A recent study to identify clinically meaningful benchmarks for gait improvement after total hip replacement (THA) has shown that the minimum clinically important improvement (MCII) in gait speed after THA is 0.32 m/sec. Currently, it remains to be investigated what preoperative factors link to suboptimal recovery of gait function after THA. This study aimed to identify preoperative lower-limb muscle predictors for gait speed improvement after THA for hip osteoarthritis. This study enrolled 58 patients who underwent unilateral primary THA. Gait speed improvement was evaluated as the subtraction of preoperative speed from postoperative speed at 6 months after THA. Preoperative muscle composition of the glutei medius and minimus (Gmed+min) and the gluteus maximus (Gmax) was evaluated on a single axial computed tomography slice at the bottom end of the sacroiliac joint. Cross-sectional area ratio of individual composition to the total muscle was calculated.Introduction
Method
The interleukin-6/gp130-associated Janus Kinases/STAT3 axis is known to play an important role in mediating inflammatory signals, resulting in production of matrix metalloproteinase-3 (MMP-3). The hip joints with rapidly destructive coxopathy (RDC) demonstrate rapid chondrolysis, probably by increased production of MMP-3 observed in the early stage of RDC. In the recent study, no apparent activation of STAT3 has been shown in the synovial tissues obtained from the osteoarthritic joint at operation. However, no data are currently available on STAT3 activation in the synovial tissues in the early stage of RDC. This study aimed to elucidate STAT3 activation in the synovial tissues in the early stage of RDC. Synovial tissues within 7 months from the disease onset were obtained from four RDC patients with femoral head destruction and high serum levels of MMP-3. RDC synovial tissues showed the synovial lining hyperplasia with an increase of CD68-positive macrophages and CD3-positive T lymphocytes. STAT3 phosphorylation was found in the synovial tissues by immunohistochemistry using anti-phospho-STAT3 antibody. The majority of phospho-STAT3-positive cells were the synovial lining cells and exhibited negative expression of macrophage or T cell marker. Treatment with tofacitinib, a Janus Kinase inhibitor, resulted in a decrease in phospho-STAT3-positive cells, especially with high intensity, indicating effective suppression of STAT3 activation in RDC synovial tissues. Inhibitory effect of tofacitinib could act through the Janus Kinase/STAT3 axis in the synovial tissues in the early stage of RDC. Therefore, STAT3 may be a potential therapeutic target for prevention of joint structural damage in RDC.
This study aimed to evaluate sagittal spinopelvic alignment (SSPA) in the early stage of rapidly destructive coxopathy (RDC) compared with hip osteoarthritis (HOA), and to identify risk factors of SSPA for destruction of the femoral head within 12 months after the disease onset. This study enrolled 34 RDC patients with joint space narrowing > 2 mm within 12 months after the onset of hip pain and 25 HOA patients showing femoral head destruction. Sharp angle was measured for acetabular coverage evaluation. Femoral head collapse ratio was calculated for assessment of the extent of femoral head collapse by RDC. The following parameters of SSPA were evaluated using the whole spinopelvic radiograph: pelvic tilt (PT), sacral slope (SS), pelvic incidence (PI), sagittal vertical axis (SVA), thoracic kyphosis angle (TK), lumbar lordosis angle (LL), and PI-LL.Aims
Methods
Using in situ hybridisation and the terminal deoxynucleotidyl transferase-mediated biotin-dUTP nick end-labelling (TUNEL) reaction in rats with osteonecrosis of the femoral head we have studied the effect of ischaemia on the gene expression of the stress proteins oxygen-regulated protein 150 (ORP150) and haemoxygenase 1 (HO1) and the death mechanism of the cells involved in osteonecrosis. Both ORP150 and HO1 have been reported to have important roles in the successful adaptation to oxygen deprivation. ORP150 and HO1 mRNA expression was induced by ischaemia in osteoblasts and osteocytes. In proliferative chondrocytes, these signals were detected constitutively. During the development of ischaemic osteonecrosis, the mechanism of cell death was apoptosis as indicated by DNA fragmentation and the presence of apoptotic bodies in osteocytes, chondrocytes and bone-marrow cells. After the initial ischaemic event, expression of ORP150 and HO1 mRNA, the TUNEL-positive reaction and empty lacunae were found sequentially. These findings were exclusive and may be considered to be markers for each stage in the development of osteonecrosis.
