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Takahiro Ochi

Publications and source records attributed to Takahiro Ochi.

At least 19 recordsLinked to original sources
PubMed2006

Cytoplasmic destruction of p53 by the endoplasmic reticulum-resident ubiquitin ligase 'Synoviolin'.

Synoviolin, also called HRD1, is an E3 ubiquitin ligase and is implicated in endoplasmic reticulum -associated degradation. In mammals, Synoviolin plays crucial roles in various physiological and pathological processes, including embryogenesis and the pathogenesis of arthropathy. However, little is known about the molecular mechanisms of Synoviolin in these actions. To clarify these issues, we analyzed the profile of protein expression in synoviolin-null cells. Here, we report that Synoviolin targets tumor suppressor gene p53 for ubiquitination. Synoviolin sequestrated and metabolized p53 in the cytoplasm and negatively regulated its cellular level and biological functions, including transcription, cell cycle regulation and apoptosis. Furthermore, these p53 regulatory functions of Synoviolin were irrelevant to other E3 ubiquitin ligases for p53, such as MDM2, Pirh2 and Cop1, which form autoregulatory feedback loops. Our results provide novel insights into p53 signaling mediated by Synoviolin.

Animals↗
PubMed2006

Isolation and expression profiling of genes upregulated in bone marrow-derived mononuclear cells of rheumatoid arthritis patients.

We have comprehensively identified the genes whose expressions are augmented in bone marrow-derived mononuclear cells (BMMC) from patients with Rheumatoid Arthritis (RA) as compared with BMMCs from Osteoarthritis (OA) patients, and named them AURA after augmented in RA. Both stepwise subtractive hybridization and microarray analyses were used to identify AURA genes, which were confirmed by northern blot analysis and/or reverse transcription polymerase chain reaction (RT-PCR). We also assessed their expression levels in individual patients by quantitative real-time RT-PCR. Of 103 AURA genes we have identified, the mRNA levels of the following 10 genes, which are somehow related to immune responses, were increased in many of the RA patients: AREG (=AURA9), FK506-binding protein 5 (FKBP5 = AURA45), C-type lectin superfamily member 9 (CLECSF9 = AURA24), tyrosylprotein sulfotransferase 1 (TPST1 = AURA52), lymphocyte G0/G1 switch gene (G0S2 = AURA8), chemokine receptor 4 (CXCR4 = AURA86), nuclear factor-kappa B (NF-kappaB = AURA25) and two genes of unknown function (FLJ11106 = AURA1, BC022398 = AURA2 and XM_058513 = AURA17). Since AREG was most significantly increased in many of the RA patients, we subjected it to further analysis and found that AREG-epidermal growth factor receptor signaling is highly activated in synovial cells isolated from RA patients, but not in OA synoviocytes. We propose that the expression profiling of these AURA genes may improve our understanding of the pathogenesis of RA.

Amphiregulin↗
PubMed2006

Pro-inflammatory cytokine tumor necrosis factor-alpha induces bone morphogenetic protein-2 in chondrocytes via mRNA stabilization and transcriptional up-regulation.

In articular chondrocytes, the inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) induces the expression of bone morphogenetic protein-2 (BMP-2), a growth factor known to be involved in the induction of cartilage and bone. A study was performed to clarify the mechanism(s) underlying the induction of BMP-2 in chondrogenic ATDC5 cells and primary cultured adult human articular chondrocytes. In ATDC5 cells, the endogenous BMP-2 expression was consistently low throughout the process of chondrogenic differentiation, and TNF-alpha induced BMP-2 expression only after the cells acquired the chondrogenic phenotype. The results of nuclear run-off assay and cycloheximide treatment consistently indicated that ATDC5 cells acquire the capacity to synthesize BMP-2 mRNA in the nuclei during the differentiation process. In an attempt to explain the discrepancy between the active nuclear mRNA synthesis and the observed low expression level in differentiated ATDC5 cells, the stability of BMP-2 mRNA was evaluated, and the cells were found to regulate the expression of BMP-2 at the post-transcriptional level. Human chondrocytes were confirmed to have a similar post-transcriptional regulation. The result of 3'-rapid amplification of cDNA end revealed that both human and mouse BMP-2 mRNAs contain multiple pentameric AUUUA motifs in a conserved manner in the 3'-untranslated regions, and transient transfection experiments demonstrated that TNF-alpha increases the stability of BMP-2 mRNA through the pentameric motifs. Further experiments revealed that TNF-alpha modulates mRNA stability via p38 signal transduction pathway, whereas the cytokine also augmented the expression of BMP-2 through transcriptional up-regulation via the transcriptional factor NF-kappaB.

