Aims. The aim of this systematic review and meta-analysis was to gather epidemiological information on selected musculoskeletal injuries and to provide pooled injury-specific incidence rates. Methods. PubMed (National Library of Medicine) and Scopus (Elsevier) databases were searched. Articles were eligible for inclusion if they reported incidence rate (or count with population at risk), contained data on adult population, and were written in English language. The number of cases and population at risk were collected, and the pooled incidence rates (per 100,000 person-years) with 95% confidence intervals (CIs) were calculated by using either a fixed or random effects model. Results. The screening of titles yielded 206 articles eligible for inclusion in the study. Of these, 173 (84%) articles provided sufficient information to be included in the pooled incidence rates. Incidences of fractures were investigated in 154 studies, and the most common fractures in the whole adult population based on the pooled incidence rates were distal radius fractures (212.0, 95% CI 178.1 to 252.4 per 100,000 person-years), finger fractures (117.1, 95% CI 105.3 to 130.2 per 100,000 person-years), and hip fractures (112.9, 95% CI 82.2 to 154.9 per 100,000 person-years). The most common sprains and dislocations were ankle sprains (429.4, 95% CI 243.0 to 759.0 per 100,000 person-years) and first-time patellar dislocations (32.8, 95% CI 21.6 to 49.7 per 100,000 person-years). The most common injuries were anterior cruciate ligament (17.5, 95% CI 6.0 to 50.2 per 100,000 person-years) and Achilles (13.7, 95% CI 9.6 to 19.5 per 100,000 person-years) ruptures. Conclusion. The presented pooled incidence estimates serve as important references in assessing the global economic and social burden of musculoskeletal injuries. Cite this article: Bone Joint Res 2022;11(11):814–825

Post-natal vasculogenesis, the process by which vascular committed bone marrow stem cells or endothelial precursor cells migrate, differentiate and incorporate into the nacent endothelium and thereby contribute to physiological and pathological neurovascularisation, has stimulated much interest. Its contribution to neovascularisation of tumours, wound healing and revascularisation associated with ischaemia of skeletal and cardiac muscles is well established. We evaluated the responses of endothelial precursor cells in bone marrow to musculoskeletal trauma in mice. Bone marrow from six C57 Black 6 mice subjected to a standardised, closed fracture of the femur, was analysed for the combined expression of cell-surface markers stem cell antigen 1 (sca-1. +. ) and stem cell factor receptor, CD117 (c-kit. +. ) in order to identify the endothelial precursor cell population. Immunomagnetically-enriched sca-1. +. mononuclear cell (MNC. sca-1+. ) populations were then cultured and examined for functional vascular endothelial differentiation. Bone marrow MNC. sca-1+,c-kit+. counts increased almost twofold within 48 hours of the event, compared with baseline levels, before decreasing by 72 hours. Sca-1. +. mononuclear cell populations in culture from samples of bone marrow at 48 hours bound together Ulex Europus-1, and incorporated fluorescent 1,1′-dioctadecyl- 3,3,3,’3′-tetramethylindocarbocyanine perchlorate-labelled acetylated low-density lipoprotein intracellularily, both characteristics of mature endothelium. Our findings suggest that a systemic provascular response of bone marrow is initiated by musculoskeletal trauma. Its therapeutic manipulation may have implications for the potential enhancement of neovascularisation and the healing of fractures

There is a disparity in sport-related injuries between sexes, with females sustaining non-contact musculoskeletal injuries at a higher rate. Anterior cruciate ligament ruptures are between two and eight times more common than in males, and females also have a higher incidence of ankle sprains, patellofemoral pain, and bone stress injuries. The sequelae of such injuries can be devastating to an athlete, resulting in time out of sport, surgery, and the early onset of osteoarthritis. It is important to identify the causes of this disparity and introduce prevention programmes to reduce the incidence of these injuries. A natural difference reflects the effect of reproductive hormones in females, which have receptors in certain musculoskeletal tissues. Relaxin increases ligamentous laxity. Oestrogen decreases the synthesis of collagen and progesterone does the opposite. Insufficient diet and intensive training can lead to menstrual irregularities, which are common in female athletes and result in injury, whereas oral contraception may have a protective effect against certain injuries. It is important for coaches, physiotherapists, nutritionists, doctors, and athletes to be aware of these issues and to implement preventive measures. This annotation explores the relationship between the menstrual cycle and orthopaedic sports injuries in pre-menopausal females, and proposes recommendations to mitigate the risk of sustaining these injuries. Cite this article: Bone Joint J 2023;105-B(7):723–728

