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Anabolic Steroids Igf Background Tendon ruptures have been linked to anabolic steroid usage, suggesting pathological changes in tendon structure due to steroid intake. The mechanisms for tendon rupture are not well-understood. However, it is now clear that there are two major pathways for pain caused by tendinosis: 1) rupture at the molecular level that leads to necrosis; or 2) breakdown of the structure of muscle fibers that results in fibrosis [5,6]. The first pathway is caused by excess and prolonged use of anabolic androgenic steroids and it is considered to be the primary and predominant cause of injury [7]. It has been proven that over-use of hormones such as estrogens and androgens can induce both hypertrophy of tendon fibers and collagen fibrotic changes (i.e. collagen breakdown) but at different levels of concentration. Therefore, in this work we investigated whether hypertrophy is a sufficient mechanism for pain.

The aim of this study is to investigate factors related to the extent of tendon injury during hypertrophy induced by the use of androgens after tendon rupture in rats.

Materials and Methods Ethics Statement Ethics approval for this study was obtained from the Local Ethic Committee of the University of Leipzig (reference no. 6/2009). Informed consent was also obtained at the University of Leipzig Human Research Ethics Committee. Rats Male Sprague–Dawley rats weighing approximately 15–18 g weighing approximately 10 g were obtained from the animal colony of the Animal Health Center Leipzig, Germany. Animals were purchased at the University of Leipzig and maintained in an animal colony on rats with a minimum body weight of 25 g. The treatment group consisted of two groups of 10 male rats with a ruptured tendon (5 in the group treated with testosterone and 5 in the group treated with oxandrolone and corticosterone at a constant dose of 5 mg/kg body weight/day, i.e. the control group). During surgery, rats were given a local injection of 50 µl of isotonic saline (I) and the tendon was punctured with a needle (A) followed by fixation of the punctured tendon by methyl methacrylate (MMA). During the experiment, 3 months after the injury, the testes were removed and treated with testosterone and dexamethasone (DEX) for a week at concentrations of 1,5 mg/ml and 50 µg/ml respectively for 6 weeks. Tendon ruptures were confirmed through histology. The control group was treated with testosterone in the same way as in the treatment group. In addition, muscle specimens of the

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