Calcific tendinopathy (CT) of the shoulder is a common, painful condition characterized by the presence of calcium deposits in the rotator cuff tendons. Current theories indicate that CT may be the result of a cell-mediated process in which, after a stage of calcium deposition, calcifications are spontaneously resorbed. However, in a minority of cases, this self-healing process is somehow disrupted, resulting in symptoms. Recent literature shows an emerging role of biological and genetic factors underlying CT. This new evidence could supplement the classic mechanical theory of rotator cuff tendinopathy complicated by calcium precipitation, and it may also explain why the majority of the therapies currently in use are only able to provide partially satisfactory outcomes. This review aims to summarize the current knowledge about the pathological processes underlying CT of the shoulder and thereby justify the quest for advanced biological treatments of this condition when it becomes symptomatic.

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The actual need for surgical reconstruction of an injured anterior cruciate ligament (ACL) is still a matter of debate. The aim of this study was to quantify and analyze the knee kinematics and the ligament force redistribution resulting from the ACL sacrifice and the consequent effects of changing the quadriceps and hamstring activity during walking. A three-dimensional musculoskeletal model was used to simulate the behavior of the knee joint during the gait cycle, in different testing conditions: an ACL-deficient knee, an ACL-deficient knee with hamstrings inactivated and an ACL-deficient knee with quadriceps inactivated. Our results showed that in the ACL-deficient knee, the medial collateral ligament (MCL) was the main passive stabilizer of the anterior translation of the tibia. Furthermore, the compensation effects produced by the hamstrings and quadriceps in the ACL-deficient knee during walking were quantified and analyzed. In the case of ACL sacrifice, reducing the quadriceps activity would allow for relieving all ligaments in general, except for the posterior cruciate ligament, which required more consistent recruitment in the support phase. Meanwhile, hamstring activity was crucial not only to compensate for the absence of ACL in limiting the anterior tibial displacement but also to reduce the risk of MCL injury.