3' Untranslated Regions↗
PubMed2006

Enhanced expression of mRNA for nuclear factor kappaB1 (p50) in CD34+ cells of the bone marrow in rheumatoid arthritis.

Bone marrow CD34+ cells from rheumatoid arthritis (RA) patients have abnormal capacities to respond to tumor necrosis factor (TNF)-alpha and to differentiate into fibroblast-like cells producing matrix metalloproteinase (MMP)-1. We explored the expression of mRNA for nuclear factor (NF)kappaB in RA bone marrow CD34+ cells to delineate the mechanism for their abnormal responses to TNF-alpha. CD34+ cells were purified from bone marrow samples obtained from 49 RA patients and 31 osteoarthritis (OA) patients during joint operations via aspiration from the iliac crest. The mRNAs for NFkappaB1 (p50), NFkappaB2 (p52) and RelA (p65) were examined by quantitative RT-PCR. The expression of NFkappaB1 mRNA in bone marrow CD34+ cells was significantly higher in RA than in OA, whereas there was no significant difference in the expression of mRNA for NFkappaB2 and RelA. The expression of NFkappaB1 mRNA was not correlated with serum C-reactive protein or with the treatment with methotrexate or oral steroid. Silencing of NFkappaB1 by small interfering RNA abrogated the capacity of RA bone marrow CD34+ cells to differentiate into fibroblast-like cells and to produce MMP-1 and vascular endothelial growth factor upon stimulation with stem cell factor, granulocyte-macrophage colony stimulating factor and TNF-alpha without influencing their viability and capacity to produce beta2-microglobulin. These results indicate that the enhanced expression of NFkappaB1 mRNA in bone marrow CD34+ cells plays a pivotal role in their abnormal responses to TNF-alpha and, thus, in the pathogenesis of RA.

Adult↗
PubMed2006

Effect of GDF-5 on ligament healing.

The effects of growth and differentiation factor-5 (GDF-5) on ligament healing were studied using a gap injury model of the medial collateral ligament in rat knee joints. The administration of GDF-5 once at the time of surgery significantly improved the mechanical properties of the femur-ligament-tibia complex. At 3 weeks after surgery, 30 microg of GDF-5 improved the ultimate tensile strength of the complex by 41%, and the stiffness by 60%, compared with the vehicle control (p < 0.05 for both; Fisher's PLSD test). The observation with a transmission electron microscopy revealed that GDF-5 increased the diameter of collagen fibrils in the repair tissue, which was considered to be a possible mechanism for the positive result in the biomechanical testing. Quantitative PCR and in situ hybridization revealed enhanced type I procollagen expression by GDF-5, and the PCR analysis also revealed that the GDF-5 treatment reduced the expression of type III procollagen relative to type I procollagen. The PCR analysis further showed that the expression of decorin and fibromodulin was relatively reduced against type I procollagen by the growth factor, which was considered to be responsible for the increase of collagen fibril diameter in the repair tissue. No adverse effects were observed, and the use of GDF-5 was considered a promising approach to facilitate ligament healing.

Animals↗
PubMed2006

Imatinib mesylate inhibits osteoclastogenesis and joint destruction in rats with collagen-induced arthritis (CIA).

Macrophage colony-stimulating factor (M-CSF) is a key factor for osteoclastogenesis at the bone-pannus interface in patients with rheumatoid arthritis as well as a receptor activator of NF-kappaB ligand (RANKL). Imatinib mesylate inhibits the phosphorylation of c-fms, a receptor for M-CSF. The present study investigates the effect of imatinib mesylate on joint destruction in rats with collagen-induced arthritis (CIA) and on osteoclastogenesis in vitro. Imatinib mesylate (50 or 150 mg/kg), dexamethasone, or vehicle was administered daily to CIA rats for 4 weeks from the onset of arthritis. Hind-paw swelling and body weight were measured weekly. At weeks 2 and 4, the metatarsophalangeal (MTP) joints and the ankle and subtalar joints were radiographically and histologically assessed. The effect of imatinib mesylate on osteoclast formation from rat bone marrow cells with M-CSF and soluble RANKL (sRANKL) in vitro was also examined. Radiographic assessment showed that 150 mg/kg imatinib mesylate suppressed the destruction of the MTP and the ankle and subtalar joints at week 2, and MTP joint destruction at week 4 in CIA rats, although hind-paw swelling was not suppressed. The number of TRAP-positive cells at the bone-pannus interface was significantly reduced in the group administered with 150 mg/kg imatinib mesylate compared with that given vehicle at week 4. Imatinib mesylate dose-dependently inhibited the proliferation of M-CSF-dependent osteoclast precursor cells in vitro as well as osteoclast formation induced by M-CSF and sRANKL. These findings suggest that imatinib mesylate could prevent joint destruction in patients with rheumatoid arthritis.

