The recent seminal discovery that an interleukin-23 (IL23) receptor positive T cell population is present in tendon and ligament attachment sites and that these cells contribute to spondyloarthritis-like joint inflammation in mice, has transformed current paradigms of the human disease. These attachment sites, commonly referred to as entheses, were earlier suggested as primary disease localization in SpA but their role in the development of chronic inflammation remained elusive. The IL23 responsive T cell population identified by Sherlock et al., is proposed as a key mediator or masterswitch in the disease process by triggering downstream inflammatory cascades as well as joint remodeling, the Janus-faced characteristics of spondyloarthritis. Interestingly the novel paradigm centered around this unexpected cell population is corroborated by further progress in genetics of spondyloarthritis, highlighted by clearly mapped molecular interactions and pathway integration. From the clinical perspective, accumulating datasets on non-radiographic axial spondyloarthritis not only support the success of anti-TNF strategies in case of failure to achieve symptom control with classical anti-inflammatory drug, but additionally trigger novel questions on the epidemiology of disease. Data obtained in cohorts of early disease patients shed new light on the demographics and likely evolution of the disease.
Biomarker research is rapidly growing and a number of novel molecules may find their way into clinical practice over time provided that the original datasets linking serum levels to radiographic progression of disease can be confirmed. With regards to the much feared radiographic progression and evolution towards ankylosis, additional evidence for a structural effect associated with non-steroidal anti-inflammatory drugs has been presented. From the therapeutic perspective, novel strategies are eagerly awaited with preliminary evidence suggesting clinical responses in patients treated with anti-interleukin 17 strategies. Early phase clinical trial data also point towards apremilast, a phosphodiesterase inhibitor as a drug that needs to be further studied.
In summary, over the last year, paradigm-shifting data have been published in the field of spondyloarthritis not only leading to novel insights into the pathophysiology but also defining novel and attractive therapeutic targets thereby suggesting that the next phase in spondyloarthritis research and therapy may be on the horizon.
Disclosure of Interest None Declared