesions.Results. Resolution of inflammation and reduction of erosions were each independently associated with the development of new backfill and fat metaplasia at 2 years on multivariate analyses. Multivariate regression analysis that included demographic features, baseline and 2-year change in parameters of inflammation and MRI structural lesion showed that reduction in erosions (P ‫؍‬ 0.0005) and increase in fat metaplasia (P ‫؍‬ 0.002) at 2 years was each independently associated with the development of new ankylosis.Conclusion. Our data support a disease model whereby ankylosis develops following repair of erosions, and fat metaplasia and backfill are key intermediary steps in this pathway.Spondyloarthritis (SpA) is an inflammatory disorder primarily of the axial spine that typically begins with sacroiliitis. The first sign of disease on radiography is the appearance of erosion of the subchondral bone of the ilium, which is seen as a blurred cortical outline. Progression results in more extensive erosion involving the sacral bone and the appearance of pseudowidening. Subsequent features include bone sclerosis and, finally, ankylosis across the joint. Magnetic resonance imaging (MRI) constitutes a major advance in the field through its ability to demonstrate active inflammation on fatsuppressed sequences, such as short tau inversion recovery (STIR), and structural lesions, such as fat metaplasia, erosions, and ankylosis, on T1-weighed sequences (1).

The ASAS HI proved to be valid, reliable and responsive. It can be used to evaluate the impact of SpA and its treatment on functioning and health. Furthermore, comparison of disease impact between populations is possible.

Our study of AS spines documents that MRI findings predict new bone formation on radiograph. Demonstration of an increased likelihood of developing new bone following resolution of inflammation after anti-TNF therapy supports the theory that TNF-α acts as a brake on new bone formation. Because the number of new syndesmophytes was low, further study is necessary to make firm conclusions.

IntroductionDespite the availability of axial spondyloarthritis (SpA) recommendations proposed by various rheumatology societies, we considered that a region‐specific guideline was of substantial added value to clinicians of the Asia‐Pacific region, given the wide variations in predisposition to infections and other patient factors, local practice patterns, and access to treatment across countries.Materials and methodsSystematic reviews were undertaken of English‐language articles published between 2000 and 2016, identified from MEDLINE using PubMed, EMBASE and Cochrane databases. The strength of available evidence was graded using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. Recommendations were developed through consensus using the Delphi technique.ResultsFourteen axial SpA treatment recommendations were developed based on evidence summaries and consensus. The first 2 recommendations cover non‐pharmacological approaches to management. Recommendations 3 to 5 describe the following: the use of non‐steroidal anti‐inflammatory drugs as first‐line symptomatic treatment; the avoidance of long‐term corticosteroid use; and the utility of conventional synthetic disease‐modifying anti‐rheumatic drugs (csDMARDs) for peripheral or extra‐articular manifestations. Recommendation 6 refers to the indications for biological DMARDs (bDMARDs). Recommendation 7 deals specifically with screening for infections endemic to Asia, prior to use of bDMARDs. Recommendations 7 to 13 cover the role of bDMARDs in the treatment of active axial SpA and include related issues such as continuing therapy and use in special populations. Recommendation 14 deals with the utility of surgical intervention in axial SpA.ConclusionThese recommendations provide up‐to‐date guidance for treatment of axial SpA to help meet the needs of patients and clinicians in the Asia‐Pacific region.

Objective. Currently available magnetic resonance imaging (MRI) assessment systems for spine inflammation in patients with spondyloarthritis (SpA) identify only the overall inflammation in the discovertebral units. We aimed to develop and illustrate a detailed anatomy-based set of definitions and an assessment system for active inflammatory lesions in the spine of patients with SpA. Methods. MRI definitions of different inflammatory lesions at various anatomical locations in the spine, and an accompanying assessment system, were agreed by consensus within the Canada-Denmark MRI working group. Subsequently, a reference image set of representative examples of the individual pathologies, as well as borderline cases and important artefacts, were collected. Results. The defined lesions were (a) vertebral body inflammatory lesions, subdivided into corner, non-corner, massive, and lateral inflammatory lesions; and (b) vertebral inflammatory lesions not involving the vertebral body, subdivided into facet joint and other posterior element inflammatory lesions. All definitions were based on presence of increased signal intensity on sagittal T2-weighted fat-suppressed or STIR-images, as compared with the normal bone marrow signal. Vertebral body inflammatory lesions are assessed at each vertebral endplate at all 23 spinal levels from C2/3 to L5/S1, whereas facet joint or posterior element inflammatory lesions are to be assessed by segmental level (cervical, thoracic, and lumbar).Conclusion. An anatomy-based set of definitions and an assessment system for active inflammatory lesions in the spine of patients with SpA was developed and illustrated. The system is designed to study the temporal and spatial patterns of inflammation and their relation to the development of structural damage.