In this retrospective study we have assessed the results of low tibial valgus osteotomy for varus-type osteoarthritis of the ankle and its indications. We performed an opening wedge osteotomy in 25 women (26 ankles). The mean follow-up was for eight years and three months (2 years 3 months to 17 years 11 months). Of the 26 ankles, 19 showed excellent or good clinical results. Their mean scores for pain, walking, and activities of daily living were significantly improved but there was no change in the range of movement. In the ankles which were classified radiologically as stage 2 according to our own grading system, with narrowing of the medial joint space, and in 11 as stage 3a, with obliteration of the joint space at the medial malleolus only, the joint space recovered. In contrast, such recovery was seen in only two of 12 ankles classified as stage 3b, with obliteration of the joint space advancing to the upper surface of the dome of the talus. Low tibial osteotomy is indicated for varus-type osteoarthritis of stage 2 or stage 3a.

To understand the molecular events coupling between cell proliferation and differentiation by elucidating genes essential for the process, we conducted a large scale gene expression analysis of an in vitro osteoclastogenesis system consisting of recombinant RANKL and mouse RAW264 cells. The entire process leading to the formation of tartrate resistant acid phosphatase-positive multinucleated cells takes 3 days and plates become fully covered with multinucleated cells at 4 days. Microarray probing at eight time points revealed 635 genes that showed greater than 2-fold differential expression for at least one time point and they could be classified into six groups by the "k-means" clustering analysis. Among a group of 106 early inducible genes (within 2-5 h after RANKL stimulation), four genes including NFAT2 were identified as genes whose enhanced expressions were fairly correlated with an efficient induction of matured osteoclasts. Moreover, cyclosporin A significantly suppressed the multinucleated cell formation accompanying the reduction of the nuclear localization of NFAT2. When the expression of NFAT2 was suppressed by introducing antisense NFAT2, multinucleated cell formation was severely hampered. Functional analysis thus combined with gene analysis by microarray technology elucidated a key role of NFAT2 in osteoclastogenesis in vitro.Specific factors/regulatory genes playing essential roles for cellular differentiation have been identified in various systems, and they have been shown to exert their effects eventually through the induction or repression of certain groups of genes (1-4). Therefore, gene expression profiling based on fine statistical analysis in addition to an elucidation of key factors/ genes might be essential to understand the molecular mechanisms underlying the differentiation process of a certain cell type. Fortunately, recent advances in the technology for assaying RNA in a highly parallel fashion (5-7), coupled with the completion/progress of several mammalian genome projects, make the approach feasible if a refined system is available. Here, we describe the broad outlines of gene expression during osteoclastogenesis in vitro, in particular during the initial stage, and explain the identification and characterization of genes essential for osteoclastogenesis on the basis of profiling characteristics. A similar approach using a different cell system was reported recently (8).Osteoclasts are multinucleated (MN) 1 giant cells and present only in bone with the capacity to resorb mineralized tissues (9). They were reported to be formed by fusion of mononuclear precursor cells derived from colony-forming unit granulocyte macrophages (CFU-GM) and branch from the monocyte-macrophage lineage during the early stage of the differentiation process (9, 10). Recently, a key factor responsible for initiating this differentiation process was identified and named receptor activator of NFB ligand (RANKL) (or osteoclast differentiation factor (ODF)/TNF-related activation-induced cytokine TRANCE) (11-13)...

Iliotibial band (ITB) syndrome is a common overuse injury in runners and cyclists. It is regarded as a friction syndrome where the ITB rubs against (and 'rolls over') the lateral femoral epicondyle. Here, we re-evaluate the clinical anatomy of the region to challenge the view that the ITB moves antero-posteriorly over the epicondyle. Gross anatomical and microscopical studies were conducted on the distal portion of the ITB in 15 cadavers. This was complemented by magnetic resonance (MR) imaging of six asymptomatic volunteers and studies of two athletes with acute ITB syndrome. In all cadavers, the ITB was anchored to the distal femur by fibrous strands, associated with a layer of richly innervated and vascularized fat. In no cadaver, volunteer or patient was a bursa seen. The MR scans showed that the ITB was compressed against the epicondyle at 30° of knee flexion as a consequence of tibial internal rotation, but moved laterally in extension. MR signal changes in the patients with ITB syndrome were present in the region occupied by fat, deep to the ITB. The ITB is prevented from rolling over the epicondyle by its femoral anchorage and because it is a part of the fascia lata. We suggest that it creates the illusion of movement, because of changing tension in its anterior and posterior fibres during knee flexion. Thus, on anatomical grounds, ITB overuse injuries may be more likely to be associated with fat compression beneath the tract, rather than with repetitive friction as the knee flexes and extends.

We have already reported that slowly progressive non-insulin-dependent diabetes mellitus (NIDDM) is produced by a single i.p. injection of a subdiabetogenic dose (100 mg/kg) of streptozotocin (STZ) to 8-week-old male ICR mice. The aim of the present study was to clarify whether or not the progressive NIDDM is induced in ddY, BALB/c, C57BL/6 and ICR mice by the administration of STZ. Eight-week-old male mice of the 4 different strains were administered a single i.p. injection of STZ at various doses (ICR, ddY and BALB/c: 100-200 mg/kg; C57BL/6: 75-150 mg/kg). Among the ddY, BALB/c and C57BL/6 mice, a time course-related rise in non-fasting serum glucose levels throughout the observation period of 1-12 weeks after STZ administration was only induced in the 125 mg/kg STZ ddY and 100 mg/kg STZ ICR mice. In contrast with serum glucose levels, the area of islets and the percentage of the relative number of insulin-immunoreactive cells (b b-cells) to glucagon-immunoreactive cells (a a-cells) in the 100 mg/kg STZ ICR and 125 mg/kg STZ ddY mice continued to decrease gradually over time. In addition, in low dose STZ mice of both strains, the insulin response to glucose stimulation was extremely impaired over time, although non-fasting serum insulin levels were maintained near normal levels. The rate of the progression of diabetes was faster in the 125 mg STZ ddY mice than in the 100 mg/kg STZ ICR mice.

The varus inclination of the articular surface of the tibial plafond progressed by stages; however, anterior opening was not significant at all stages. The valgus inclination of the subtalar joint progressed until the intermediate stage and converted to varus position at the later stage. CONCLUSION The compensatory function of the subtalar joint was most pronounced at the intermediate ankle arthritis stage.