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Is osteoarthritis (OA) only one and the same disease or is it actually a nebula of several diseases for which we still lack markers allowing to differentiate them? This issue is currently the subject of much debate in the medical and scientific community and remains unresolved. It is not a trivial question because deciphering disease phenotypes could be used to select a group of patients for whom a particular treatment will be effective or for whom the prognosis will be better or worse.
According to the Osteoarthritis Research Society International (OARSI), OA is a disorder involving movable joints characterised by cell stress and extracellular matrix degradation initiated by microinjury and macroinjury that activate maladaptive repair responses, including proinflammatory pathways of innate immunity. The disease manifests first as a molecular derangement (abnormal joint tissue metabolism), followed by anatomical and/or physiological derangements (characterised by cartilage degradation, bone remodelling, osteophyte formation, joint inflammation and loss of normal joint function), which can culminate in illness.1 It is clear that this complex definition reveals, on the one hand, a poor understanding of the underlying mechanisms, and on the other hand the potential extent of heterogeneity of the disease. With such a definition, it is easy to imagine the theoretical possibility of many different disease subgroups, depending on clinical, biological, genetics and/or imaging variables.
Some believe that the successive failures of the many therapeutic trials carried out in recent years to delay OA are due to the phenotypic heterogeneity of the patients included in these trials, masking the possible efficacy of the drug X reserved for the only phenotype Y. This reasoning is analogous to what is now consensually accepted in cancer, where drugs used to be poorly effective in clinical trials before patient selection have become remarkably effective in specific phenotypes based on tumour gene signatures. …
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