Introduction. Pain is an expected and appropriate experience following traumatic musculoskeletal injury. By contrast, chronic pain and disability are unhelpful yet common sequelae of trauma-related injuries. Presently, the mechanisms that underlie the transition from acute to chronic disabling post-traumatic pain are not fully understood. The aim of this study is to identify prognostic factors for risk of developing chronic pain and disability following acute musculoskeletal trauma. Methods. A prospective observational study will recruit two temporally staggered cohorts (n=250 each cohort; 10 cases per candidate predictor) of consecutive acute musculoskeletal trauma patients aged ≥16 years, who are emergency admissions into a Major Trauma Centre in the United Kingdom, with an episode inception defined as the traumatic event. The first cohort will identify prognostic factors to develop a screening tool to predict development of chronic and disabling pain, and the second will allow evaluation of the predictive performance of the tool (validation). The outcome being predicted is an individual's absolute risk of poor outcome measured at 6-months follow-up using the Chronic Pain Grade Scale (poor outcome ≥Grade II). Candidate predictors encompass the four primary mechanisms of pain: nociceptive (e.g. injury characteristics), neuropathic (e.g. painDETECT), inflammatory (biomarkers), and central hypersensitivity (e.g. quantitative sensory testing). Concurrently, patient-reported outcome measures will assess general health and psychosocial factors. Risk of poor outcome will be calculated using multiple variable regression analysis. Conclusion. A prognostic screening tool for post-trauma pain will inform precision rehabilitation, targeting interventions to individual patients to improve clinical and cost effectiveness. Conflicts of interest: None. Sources of funding: NIHR Surgical Reconstruction and Microbiology Research Centre

Background: Circulating endothelial precursor cells (CEPS) are thought to play a role in postnatal angiogenesis. We investigated the angiogenic stress of musculoskeletal trauma on CEP kinetics in trauma patients and their bone marrow progenitor populations in a murine model. Methods: Peripheral blood mononuclear cells (PB-MNCs) were isolated from patients (n=12) on consecutive days following closed lower-limb diaphyseal fractures. CEP levels, defined by the surface expression patterns of VEGFR2, CD34 and AC133 were determined and cytokine analysis of collected serum was performed. Bone marrow precursors defined by Ly-6A/E and c-Kit expression were harvested following traumatic insult from the murine model and quantified on flow cytometry. Human and murine progenitor populations were cultured on fibronectin and examined for markers of endothelial cell linage (Ulexeuropaeus- agglutinin- 1 binding and acetylated-LDL uptake) and cell morphology. Statistical analysis was performed using variance analysis. Results: A consistent increase in human CEPs levels was noted within 72 hours of the initial insult, the percentage increase over day 1 reaching 300%. Conclusion: We propose that musculoskeletal trauma through the release of chemokines such as VEGF, promotes rapid mobilisation of CEP from born marrow, which have the potential to contribute to reparative neovascularisation. Strategies to enhance CEPs kinetics may accelerate this process and offer a therapeutic role in aberrant fracture healing

Aims: Circulating endothelial precursor cells (CEPs) are thought to play a role in angiogenesis. We investigated the angiogenic stress of musculoskeletal trauma on CEP kinetics in trauma patients and their bone marrow progenitor populations in a murine model. Methods: Peripheral blood mononuclear cells (PB-MNCs) were isolated from patients (n=12) on consecutive days following closed lower-limb diaphyseal fractures. CEP levels, deþned by the surface expression patterns of VEGFR2, CD34 and AC133 were determined and cytokine analysis of collected serum was performed. Bonemarrow precursors deþned byLy-6A/E and c-Kit expression were harvested following the traumatic insult from the murine model and quantiþed on ßow cytometry. Human and murine progenitor populations were cultured on þbronectin and examined for markers of endothelial cell lineage (Ulexeuropaeus- agglutinin-1 binding and acetylated-LDL uptake) and cell morphology. Statistical analysis was performed using variance analysis. Results: A consistent increase in human CEPs levels was noted within 72 hours of the initial insult, the percentage increase over day 1 reaching 300% (p=0.008) and returning to normal levels by day 10. Murine bone marrow precursors were mobilisd within 24 hrs peaking at 48hrs (900% p=0.035). On culture, morphologically characteristic endotheliallike cells binding UEA-1 and incorporating LDL were identiþed. Serum VEGF levels increased signiþcantly within 24 hrs of the insult, (p=0.018) preceeding the peak in CEP mobilisation. Conclusion: We propose that musculoskeletal trauma through the release of chemokines such as VEGF, promotes rapid mobilisation of CEPs from born marrow, which have the potential to contribute to reparative neovascularisation. Strategies to enhance CEPs kinetics may accelerate this process and offer a therapeutic role in aberrant fracture healing

