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In this issue Jacques et al1 provide proof of concept that experimental spondyloarthritis (SpA) may be a biomechanically triggered process. The implication is that an aberrant mesenchymal tissue response to physiological mechanical forces that occur during joint movement may trigger inflammation associated with SpA. Given the long-known genetic association of human SpA with human leukocyte antigen (HLA)-B27,2 which governs initiation of adaptive immune responses, the concept that SpA resembles a biomechanically driven rather than autoimmune disease may come as a great surprise. The en face argument that mechanically driven animal models bear no resemblance to human SpA, however, has to be taken with caution, given that the role of mechanics in human SpA has several supporting strands of evidence that date back over 50 years.
Jacques and colleagues show that the earliest lesions in their model are localised at the Achilles tendon. As far back as 1959, La Cava, in his prophetic commentary on enthesitis, but not specifically in relationship to SpA, recognised that “the continually recurring concentration of muscle stress at these points provokes a reaction of inflammation with a strong tendency to the formation of fibrosis and calcification”.3 He also stated that insertions appeared to show ‘a peculiar reaction to irritative stimuli’ and that such stimuli were most frequently ‘microtraumatic in origin’. Since that time evidence has accumulated that supports all aspects of these suppositions.
In the 1970s, Moll and Wright deduced the clinical concept of SpA.4–6 Although they did not pinpoint the ‘invisible unifying concept’, which appears to be mechanical stress, they recognised that physical trauma to joints appeared to trigger psoriatic arthritis and speculated that psoriatic arthritis (PsA) represented a ‘Deep Koebner response’. However, they did not specifically recognise the importance of the entheseal organ as the link between biomechanics and …
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