Biochemical markers of bone-turnover have long been used to complement the radiological assessment of patients with metabolic bone disease. Their implementation in daily clinical practice has been helpful in the understanding of the pathogenesis of osteoporosis, the selection of the optimal dose and the understanding of the progression of the onset and resolution of treatment. Since they are derived from both cortical and trabecular bone, they reflect the metabolic activity of the entire skeleton rather than that of individual cells or the process of mineralisation.

Quantitative changes in skeletal-turnover can be assessed easily and non-invasively by the measurement of bone-turnover markers. They are commonly subdivided into three categories; 1) bone-resorption markers, 2) osteoclast regulatory proteins and 3) bone-formation markers. Because of the rapidly accumulating new knowledge of bone matrix biochemistry, attempts have been made to use them in the interpretation and characterisation of various stages of the healing of fractures. Early knowledge of the individual progress of a fracture could help to avoid delayed or nonunion by enabling modification of the host’s biological response.

The levels of bone-turnover markers vary throughout the course of fracture repair with their rates of change being dependent on the size of the fracture and the time that it will take to heal. However, their short-term biological variability, the relatively low bone specificity exerted, given that the production and destruction of collagen is not limited to bone, as well as the influence of the host’s metabolism on their concentration, produce considerable intra- and inter-individual variability in their interpretation. Despite this, the possible role of bone-turnover markers in the assessment of progression to union, the risks of delayed or nonunion and the impact of innovations to accelerate fracture healing must not be ignored.

Non-accidental injury (NAI) in children includes orthopaedic trauma throughout the skeleton. Fractures with soft-tissue injuries constitute the majority of manifestations of physical abuse in children. Fracture and injury patterns vary with age and development, and NAI is intrinsically related to the mobility of the child. No fracture in isolation is pathognomonic of NAI, but specific abuse-related injuries include multiple fractures, particularly at various stages of healing, metaphyseal corner and bucket-handle fractures and fractures of ribs. Isolated or multiple rib fractures, irrespective of location, have the highest specificity for NAI. Other fractures with a high specificity for abuse include those of the scapula, lateral end of the clavicle, vertebrae and complex skull fractures.

Injuries caused by NAI constitute a relatively small proportion of childhood fractures. They may be associated with significant physical and psychological morbidity, with wide- ranging effects from deviations in normal developmental progression to death.

Orthopaedic surgeons must systematically assess, recognise and act on the indicators for NAI in conjunction with the paediatric multidisciplinary team.

This paper reviews the current literature concerning the main clinical factors which can impair the healing of fractures and makes recommendations on avoiding or minimising these in order to optimise the outcome for patients. The clinical implications are described.

The survivorship of contemporary resurfacing arthroplasty of the hip using metal-on-metal bearings is better than that of first generation designs, but short-term failures still occur. The most common reasons for failure are fracture of the femoral neck, loosening of the component, osteonecrosis of the femoral head, reaction to metal debris and malpositioning of the component. In 2008 the Australian National Joint Registry reported an inverse relationship between the size of the head component and the risk of revision in resurfacing hip arthroplasty. Hips with a femoral component size of ≤ 44 mm have a fivefold increased risk of revision than those with femoral components of ≥ 55 mm irrespective of gender. We have reviewed the literature to explore this observation and to identify possible reasons including the design of the implant, loading of the femoral neck, the orientation of the component, the production of wear debris and the effects of metal ions, penetration of cement and vascularity of the femoral head. Our conclusion is that although multifactorial, the most important contributors to failure in resurfacing arthroplasty of the hip are likely to be the design and geometry of the component and the orientation of the acetabular component.