Construction of a functional skeleton is accomplished through co-ordination of the developmental processes of chondrogenesis, osteogenesis, and synovial joint formation. Infants whose movement in utero is reduced or restricted and who subsequently suffer from joint dysplasia (including joint contractures) and thin hypo-mineralised bones, demonstrate that embryonic movement is crucial for appropriate skeletogenesis. This has been confirmed in mouse, chick, and zebrafish animal models, where reduced or eliminated movement consistently yields similar malformations and which provide the possibility of experimentation to uncover the precise disturbances and the mechanisms by which movement impacts molecular regulation. Molecular genetic studies have shown the important roles played by cell communication signalling pathways, namely Wnt, Hedgehog, and transforming growth factor-beta/bone morphogenetic protein. These pathways regulate cell behaviours such as proliferation and differentiation to control maturation of the skeletal elements, and are affected when movement is altered. Cell contacts to the extra-cellular matrix as well as the cytoskeleton offer a means of mechanotransduction which could integrate mechanical cues with genetic regulation. Indeed, expression of cytoskeletal genes has been shown to be affected by immobilisation. In addition to furthering our understanding of a fundamental aspect of cell control and differentiation during development, research in this area is applicable to the engineering of stable skeletal tissues from stem cells, which relies on an understanding of developmental mechanisms including genetic and physical criteria. A deeper understanding of how movement affects skeletogenesis therefore has broader implications for regenerative therapeutics for injury or disease, as well as for optimisation of physical therapy regimes for individuals affected by skeletal abnormalities. Cite this article: Bone Joint Res 2015;4:105–116

In May 2012, in airports across the globe, seven orthopaedic surgeons bravely said goodbye to their loved ones, and slowly turned towards their respective aircraft. Filled with expectation and mild trepidation they stepped into the unknown… the ABC fellowship of 2012.

Drug therapy forms an integral part of the management of many orthopaedic conditions. However, many medicines can produce serious adverse reactions if prescribed inappropriately, either alone or in combination with other drugs. Often these hazards are not appreciated. In response to this, the European Union recently issued legislation regarding safety measures which member states must adopt to minimise the risk of errors of medication.

In March 2014 the Medicines and Healthcare products Regulatory Agency and NHS England released a Patient Safety Alert initiative focussed on errors of medication. There have been similar initiatives in the United States under the auspices of The National Coordinating Council for Medication Error and The Joint Commission on the Accreditation of Healthcare Organizations. These initiatives have highlighted the importance of informing and educating clinicians.

Here, we discuss common drug interactions and contra-indications in orthopaedic practice. This is germane to safe and effective clinical care.

Cite this article: Bone Joint J 2015;97-B:434–41.

Severe acute respiratory syndrome (SARS) is a newly described infectious disease caused by the SARS coronavirus which attacks the immune system and pulmonary epithelium. It is treated with regular high doses of corticosteroids. Our aim was to determine the relationship between the dosage of steroids and the number and distribution of osteonecrotic lesions in patients treated with steroids during the SARS epidemic in Beijing, China in 2003.

We identified 114 patients for inclusion in the study. Of these, 43 with osteonecrosis received a significantly higher cumulative and peak methylprednisolone-equivalent dose than 71 patients with no osteonecrosis identified by MRI. We confirmed that the number of osteonecrotic lesions was directly related to the dosage of steroids and that a very high dose, a peak dose of more than 200 mg or a cumulative methylprednisolone-equivalent dose of more than 4000 mg, is a significant risk factor for multifocal osteonecrosis with both epiphyseal and diaphyseal lesions. Patients with diaphyseal osteonecrosis received a significantly higher cumulative methylprednisolone-equivalent dose than those with epiphyseal osteonecrosis. Multifocal osteonecrosis should be suspected if a patient is diagnosed with osteonecrosis in the shaft of a long bone.