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Musculoskeletal pain in athletes is common, but not always associated with injury (ie, tissue damage).1 Damage occurs when load exceeds tissue tolerance, such as ligament tear or a fracture. However, pain in athletes that occurs in the absence of trauma and tissue damage is still often labelled an ‘injury’ by clinicians, coaches and athletes themselves. This highlights a gap between knowledge (tissue damage is not necessary for pain) and practice (assuming that all pain arises from tissue damage) in our clinical community.1 2 This applies particularly in the area of acute non-traumatic pain (such as back and joint pain). To help bridge this gap, we outline eight principles to guide clinicians who manage musculoskeletal pain in sport (see infographic in figure 1). Figure 1 Infographic—principles to guide care of acute non-traumatic pain in sport. ### 1. In the absence of trauma, do not assume that pain indicates tissue damage

Objective: To compare the long term outcomes of the two treatment options for navicular stress fractures: non-weightbearing cast immobilisation and surgical fixation. Design: Retrospective case study. Participants: Subjects aged 18 years and older who had been treated for a navicular stress fracture more than two years previously. Main outcome measures: Questionnaire based analogue pain score and function score; tenderness on palpation; abnormality detected on computed tomography (CT). Results: In all, 32 fractures in 26 subjects were investigated. No significant differences were found between surgical and conservative management for current pain (p = 0.984), current function (p = 0.170), or abnormality on CT (p = 0.173). However, surgically treated patients more often remained tender over the “N spot” (p = 0.005), even after returning to competition for two years or more. Conclusions: Surgical fixation of navicular stress fractures appears to be as effective as conservative management over the longer term. However, there remains a small but measurable degree of pain and loss of function over this period. The value of using “N spot” tenderness as the sole clinical predictor of treatment success requires further investigation, as some patients remained tender despite successful completion of treatment and return to competition.

To use a randomised, double blind, placebo controlled trial to establish the effect on straight leg raise, hip internal rotation, and muscle pain of dry needling treatment to the gluteal muscles in athletes with posterior thigh pain referred from gluteal trigger points.A randomised, double blind, placebo controlled trial of 59 male runners was performed during the 2002 Australian Rules football season. Subjects were thoroughly screened and had magnetic resonance imaging of their hamstring muscles to exclude local pathology. The inclusion criterion was reproduction of recognisable posterior thigh pain with the application of digital pressure to the gluteal trigger points. Subjects randomly received either therapeutic or placebo needle treatment on one occasion at their gluteal trigger points. Range of motion and visual analogue scale data were collected immediately before, immediately after, 24 hours after, and 72 hours after the intervention. Range of motion was measured with passive straight leg raise and hip internal rotation. Visual analogue scales were completed for hamstring and gluteal pain and tightness at rest and during a running task.Magnetic resonance imaging scans revealed normal hamstring musculature in most subjects. Straight leg raise and hip internal rotation remained unchanged in both groups at all times. Visual analogue scale assessment of hamstring pain and tightness and gluteal tightness after running showed improvements immediately after the intervention in both groups (p = 0.001), which were maintained at 24 and 72 hours. The magnitude of this improvement was the same for therapeutic and placebo interventions. Resting muscle pain and tightness were unaffected.Neither dry needling nor placebo needling of the gluteal muscles resulted in any change in straight leg raise or hip internal rotation. Both interventions resulted in subjective improvement in activity related muscle pain and tightness. Despite being commonly used clinical tests in this situation, straight leg raise and hip internal rotation are not likely to help the therapist assess response to treatment. Patient reports of response to such treatment are better indicators of its success. The mechanisms by which these responses occur and the reasons for the success of the placebo needling treatment are areas for further investigation.