Animals↗
PubMed2006

Effects of unipedal standing balance exercise on the prevention of falls and hip fracture among clinically defined high-risk elderly individuals: a randomized controlled trial.

BACKGROUND: The aim of this study was to assess the effectiveness of the unipedal standing balance exercise for 1 min to prevent falls and hip fractures in high-risk elderly individuals with a randomized controlled trial. This control study was designed as a 6-month intervention trial. SUBJECTS: Subjects included 553 clinically defined high-risk adults who were living in residences or in the community. They were randomized to an exercise group and a control group. METHODS: Randomization to the subjects was performed by a table of random numbers. A unipedal standing balance exercise with open eyes was performed by standing on each leg for 1 min three times per day. As a rule, subjects of the exercise group stood on one leg without holding onto any support, but unstable subjects were permitted to hold onto a bar during the exercise time. Falls and hip fractures were reported by nurses, physical therapists, or facility staff with a survey sheet every month. This survey sheet was required every month for both groups. RESULTS: Registered subjects were 553 persons ranging in age from 37 to 102 years (average, 81.6 years of age). Twenty-six subjects dropped out. The number of falls and hip fractures for the 6-month period after the trial for 527 of the 553 subjects for whom related data were available were assessed. The exercise group comprised 315 subjects and the control group included 212 subjects. The cumulative number of falls of the exercise group, with 1 multiple faller omitted, was 118, and the control group recorded 121 falls. A significant intergroup difference was observed. However, the cumulative number of hip fractures was only 1 case in both groups. This difference was not statistically significant. CONCLUSIONS: The unipedal standing balance exercise is effective to prevent falls but was not shown to be statistically significant in the prevention of hip fracture in this study.

Accidental Falls↗
PubMed2006

Adrenocorticotropic hormone and dehydroepiandrosterone sulfate levels of rheumatoid arthritis patients treated with glucocorticoids.

To assess adrenal function with respect to the presence or absence of steroid therapy, we investigated differences in the blood levels of adrenocorticotropic hormone (ACTH) and dehydroepiandrosterone sulfate (DHEAS) in relation to steroid (prednisolone) administration in 123 patients with rheumatoid arthritis (RA). Levels of ACTH and DHEAS were significantly lower in the steroid-treated group than in the non-treated group (ACTH: 11.79 pg/ml vs 27.92 pg/ml) (DHEAS: 418.12 ng/ml vs 883.91 ng/ml) (P<0.0001). We observed no steroid dose-related differences in ACTH levels. However, DHEAS levels showed a slight decrease at a prednisolone dose of 2.5 mg/day, with a significant decrease being observed at a dose of 5 mg/day when statistical adjustments were made for age and sex (P<0.0001). At doses of 7.5 mg/day or greater, DHEAS levels were significantly lower than those for 5 mg/day (P<0.0006). These results suggest that low-dose prednisolone reduces adrenal function in patients with RA. We recommend that doses of prednisolone should be limited to 5 mg/day or less in consideration of adrenal function when treating RA patients. The measurement of ACTH and DHEAS may be useful for evaluating adrenal function in patients with RA.

Adrenal Glands↗
PubMed2006

Soft-tissue balance evaluation system for total hip arthroplasty by intraoperative contact pressure measurement at the hip joint.

We developed a system for measurement of contact pressure at the hip joint surfaces that enables checking of the artificial hip joint condition during surgery. First, we constructed the pressure sensor that forms the artificial joint. We installed eight small pressure sensors to the spherical head component, a part of the ball-socket joint. Next, we developed software for recording and visualizing the detected pressures that were recorded every 1 ms. The pressure distribution was displayed with the 3D computer graphics in real-time. The system enabled intuitive recognition of pressure direction 3-dimensions. Next, using the system, we conducted measurements during total hip arthroplasty. Although it requires some improvements in its measurement accuracy, the system allows real-time acquisition of information on the artificial hip joint in real-time. Further improvements of the calibration method should enable more accurate measurements. As a complete system, it will be a useful tool for selecting an appropriate implant that fits a patient's hip joint or for estimating the risk of complications after surgery.

Arthroplasty, Replacement, Hip↗
PubMed2005

Prostaglandin E2 strongly inhibits human osteoclast formation.

