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Studies in the spontaneous ankylosis model in ageing male DBA/1 mice and in patients with ankylosing spondylitis have provided evidence that inflammation and new tissue formation leading to joint or spine ankylosis are likely to be linked but are largely uncoupled processes. We have previously proposed the ‘entheseal stress’ hypothesis that defines microdamage to the enthesis as a starting point for these murine and human diseases.
To study the involvement of inflammatory pathways in …
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