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Effect of non-steroidal anti-inflammatory drugs on radiographic spinal progression in patients with axial spondyloarthritis: results from the German Spondyloarthritis Inception Cohort

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TLDR
A high NSAIDs intake over 2 years is associated with retarded radiographic spinal progression in AS, and in non-radiographic axial SpA this effect is less evident, probably due to a low grade of new bone formation in the spine at this stage.
Abstract
Objective To investigate the influence of non-steroidal anti-inflammatory drugs (NSAIDs) intake on radiographic spinal progression over 2 years in patients with ankylosing spondylitis (AS) and non-radiographic axial spondyloarthritis (SpA). Methods 164 patients with axial SpA (88 with AS and 76 with non-radiographic axial SpA) were selected for this analysis based on availability of spinal radiographs at baseline and after 2 years of follow-up and the data on NSAIDs intake. Spinal radiographs were scored by two trained readers in a concealed randomly selected order according to the modified Stoke Ankylosing Spondylitis Spine Score (mSASSS) system. An index of the NSAID intake counting both dose and duration of drug intake was calculated. Results High NSAIDs intake (NSAID index≥50) in AS was associated with lower likelihood of significant radiographic progression defined as an mSASSS worsening by ≥2 units: OR=0.15, 95% CI 0.02 to 0.96, p=0.045 (adjusted for baseline structural damage, elevated C reactive protein (CRP) and smoking status) in comparison with patients with low NSAIDs intake (NSAID index Conclusion A high NSAIDs intake over 2 years is associated with retarded radiographic spinal progression in AS. In non-radiographic axial SpA this effect is less evident, probably due to a low grade of new bone formation in the spine at this stage.

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Journal ArticleDOI

The impact of tumor necrosis factor α inhibitors on radiographic progression in ankylosing spondylitis.

TL;DR: Treatment with TNFα inhibitors appears to reduce radiographic progression in patients with ankylosing spondylitis, especially with early initiation and with longer duration of followup, and the protective effect of TNF α inhibitors was stronger after propensity score matching.
Journal ArticleDOI

Enthesitis: from pathophysiology to treatment

TL;DR: The role of biomechanics, prostaglandin E2-mediated vasodilation and the activation of innate immune cells in the initiation phase of enthesitis, as well as the role of entheseal IL-23-responsive cells that augment inflammation by producing pro-inflammatory mediators such as IL-17A, IL-22 and TNF are addressed.
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Continuous long-term anti-TNF therapy does not lead to an increase in the rate of new bone formation over 8 years in patients with ankylosing spondylitis

TL;DR: The radiographic progression of ankylosing spondylitis patients treated with infliximab versus historical controls never treated with tumour necrosis factor (TNF)-blockers over 8 years argues against a major role for the TNF-brake hypothesis.
References
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Journal ArticleDOI

Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria.

TL;DR: The study showed the clinical history screening test for AS to be moderately sensitive, but it might be better in clinical practice, and substitution of the Rome pain criterion for the New York pain criterion is proposed.
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The European spondylarthropathy study group preliminary criteria for the classification of spondylarthropathy

TL;DR: The proposed classification criteria for spondylarthropathy are easy to apply in clinical practice and performed well in all 7 participating centers and are regarded as preliminary until they have been further evaluated in other settings.
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2010 update of the ASAS/EULAR recommendations for the management of ankylosing spondylitis

TL;DR: The ASAS/EULAR recommendations on the management of ankylo sing spondylitis (AS) are based on the original paper, a systematic review of existing recommendations and the literature since 2005 and the discussion and agreement among 21 international experts, 2 patients and 2 physiotherapists in a meeting in February 2010 as mentioned in this paper.
Journal ArticleDOI

Cyclooxygenase-2 regulates mesenchymal cell differentiation into the osteoblast lineage and is critically involved in bone repair

TL;DR: It is demonstrated that COX-2 plays an essential role in both endochondral and intramembranous bone formation during skeletal repair and regulates the induction of cbfa1 and osterix to mediate normal skeletal repair.
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