The FIFA 11+ warm-up program is effective in reducing the rates of injuries in elite male basketball players.

Rotator cuff disease is among the most common musculoskeletal disorders with high direct and indirect costs in industrialized countries. Not all rotator cuff tears are symptomatic. Genetics has recently been investigated as a factor involved in the pathogenesis of rotator cuff pathology. Genetic factors seem to be involved in symptom presentation and tear progression. As rotator cuff disease is multifactorial, no single gene is directly involved in the pathology. Phenotypic expression of genetic susceptibility manifests at the level of ultrastructure of the tendon. Predisposing genes may also operate through apoptosis and regenerative capacity. Studies on cellular and molecular biology are more numerous, but still incomplete, and recently have focussed on the role of apoptosis in tendinopathy, analyzing its key mediators and cellular changes. Oxidative stress is responsible for reduction of collagen synthesis. Biological investigations have identified recently new risk factors. Preliminary reports introduced the possible role of glucose as a risk factor for rotator cuff tear. Further studies are required to fully clarify the genetic and biological factors involved in rotator cuff tears.

The pathogenesis of rotator cuff tears is multifactorial. Tendon abnormalities of the rotator cuff include alteration of collagen fiber structure, tenocytes, cellularity, and vascularity. Ruptured tendons show marked collagen degeneration and disordered arrangement of collagen fibers. Fibroblast population decreases as the size of the tear in the rotator cuff increases. The larger fibroblast population seen in the smaller tears is also actively proliferating and is part of an active reparative process. Inflammatory cell infiltrate correlates inversely to rotator cuff tear size in the torn supraspinatus tendon samples, with larger tears showing a marked reduction in all cell types. As tear size increase, there is also a progressive decrease in the number of blood vessels. Whether rotator cuff tear heals spontaneously is an important pathologic and clinical question. Histologic changes indicative of repair and inflammation lead to consider biological options in addition to biomechanical treatment of the rotator cuff tears.

Systematic review, Level IV.

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Cartilage defects represent a common problem in orthopaedic practice. Predisposing factors include traumas, inflammatory conditions, and biomechanics alterations. Conservative management of cartilage defects often fails, and patients with this lesions may need surgical intervention. Several treatment strategies have been proposed, although only surgery has been proved to be predictably effective. Usually, in focal cartilage defects without a stable fibrocartilaginous repair tissue formed, surgeons try to promote a natural fibrocartilaginous response by using marrow stimulating techniques, such as microfracture, abrasion arthroplasty, and Pridie drilling, with the aim of reducing swelling and pain and improving joint function of the patients. These procedures have demonstrated to be clinically useful and are usually considered as first-line treatment for focal cartilage defects. However, fibrocartilage presents inferior mechanical and biochemical properties compared to normal hyaline articular cartilage, characterized by poor organization, significant amounts of collagen type I, and an increased susceptibility to injury, which ultimately leads to premature osteoarthritis (OA). Therefore, the aim of future therapeutic strategies for articular cartilage regeneration is to obtain a hyaline-like cartilage repair tissue by transplantation of tissues or cells. Further studies are required to clarify the role of gene therapy and mesenchimal stem cells for management of cartilage lesions.