Objective: To describe the histological features of the fascial-periosteal interface at the medial tibial border of patients surgically treated for chronic deep posterior compartment syndrome and to make statistical comparisons with control tissue. Methods: Nineteen subjects and 11 controls were recruited. Subject tissue was obtained at operation, and control tissue from autopsy cases. Tissue samples underwent histological preparation and then examination by an independent pathologist. Samples were analysed with regard to six histological variables: fibroblastic activity, chronic inflammatory cells, vascularity, collagen regularity, mononuclear cells, and ground substance. Collagen regularity was measured with respect to collagen density, fibre arrangement, orientation, and spacing. The observed changes were graded from 1 to 4 in terms of abnormality. Mann-Whitney U test, Spearman correlation coefficients, and intraobserver reliability scores were used. Results: With regard to collagen arrangement, control tissue showed greater degrees of irregularity than subject tissue (p = 0.01). Subjects with a symptom duration of greater than 12 months (as opposed to less than 12 months) showed greater degrees of collagen irregularity (p = 0.043). Vascular changes approached significance (p = 0.077). With regard to the amount of fibrocyte activity, chronic inflammatory cell activity, mononuclear cells, or ground substance, there were no significant differences between controls and subjects. Good correlation was seen in scores measuring chronic inflammatory cell activity and mononuclear cells (r = 0.649), and moderate correlation was seen between fibrocyte activity and vascular changes (r = 0.574). Intraobserver reliability scores were good for chronic inflammatory cell activity and moderate for vascular changes, but were poor for collagen and fibrocyte variables. Individual cases showed varying degrees of fibrocyte activity, chronic inflammatory cellular infiltration, vascular abnormalities, and collagen fibre disruption. Conclusions: Statistical analysis showed no histological differences at the fascial-periosteal interface in cases of chronic deep posterior compartment syndrome, except for collagen, which showed less irregularity in subject samples. The latter may indicate a remodelling process, and this is supported by greater collagen irregularity in subjects with longer duration of symptoms.

It would seem that the development of a stress fracture results from unsuccessful adaptation of bone to a change in its mechanical environment caused by repetitive loading. It involves the physiological processes of microdamage production and remodelling. Whether the initiating factor is microdamage production or activation of remodelling through direct effects of strain is unclear. The remodelling process involves both the removal of bone which has become fatigue damaged or is extraneous to the requirements of the new loading environment, and the addition of new bone in an manner that is best suited to withstand the new mechanical strain. Normally this process is well modulated and does not cause symptoms. If the amount of bone removed is not sufficient to unduly weaken bone structure and the addition of new bone occurs sufficiently rapidly to correct any weakness before failure occurs or to repair microdamage, the process will successfully lead to a bone with appropriate material strength and geometry to withstand the new strain environment. However, if there is imbalance between bone removal and replacement, together with accumulation of microdamage, signs and symptoms of a stress fracture may result. Any factors which influence bone load, bone strength, or remodelling have the potential to result in a stress fracture. Attention should be paid to the identification of these factors in an attempt to prevent this overuse injury in athletes.

It is apparent that bone density in male athletes can be reduced without a concomitant decrease in testosterone, suggesting that bone density and testosterone concentrations in the normal range are not closely related in male athletes. Further research is necessary to monitor concurrent changes in bone density and testosterone over a period of time in exercising males. In any case, the effect of exercise on the male reproductive system does not appear as extreme as that which can occur in female athletes, and any impact on bone density is not nearly as evident. These results imply that factors apart from testosterone concentrations must be responsible for the observed osteopenia in some male athletes. Many factors have the potential to adversely affect bone density, independently of alterations in reproductive function. These include low calcium intake, energy deficit, weight loss, psychological stress, and low body fat, all of which may be associated with intense endurance training. Future research investigating skeletal health in male athletes should include a thorough assessment of reproductive function in addition to these other factors.

Let's start with a couple of quiz questions. Put your hands up if you have given the following pieces of advice to your patients/athletes. (1) Thirst is not a good indicator of hydration. You must drink lots of fluids before, during and after exercise. (2) The optimum diet for weight control, general health and athletic performance consists of low fat, high carbohydrate. Well, both my hands are up, and I suspect I am in good company among sports medicine professionals. For the past 30 years, these have been two of the basic tenets of sports nutrition. Recently, however, both these universally regarded ‘truths’ have been challenged. We now know that excessive intake of fluid during endurance events can lead to exercise-associated hyponatraemic encephalopathy (EAHE) or ‘water intoxication’.1 There have been a number of deaths reported from this syndrome. One of the researchers who has been prominent in researching this topic is Professor Tim Noakes from the University of Cape Town. In his recent book ‘Waterlogged’,2 Noakes explains how drinking too much water can lead to fluid retention and EAHE in those who also have the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Endurance athletes have been encouraged for the past three decades to not wait until they were thirsty, but to drink large amounts of water or sports drinks to prevent dehydration and heat illness. Noakes advises that excessive fluid overload is the major danger in endurance exercise, not …

I was excited when I saw this book as the five authors are all well known to me as prominent in their respective fields. Nicola Maffulli of Stoke on Trent via Aberdeen and Hong Kong is an orthopaedic surgeon with a special interest in children's injuries, Kai Ming Chan from Hong Kong is a widely published orthopaedic surgeon, Rose McDonald has been prominent in sports physiotherapy in the United Kingdom for many years, Bob Malina from Michigan State University is one of the foremost experts in children's growth, and Tony Parker has been a leading FIMS official for many years. Their stated aim is “to address in one volume the …