As the population ages, the number of operations performed on bone is expected to increase. Diseases such as arthritis, tumours, and trauma can lead to defects in the skeleton requiring an operation to replace or restore the lost bone. Surgeons can use autografts, allografts, and/or bone graft substitutes to restore areas of bone loss. Surgical implants are also used in addition or in isolation to replace the diseased bone. This review considers the application of available bone grafts in different clinical settings. It also discusses recently introduced bioactive biomaterials and highlights the clinical difficulties and technological deficiencies that exist in our current surgical practice.

There is a pressing clinical need to develop cell-based bone therapies due to a lack of viable, autologous bone grafts and a growing demand for bone grafts in musculoskeletal surgery. Such therapies can be tissue engineered and cellular, such as osteoblasts, combined with a material scaffold. Because mesenchymal stem cells (MSCs) are both available and fast growing compared to mature osteoblasts, therapies that utilize these progenitor cells are particularly promising. We have developed a nanovibrational bioreactor that can convert MSCs into bone-forming osteoblasts in two- and three-dimensional, but the mechanisms involved in this osteoinduction process remain unclear. Here, to elucidate this mechanism, we use increasing vibrational amplitude, from 30 nm (N30) to 90 nm (N90) amplitudes at 1000 Hz and assess MSC metabolite, gene, and protein changes. These approaches reveal that dose-dependent changes occur in MSCs’ responses to increased vibrational amplitude, particularly in adhesion and mechanosensitive ion channel expression and that energetic metabolic pathways are activated, leading to low-level reactive oxygen species (ROS) production and to low-level inflammation as well as to ROS- and inflammation-balancing pathways. These events are analogous to those that occur in the natural bone-healing processes. We have also developed a tissue engineered MSC-laden scaffold designed using cells’ mechanical memory, driven by the stronger N90 stimulation. These mechanistic insights and cell-scaffold design are underpinned by a process that is free of inductive chemicals.

Infection rates after arthroplasty surgery are between 1-4 %, rising significantly after revision procedures. To reduce the associated costs of treating these infections, and the patients' post-operative discomfort and trauma, a new preventative method is required. High intensity narrow spectrum (HINS) 405 nm light has bactericidal effects on a wide range of medically important bacteria, and it reduced bacterial bioburden when used as an environmental disinfection method in a Medical Burns Unit. To prove its safety for use for environmental disinfection in orthopaedic theatres during surgery, cultured osteoblasts were exposed to HINS-light of intensities up to 15 mW/cm 2 for 1 h (54 J/ cm 2 ). Intensities of up to 5 mW/cm 2 for 1 h had no effect on cell morphology, activity of alkaline phosphatase, synthesis of collagen or osteocalcin expression, demonstrating that under these conditions this dose is the maximum safe exposure for osteoblasts; after exposure to 15 mW/cm 2 all parameters of osteoblast function were significantly decreased. Viability (measured by protein content and Crystal Violet staining) of the osteoblasts was not influenced by exposure to 5 mW/cm 2 for at least 2 h. IntroductionHealthcare associated infections (HAI), defined as infections which are not present at the time the patient enters hospital, are an ever increasing problem in modern healthcare affecting approximately 1 in 10 patients admitted to UK hospitals (Reilly et al., 2007). Despite current attempts to resolve the problem, including campaigns to improve hygiene in hospitals, particularly hand washing, HAI still causes significant patient mortality. A report published by the House of Commons in 2004 found that HAIs are responsible for over 5,000 deaths in the UK each year, and are a contributory factor in over 1,500 deaths (National Audit Office, 2004). In the USA, deaths associated with HAI in hospitals exceeded the number attributable to several of the top ten leading causes of death. A survey performed in 2002 found 1.7 million patients with an HAI, of which 155,668 died (Klevens et al., 2007). The rise in prevalence of HAI can partly be attributed to the increased use of antibiotics leading to antibiotic resistant strains of many bacteria (McGowan, 1983). It is clear that novel approaches to bacterial inactivation are required.HAI take many forms. The most common type of infection reported by the Scottish National HAI Prevalence Survey was found to be urinary tract infection (UTI), accounting for 17.9 % of cases (Reilly et al., 2008), with a major risk factor being the use of indwelling catheters. Surgical site infections (SSI) are the next most common, accounting for 16 %. The use of indwelling or implanted medical devices is increasing with technological advances, and so the incidence of device-related infection is increasing (von Eiff et al., 2005). Taking infection acquired during hip replacement surgery as a specific example of HAI, studies have shown incidence rates from 1-5 %, increasing considerably after revi...

The 'cement in cement' technique for revision hip arthroplasty has become popular in recent years, particularly in relation to polished taper stems. Since 2006 a short Exeter stem with 44 mm offset has been available specifically for this purpose. We report a fracture of such a stem in the absence of trauma 5 years after the revision procedure. The patient had a BMI of 27.8 and the proximal cement mantle gave good support to the stem. The fracture initiated and propagated from the introducer hole on the shoulder of the prosthesis. Macroscopically there was no defect in this area. This may be an unusual case of fatigue failure.

This study examined the expression of inducible nitric oxide synthase (iNOS) and transforming growth factor-beta (TGF-beta) in macrophage infiltrates within crush-injured digital flexor tendon and synovium of control rats and rats treated with N(G)-nitro-1-arginine methyl ester (L-NAME) (5 mg/kg). Release of TGF-beta from organ cultures of tendon, muscle, and synovium, and the effects of L-NAME treatment (in vitro and in vivo), on adhesion of peritoneal macrophages to epitenon monolayers were also investigated. The results showed that during normal tendon healing the levels of TGF-beta are high at first and gradually decrease after 3 weeks of injury to slightly above control uninjured levels. However, when L-NAME was administered at the time of injury, the macrophage infiltrates were expressing high levels of TGF-beta even at 5 weeks after the injury, with no evidence of reduction. In the standard injury, iNOS activity was greatest at the acute phase of the inflammatory response and then gradually returned to normal. Treatment with L-NAME, however, resulted in inhibition of iNOS activity at 3 days and a reduction in the activity at the later time points examined after injury. We also found greatly increased levels of adhesion of peritoneal macrophages from L-NAME-treated rats to epitenon monolayers in vitro, which reflect a chronic imbalance in expression of TGF-beta, which is overexpressed, and nitric oxide, which is underexpressed. The results of the current study show that formation of nitric oxide is an important event in the course of tendon healing since its inhibition results in chronic inflammation and fibrosis due to an imbalance in TGF-beta expression in vivo.