Total hip replacement for high dislocation of the hip joint remains technically difficult in terms of preparation of the true acetabulum and restoration of leg length. We describe our experience of cementless total hip replacement combined with a subtrochanteric femoral shortening osteotomy in 20 hips with Crowe grade IV dislocation with a mean follow-up of 8.1 years (4 to 11.5). There was one man and 17 women with a mean age of 55 years (44 to 69) at the time of the operation. After placement of the acetabular component at the site of the natural acetabulum, a cementless porous-coated cylindrical femoral component was implanted following a subtrochanteric femoral shortening osteotomy. The mean Japanese Orthopedic Association hip score improved from a mean of 38 (22 to 62) to a mean of 83 points (55 to 98) at the final follow-up. The mean lengthening of the leg was 14.8 mm (-9 to 34) in patients with iliofemoral osteoarthritis and 35.3 mm (15 to 51) in patients with no arthritic changes. No nerve palsy was observed. Total hip replacement combined with subtrochanteric shortening femoral osteotomy in this situation is beneficial in avoiding nerve injury and still permits valuable improvement in inequality of leg length.

Alcohol-induced osteonecrosis of the femoral head (ONFH) is observed in alcohol abusers and patients with alcoholic fatty liver disease. It has been reported that Toll-like receptor 4 (TLR4) signalling plays a crucial role in the pathogenesis of alcoholic fatty liver disease. We previously reported a corticosteroid-induced ONFH rat model, and suggested that TLR4 signalling contributes to the pathogenesis of ONFH. Thus, it is thought that the pathogenesis of alcohol-induced ONFH is probably similar to that of corticosteroid-induced ONFH. The aim of this study was to develop a new animal model for alcohol-induced ONFH and to evaluate the relationship between the pro-inflammatory response via TLRs and the development of ONFH in rats. Male Wistar rats were fed a Lieber–DeCarli liquid diet containing 5% ethanol (experimental group) or dextran (control group) for 1–24 weeks. Histopathological and biochemical analyses were performed. Feeding the ethanol-containing liquid diet resulted in the development of ONFH with hepatic steatosis, hepatic dysfunction and hyperlipidaemia, whereas feeding the dextran-containing diet did not cause ONFH. However, we could not recognize any relationship between the pro-inflammatory response via TLR4 and the development of alcohol-induced ONFH. Thus in this study we have developed a new rat model for alcohol-induced ONFH based on the feeding of an ethanol liquid diet. ONFH was observed within seven days from the start of feeding with 5% ethanol-containing liquid diet. Although this was linked to hepatic steatosis, a TLR4 association was not a feature of this model.

We evaluated triple-phase bone scintigraphy in the differential diagnosis of peri-prosthetic infection in 46 patients with a total hip replacement or bipolar hemiarthroplasty who were due for revision surgery. There were 18 men and 28 women, with a mean age at operation of 64.6 years (28 to 81). We defined peri-prosthetic infection as an increased uptake of radioisotope in all the phases of triple-phase bone scintigraphy and validated these results against the histological and/or microbiology results in every case.The positive and negative predictive values for the presence of infection were 83% and 93%, respectively. The diagnostic sensitivity was 88% and the specificity was 90%.This study indicates that triple-phase bone scintigraphy is a useful tool in the detection of peri-prosthetic infection and offers a cost-effective method of screening.

We previously reported that ethanol consumption affects morbidity and mortality after traumatic brain injury (TBI) by accelerating brain edema via oxidative stress after TBI. Aquaporin-4 (AQP4), a water channel, is involved in brain edema formation. In this study, we found that acute ethanol administration increased AQP4 expression after TBI, leading to severe brain edema in rats. Rats were pretreated with ethanol (3 g/kg) or dl-buthionine-(S,R)-sulfoximine (BSO; 100 mg/kg), an oxidative stressor, before TBI. Acetazolamide, an AQP4 inhibitor, was administered to ethanol-pretreated rats 3 or 12 hours after TBI. Brain edema was increased 24 hours after TBI in both the ethanol- and BSO-pretreated groups. Ethanol pretreatment induced lipid peroxidation 24 hours after TBI. Transcription factors, NF-κB and hypoxia-inducible factor-1α, were activated 3 and 24 hours after TBI in the BSO- and ethanol-pretreated groups, respectively. In the ethanol-pretreated group, AQP4 was accumulated, particularly in astrocyte end feet, 24 hours after TBI. Acetazolamide treatment improved the survival rate to 100% and decreased brain edema and AQP4 in ethanol-pretreated rats. These findings suggest that ethanol induces up-regulation of AQP4, leading to brain edema. The accumulation of AQP4 may play an important role in the augmentation of brain edema after TBI under ethanol consumption.

Denosumab is one of a number of anti-osteoporotic agents to have a definitive effect on the restoration of proximal periprosthetic bone loss, especially in zone 7, after cementless THA. Denosumab contributed to the restoration of decreased periprosthetic BMD to normal levels. As the decrease in BMD in the proximal femur after THA is considered to be apparent at 6-12 months after surgery, it is believed that prevention of the deterioration of bone quality is important in the proximal femur immediately after cementless THA for elderly female patients with osteoporosis.