Introduction Osteoarthritis (OA) is one of the most common forms of arthritis. There is accumulating evidence to suggest that OA is an inflammatory disease of the entire synovial joint and has multiple phenotypes. This presents the OA research community with new challenges and opportunities. The main challenge is to understand the root cause of the disease and identify differences and similarities between OA phenotypes. The key opportunity is the possibility of developing personalized and individualized prevention and treatment strategies for OA patients that havewith different forms phenotypes of the disease. Indeed, it has been suggested that this is the era of 'personalized prevention' for OA. The aim of this mini-review paper is to focus on the pathophysiological aspects of OA development and progression, review the current concepts and discuss the future of personalized medicine for OA.

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Osteoarthritis (OA) represents a final and common pathway for all major traumatic insults to synovial joints. OA is the most common form of degenerative joint disease and a major cause of pain and disability. Despite the global increase in the incidence of OA, there are no effective pharmacotherapies capable of restoring the original structure and function of damaged articular cartilage. Consequently cell-based and biological therapies for osteoarthritis (OA) and related orthopaedic disorders have become thriving areas of research and development. Autologous chondrocyte implantation (ACI) has been used for treatment of osteoarticular lesions for over two decades. Although chondrocyte-based therapy has the capacity to slow down the progression of OA and delay partial or total joint replacement surgery, currently used procedures are associated with the risk of serious adverse events. Complications of ACI include hypertrophy, disturbed fusion, delamination, and graft failure. Therefore there is significant interest in improving the success rate of ACI by improving surgical techniques and preserving the phenotype of the primary chondrocytes used in the procedure. Future tissue-engineering approaches for cartilage repair will also benefit from advances in chondrocyte-based repair strategies. This review article focuses on the structure and function of articular cartilage and the pathogenesis of OA in the context of the rising global burden of musculoskeletal disease. We explore the challenges associated with cartilage repair and regeneration using cell-based therapies that use chondrocytes and mesenchymal stem cells (MSCs). This paper also explores common misconceptions associated with cell-based therapy and highlights a few areas for future investigation.

The definitions and methodology proposed for recording injuries and illnesses sustained during tennis activities will lead to more consistent and comparable data being collected. The surveillance procedures presented here may also be applicable to other racket sports.

For some subjects, the maintenance of similar peak impact forces for different running surfaces was explained by observed kinematic adjustments. For example, when running on the surface providing the least impact absorption, an increased initial knee flexion was observed for some subjects, suggesting an increased lower extremity compliance. However, for some subjects, sagittal plane kinematic data were not sufficient for the explanation of peak impact force results. It appears that the mechanism of adaptation varies among runners, highlighting the requirement of individual subject analyses.

ObjectivesTo determine the prevalence of knee pain, radiographic knee osteoarthritis (RKOA), total knee replacement (TKR) and associated risk factors in male ex-professional footballers compared with men in the general population (comparison group).Methods1207 male ex-footballers and 4085 men in the general population in the UK were assessed by postal questionnaire. Current knee pain was defined as pain in or around the knees on most days of the previous month. Presence and severity of RKOA were assessed on standardised radiographs using the Nottingham Line Drawing Atlas (NLDA) in a subsample of 470 ex-footballers and 491 men in the comparison group. The adjusted risk ratio (aRR) and adjusted risk difference (aRD) with 95% CI in ex-footballers compared with the general population were calculated using the marginal model in Stata.ResultsEx-footballers were more likely than the comparison group to have current knee pain (aRR 1.91, 95% CI 1.77 to 2.06), RKOA (aRR 2.21, 95% CI 1.92 to 2.54) and TKR (aRR 3.61, 95% CI 2.90 to 4.50). Ex-footballers were also more likely to present with chondrocalcinosis (aRR 3.41, 95% CI 2.44 to 4.77). Prevalence of knee pain and RKOA were higher in ex-footballers at all ages. However, even after adjustment for significant knee injury and other risk factors, there was more than a doubling of risk of these outcomes in footballers.ConclusionsThe prevalence of all knee osteoarthritis outcomes (knee pain, RKOA and TKR) were two to three times higher in male ex-footballers compared with men in the general population group. Knee injury is the main attributable risk factor. Even after adjustment for recognised risk factors, knee osteoarthritis appear to be an occupational hazard of professional football.

Chest pain in the athlete has a wide differential diagnosis. Pain may originate from structures within the thorax, such as the heart, lungs or oesophagus. However, musculoskeletal causes of chest pain must be considered. The aim of this review is to help the clinician to diagnose chest wall pain in athletes by identifying the possible causes, as reported in the literature. Musculoskeletal problems of the chest wall can occur in the ribs, sternum, articulations or myofascial structures. The cause is usually evident in the case of direct trauma. Additionally, athletes' bodies may be subjected to sudden large indirect forces or overuse, and stress fractures of the ribs caused by sporting activity have been extensively reported. These have been associated with golf, rowing and baseball pitching in particular. Stress fractures of the sternum reported in wrestlers cause pain and tenderness of the sternum, as expected. Diagnosis is by bone scan and limitation of activity usually allows healing to occur. The slipping rib syndrome causes intermittent costal margin pain related to posture or movement, and may be diagnosed by the 'hooking manoeuvre', which reproduces pain and sometimes a click. If reassurance and postural advice fail, good results are possible with resection of the mobile rib. The painful xiphoid syndrome is a rare condition that causes pain and tenderness of the xiphoid and is self-limiting. Costochondritis is a self-limiting condition of unknown aetiology that typically presents with pain around the second to fifth costochondral joints. It can be differentiated from Tietze's syndrome in which there is swelling and pain of the articulation. Both conditions eventually settle spontaneously although a corticosteroid injection may be useful in particularly troublesome cases. The intercostal muscles may be injured causing tenderness between the ribs. Other conditions that should be considered include epidemic myalgia, precordial catch syndrome and referred pain from the thoracic spine.

The purpose of this study was to investigate the use of magnetic resonance (MR) imaging and image processing software to determine the functional cross-sectional area (FCSA) (the area of muscle isolated from fat) of the lumbar paraspinal muscles. The measurement of the morphology of the lumbar paraspinal muscles has become the focus of several recent investigations into the aetiology of low back pain. However, the reliability and validity of determining the FCSA of the lumbar paraspinal muscles using MR imaging are yet to be reported. T2 axial MR scans at the L1-S1 spinal levels of six subjects were obtained using identical MR systems and scanning parameters. Lean paraspinal muscle, vertebral body bone and intermuscular fat were manually segmented using image analysis software to assign a grey scale range to the MR signal intensity emitted by each tissue type. The resultant grey scale range for muscle was used to determine FCSA measurements for each of the paraspinal muscles, psoas, quadratus lumborum, erector spinae and lumbar multifidus on each scan slice. As various biological, instrument and measurement factors can affect MR signal intensity, a sensitivity analysis was conducted to determine the error associated in calculating FCSA for paraspinal muscle using a discrete grey scale range. Cross-sectional area and FCSA measurements were repeated three times and reliability indices for the FCSA measurements were obtained, showing excellent reliability, intra class correlation coefficient (mean=0.97, range 0.90-0.99) and %SEM (mean=2.6%, range 0.7-4.8%). In addition, the error associated with miscalculation of the grey scale range for the MR signal intensity of muscle was calculated and found to be low with an error of 20 grey scale units at the upper end of the muscle's grey scale range resulting in a very small error in the measured muscle FCSA. The method presented in this paper has a variety of practical applications in areas such as evidence-based rehabilitation, biomechanical modelling and the determination of segmental inertial parameters.