Myostatin (GDF-8) is known to play an important role in muscle regeneration, and myostatin is also expressed during the early phases of fracture healing. In this study we used fluorescent immunohistochemistry to define the temporal and spatial localization of myostatin during muscle and bone repair following deep penetrant injury in a mouse model. We then used hydrogel delivery of exogenous myostatin in the same injury model to determine the effects of myostatin exposure on muscle and bone healing. Results show that while myostatin was constitutively expressed in the cytoplasm of intact skeletal muscle fibers, a pool of intense myostatin staining was observed amongst injured skeletal muscle fibers 12-24 hours post-surgery. Myostatin was also expressed in the soft callus chondrocytes 4 days following osteotomy. Hydrogel delivery of 10 or 100 ug/ml recombinant myostatin decreased fracture callus cartilage area relative to total callus area in a dose-dependent manner by 41% and 80% (p<0.05), respectively, compared to vehicle treatment. Myostatin treatment also dose-dependently decreased fracture callus total bone volume by 23% and 47% (p<0.05), with the higher dose of recombinant myostatin yielding the greatest decrease in callus bone volume. Finally, exogenous myostatin treatment caused a significant, dose-dependent increase in fibrous tissue formation in skeletal muscle. Together, these findings suggest that myostatin may inhibit bone repair after traumatic musculoskeletal injury through both autocrine (soft-callus chondrocytes) and paracrine (surrounding injured muscle fibers) mechanisms. Thus, early pharmacological inhibition of myostatin is likely to improve the regenerative potential of both muscle and bone following deep penetrant musculoskeletal injury

Acute respiratory distress syndrome is a long established complication and continuing cause of significant morbidity and mortality in the multiply injured patient. Systemic inflammatory response syndrome (SIRS) is classically associated with acute pulmonary dysfunction. A variety of insults including trauma, sepsis, hypoxia, ischaemia reperfusion, can trigger systemic inflammatory response and acute lung injury. In models of sepsis, endotoxaemia and ischaemia-reperfusion, acute lung injury is characterised by widespread endothelial-neutrophil interaction and neutrophil activation. Another associated finding in these models of injury, is evidence of induced diaphragm muscle dysfunction, by electrophysiological testing of muscle strips post injury. An established model of incremental increasing skeletal trauma was employed. Adult male sprague dawley rats (mean weight 476grams, 370–520g) were randomised to control, single hindlimb fracture, bilateral hindlimb fracture and bilateral hind limb fracture + 20% haemorrhage. Indices of acute lung injury studied 2 hours post injury were bronchalveolar lavage, cell counts, and protein assays. Pulmonary tissue myeloperoxidase activity was assayed as an indicator of neutrophil activation and pulmonary wet/dry weights were measured as a marker of pulmonary oedema. Diaphragmatic electrophysiological testing was also performed 2 hours post injury. Freshly harvested diaphragmatic muscle strips had peak evoked muscle twitches measured, the maximal tetanic twitch and muscle strip fatigue times were also assessed. Statistical analysis was performed by means of analysis of variance (ANOVA). Results: The cohort of animals with the greatest injury severity manifested evidence of acute lung injury when compared with controls, this was associated with evidence of interstitial leucosequestration. This data suggests that neutrophils are involved in mediating an acute lung injury following musculoskeletal trauma

Background

Serious traumatic injury is a leading cause of death and disability globally, with the majority of survivors developing chronic pain.

Interest in football continues to increase, with ever younger age groups participating at a competitive level. Football academies have sprung up under the umbrella of professional clubs in an attempt to nurture and develop such talent in a safe manner. However, increased participation predisposes the immature skeleton to injury. Over a five-year period we have prospectively collected data concerning all injuries presenting to the medical team at Newcastle United football academy. We identified 685 injuries in our cohort of 210 players with a mean age of 13.5 years (9 to 18). The majority of injuries (542;79%) were to the lower limb. A total of 20 surgical procedures were performed. Contact injuries accounted for 31% (210) of all injuries and non-contact for 69% (475).The peaks of injury occurred in early September and March. The 15- and 16-year-old age group appeared most at risk, independent of hours of participation. Strategies to minimise injury may be applicable in both the academy setting and the wider general community.

Aims

As an increasing number of female surgeons are choosing orthopaedics, it is important to recognize the impact of pregnancy within this cohort. The aim of this review was to examine common themes and data surrounding pregnancy, parenthood, and fertility within orthopaedics.

The subject of noise in the operating theatre was recognized as early as 1972 and has been compared to noise levels on a busy highway. While noise-induced hearing loss in orthopaedic surgery specifically has been recognized as early as the 1990s, it remains poorly studied. As a result, there has been renewed focus in this occupational hazard. Noise level is typically measured in decibels (dB), whereas noise adjusted for human perception uses A-weighted sound levels and is expressed in dBA. Mean operating theatre noise levels range between 51 and 75 dBA, with peak levels between 80 and 119 dBA. The greatest sources of noise emanate from powered surgical instruments, which can exceed levels as high as 140 dBA. Newer technology, such as robotic-assisted systems, contribute a potential new source of noise. This article is a narrative review of the deleterious effects of prolonged noise exposure, including noise-induced hearing loss in the operating theatre team and the patient, intraoperative miscommunication, and increased cognitive load and stress, all of which impact the surgical team’s overall performance. Interventions to mitigate the effects of noise exposure include the use of quieter surgical equipment, the implementation of sound-absorbing personal protective equipment, or changes in communication protocols. Future research endeavours should use advanced research methods and embrace technological innovations to proactively mitigate the effects of operating theatre noise.

Cite this article: Bone Joint J 2024;106-B(10):1039–1043.