Tendon injuries and other tendon disorders represent a common diagnostic and therapeutic challenge in sports medicine, resulting in chronic and long‐lasting problems. Tissue degeneration is a common finding in many sports‐related tendon complaints. In the great majority of spontaneous tendon ruptures, chronic degenerative changes are seen at the rupture site of the tendon (1). Systemic diseases and diseases specifically deteriorating the normal structure of the tendon (i.e. foreign bodies, and metabolic, inherited and infectious tendon diseases) are only rarely the cause of tendon pathology. Inherited diseases, such as various hereditary diseases with disturbed collagen metabolism and characteristic pathological structural alterations (Ehlers‐Danlos syndrome, Marfani syndrome, homocystinuria (ochronosis)), represent approximately 1% of the causes of chronic tendon complaints (2), whereas foreign bodies are somewhat more common and are found in less than 10% of all chronic tendon problems (1). Rheumatoid arthritis and sarcoidosis are typical systemic diseases that cause chronic inflammation in tendon and peritendinous tissues. Altogether, these ‘specific’disorders represented less than 2% of the pathological alterations found in the histological analysis of more than 1000 spontaneously ruptured tendons (1, 3, 4). In this material, degenerative changes were seen in a great majority of the tendons, indicating that aspontaneous tendon rupture is a typical clinical end‐state manifestationof a degenerative process in the tendon tissue. The role of overuse in the pathogenesis of chronic tendon injuries and disorders is not completely understood. It has been speculated that when tendon is overused, it becomes fatigued and loses its basal reparative ability, the repetitive microtraumatic processes thus overwhelming the ability of the tendon cells to repair the fiber damage. The intensive repetitive activity, which often is eccentric by nature, may lead to cumulative microtrauma which further weakens the collagen cross‐linking, non‐collagenous matrix, and vascular elements of the tendon. Overuse has also been speculated to cause chronic tendon problems, by disturbing the micro‐ and macrovasculature of the tendon and resulting in insufficiency in the local blood circulation. Decreased blood flow simultaneous with an increased activity may result in local tissue hypoxia, impaired nutrition and energy metabolism, and together these factors are likely to play an important role in the sequence of events leading to tendon degeneration (4). A sedentary lifestyle has been proposed as a main reason for poor basal circulation of the tendon, and presumably is at least partly responsible for the high number of tendon problems in people with a sedentary lifestyle who occasionally take part in high physical activity sports events.

The concept and need for a gender-specific or female-specific total knee prosthesis have generated interest and discussion in the orthopaedic community and the general public. This concept relies on the assumption of a need for such a design and the opinion that there are major anatomic differences between male and female knees. Most of the information regarding this subject has been disseminated through print and Internet advertisements, and through direct-to-patient television and magazine promotions. These sources and a recent article in a peer-reviewed journal, which support the need for a female-specific implant design, have proposed three gender-based anatomic differences: (1) an increased Q angle, (2) less prominence of the anterior medial and anterior lateral femoral condyles, and (3) reduced medial-lateral to anterior-posterior femoral condylar aspect ratio. We examined the peer-reviewed literature to determine whether women have had worse results than men after traditional TKAs. We found women have equal or better results than men. In addition, we reviewed the evidence presented to support these three anatomic differences. We conclude the first two proposed differences do not exist, and the third is so small that it likely has no clinical effect.

The management of neglected tears of the Achilles tendon by free gracilis tendon grafting is safe but technically demanding. It affords good recovery, even in patients with a neglected rupture of a duration of 9 months. These patients should be warned that they are at risk for postoperative complications, and that their ankle plantar flexion strength can remain reduced.

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