Osteoarthritis (OA) is a pretty old disease, which has “accompanied” mankind since the beginning: anthropologists have found remnants of osteoarthritic joints in mummies of Ancient Egypt, not to mention the description of OA present in literary works, such as some Roman medical treatises, and also more “recent” pictorial representations of OA in works realized from the Middle ages onwards [1]. To be more accurate, OA even precedes mankind, since there is evidence of this disease affecting joints of Early Cretaceous birds and dinosaurs, 110–130 million years ago [2]. Joint degeneration seems something unavoidably, especially for bipedal animals. This premise justifies the increasing interest towards OA, not only by basic researchers and physicians but also by patients themselves who are struggling against a pathology that severely affects their quality of life: FDA has recognized OA as a serious disease with an “unmet clinical need” for strategies that modify the course and progression of the disease [3]. This explains the great efforts made in the last 20 years to better define the aetiopathogenetic pathways of OA and identifying novel therapeutic strategies [4, 5]: this was possible due to an increasing interaction among basic researchers and clinicians, whose actions, taken singularly, would not have led to any significant achievement in the approach to OA. The necessity of such interaction was the primum movens which stimulated us to propose a Special Issue on “Biologic strategies for Osteoarthritis and around: from early diagnosis to treatment,” with the goal of collecting high-quality studies investigating different but complementary aspects of OA, from diagnostic tools to novel therapeutic options. There are many open questions regarding OA, which is a multi-faceted disease: the word OA may in fact include different clinical entities, presenting with different signs and symptoms. Experienced clinicians know that many “phenotypes” exist, from inflammatory ones, where swelling is predominant, to mechanical ones where the patient’s status is mainly influenced by joint deformity with only mild signs of chronic inflammation [4]. We know that some risk factors exist, such as obesity, mal-alignment, previous traumatic injuries or previous meniscectomy, but we are also aware that OA can involve patients without any of the aforementioned factors. Pain and functional limitations are common findings among osteoarthritic patients, but the etiopathogenetic pathways triggering the onset and progression of OA are several, and also many molecules are involved [6]. Furthermore, each joint has peculiar biomechanical features that could play a role in the pathogenesis of articular degeneration, favouring specific molecular pathways compared with others. Therefore, a deeper insight into the biology of OA and its correlation with biomechanics will lead us to differentiate joint-specific OA phenotypes and, perhaps, better target our treatments.
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