Entheses (insertion sites, osteotendinous junctions, osteoligamentous junctions) are sites of stress concentration at the region where tendons and ligaments attach to bone. Consequently, they are commonly subject to overuse injuries (enthesopathies) that are well documented in a number of sports. In this review, we focus on the structurefunction correlations of entheses on both the hard and the soft tissue sides of the junction. Particular attention is paid to mechanical factors that influence form and function and thus to exploring the relationship between entheses and exercise. The molecular parameters indicative of adaptation to mechanical stress are evaluated, and the basis on which entheses are classified is explained. The application of the 'enthesis organ' concept (a collection of tissues adjacent to the enthesis itself, which jointly serve the common function of stress dissipation) to understanding enthesopathies is considered and novel roles of adipose tissue at entheses are reviewed. A distinction is made between different locations of fat at entheses, and possible functions include space-filling and proprioception. The basic anchorage role of entheses is considered in detail and comparisons are explored between entheses and other biological 'anchorage' sites. The ability of entheses for self-repair is emphasized and a range of enthesopathies common in sport are reviewed (e.g. tennis elbow, golfer's elbow, jumper's knee, plantar fasciitis and Achilles insertional tendinopathies). Attention is drawn to the degenerative, rather than inflammatory, nature of most enthesopathies in sport. The biomechanical factors contributing to the development of enthesopathies are reviewed and the importance of considering the muscle-tendon-bone unit as a whole is recognized. Bony spur formation is assessed in relation to other changes at entheses which parallel those in osteoarthritic synovial joints.

The study suggests that the extended nature of the enthesis organ associated with the DIP joint may explain the diffuse nature of the inflammatory response around the nail in PsA. Therefore the nail is as much an integral part of the enthesis organ as it is of the skin, which has implications for a better understanding of the disease.

Stretch injury to the myotendinous junction is a common problem in competitive athletes and those involved in regular physical activity. The major risk factor for recurrent injury appears to be the primary injury itself. Physicians, physical therapists, athletic trainers and athletes alike continue to search for optimal treatment and prevention strategies. Acute inflammation is regarded as the body's generalized protective response to tissue injury. An especially important and unexplored aspect of inflammation following injury is the role of inflammatory cells in extending injury and possibly directing muscle repair. It has been suggested that the inflammatory reaction, although it typically represents a reaction to damage and necrosis, may even bring about some local damage of its own and therefore increase the possibility for scarring and fibrosis. Limiting certain aspects of inflammation may theoretically reduce muscle damage as well as signals for muscle scarring. Here we focus on the role of neutrophils in injury and repair of stretch-injured skeletal muscle. A minimally invasive model that generates a reproducible injury to rabbit skeletal muscle is presented. We present a plausible theory that neutrophil-derived oxidants resulting from the initial stretch injury are responsible for extending the damage. An anti-CD11b antibody that blocks the neutrophil's respiratory burst is employed to reduce myofibre damage. An intriguing area that is currently being explored in our laboratory and others is the potential role for neutrophils to contribute to muscle growth and repair. It may be possible that neutrophils facilitate muscle repair through removal of tissue debris as well as by activation of satellite cells. Recent and ongoing investigations point to interleukin-6 as a possible key cytokine in muscle inflammation and repair. Studies to elucidate a clearer understanding of this possibility will be reviewed.Key words macrophages; muscle; neutrophils; stretch; tendon. The clinical problem 460Physicians, physical therapists, athletic trainers and athletes alike continue to search for optimal treatment and prevention strategies. An area of controversy and ongoing study is the role of stretching in preventing and treating injury. A recent systematic review of the literature using the six available published studies concluded that stretching was not significantly associated with a reduction in musculoskeletal injuries (Thacker et al. 2004). This meta-analysis combined five studies on pre-exercise stretching with one article on regular stretching outside of exercise to obtain an overall summary that stretching does not prevent injury (odds ratio (OR) = 0.93; CI 0.78-1.11). As with stretching, little

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Objective. To describe the basis for enthesealassociated bone disease in the spondylarthritides, by analyzing microanatomic and histopathologic relationships between soft tissue, bone cortex, and adjacent trabeculae.Methods. Serial sections from 52 entheses were examined; these entheses encompassed small and large insertions in the upper limb (n ‫؍‬ 21), lower limb (n ‫؍‬ 27), and spine (n ‫؍‬ 4) from 60 cadavers. Enthesis microdamage (fissuring) as well as vascular and reparative changes were evaluated. Contact radiographs were used to ascertain the relationship between entheses and the trabecular network.Results. At virtually all fibrocartilaginous entheses, the deep cortical boundary was extremely thin (typically 50-600 m) or indistinguishable, and 96% of entheses had small holes in the cortical shell (typically 100-400 m wide). Such regions were frequent sites of bone formation and renewal (96%) and microdamage (31%); these changes were more common in the lower limb. The presence of blood vessels near holes in the cortical shell was common; in 85% of attachments, blood vessels were present on the soft tissue side of the enthesis. Highly orientated trabeculae were more obvious in the lower limb than the upper limb (59% versus 29%).Conclusion. The trabecular network supporting the cortical shell is an integral part of the enthesis, transferring load to an extensive skeletal region. In many cases, tendons/ligaments are anchored directly to such networks. This functional integration is associated with microdamage and repair at the hard tissue-soft tissue interface. These findings have implications for understanding bone involvement in SpA and for the SpA concept in general, especially the hypothesis that enthesis-bone architecture may be important in disease initiation.