Prostaglandin E(2) (PGE(2)) enhances osteoclast formation in mouse macrophage cultures treated with receptor activator of nuclear factor-kappaB ligand (RANKL). The effects of PGE(2) on human osteoclast formation were examined in cultures of CD14(+) cells prepared from human peripheral blood mononuclear cells. CD14(+) cells differentiated into osteoclasts in the presence of RANKL and macrophage colony-stimulating factor. CD14(+) cells expressed EP2 and EP4, but not EP1 or EP3, whereas CD14(+) cell-derived osteoclasts expressed none of the PGE(2) receptors. PGE(2) and PGE(1) alcohol (an EP2/4 agonist) stimulated cAMP production in CD14(+) cells. In contrast to mouse macrophage cultures, PGE(2) and PGE(1) alcohol inhibited RANKL-induced human osteoclast formation in CD14(+) cell cultures. H-89 blocked the inhibitory effect of PGE(2) on human osteoclast formation. These results suggest that the inhibitory effect of PGE(2) on human osteoclast formation is mediated by EP2/EP4 signals. SaOS4/3 cells have been shown to support human osteoclast formation in cocultures with human peripheral blood mononuclear cells in response to PTH. PGE(2) inhibited PTH-induced osteoclast formation in cocultures of SaOS4/3 cells and CD14(+) cells. Conversely, NS398 (a cyclooxygenase 2 inhibitor) enhanced osteoclast formation induced by PTH in the cocultures. The conditioned medium of CD14(+) cells pretreated with PGE(2) inhibited RANKL-induced osteoclast formation not only in human CD14(+) cell cultures, but also in mouse macrophage cultures. These results suggest that PGE(2) inhibits human osteoclast formation through the production of an inhibitory factor(s) for osteoclastogenesis of osteoclast precursors.

Adult↗
PubMed2005

Nurse-like cells from patients with rheumatoid arthritis support the survival of osteoclast precursors via macrophage colony-stimulating factor production.

OBJECTIVE: To elucidate the role of nurse-like cells (NLCs) obtained from rheumatoid arthritis (RA) patients in bone loss during progressive synovial expansion. METHODS: CD14+ monocytes were cocultured with NLCs for 4 weeks and collected as NLC-supported CD14+ (NCD14+) monocytes. To determine their ability to differentiate into osteoclasts, NCD14+ monocytes were further cultured with macrophage colony-stimulating factor (M-CSF) together with RANKL or tumor necrosis factor alpha (TNFalpha). NCD14+ monocytes were also cocultured with SaOS-4/3 cells, which were shown to support osteoclastogenesis in response to parathyroid hormone (PTH). CD14+ monocytes were cocultured with SaOS-4/3 cells to elucidate how SaOS-4/3 cells and NLCs supported CD14+ monocytes for a long period. Synovial expansion adjacent to bone in RA patients was examined immunohistochemically to detect osteoclast precursors such as NCD14+ monocytes. RESULTS: NLCs supported the survival of CD14+ monocytes for 4 weeks. NCD14+ as well as CD14+ monocytes differentiated into osteoclasts in the presence of M-CSF together with RANKL or TNFalpha. NCD14+ monocytes also differentiated into osteoclasts in PTH-treated cocultures with SaOS-4/3 cells. SaOS-4/3 cells supported the survival of CD14+ monocytes for 4 weeks in the presence, but not absence, of PTH. Treatment of SaOS-4/3 cells with PTH up-regulated the expression of M-CSF messenger RNA. Neutralizing antibodies against M-CSF inhibited the NLC-supported survival of CD14+ monocytes. CD68+ monocytes and M-CSF+ fibroblast-like synoviocytes were colocalized in regions adjacent to the destroyed bone of RA patients. CONCLUSION: Our findings suggest that NLCs are involved in RA-induced bone destruction by maintaining osteoclast precursors via production of M-CSF.

Aged↗
PubMed2005

Production of interleukin-6 and interleukin-8 by nurse-like cells from rheumatoid arthritis patients after stimulation with monocytes.

It has been reported that nurse-like cells (NLCs) play a critical role in the pathogenesis of rheumatoid arthritis (RA). The interaction between NLCs established from RA patients (RA-NLCs), and freshly isolated blood monocytes was analyzed to further elucidate the pathogenesis of RA. RA-NLC lines were established from the synovium of RA patients. The RA-NLCs were cultured with monocytes freshly isolated from peripheral blood of healthy donors, and induction of interleukin (IL)-6 and IL-8 as well as the mRNA expression of these cytokines was examined. The levels of IL-6 were over 400 times higher in the supernatant from coculture of RA-NLCs and monocytes than in those from cultures of RA-NLCs alone. Anti-tumor necrosis factor (TNF)-alpha monoclonal antibody inhibited the induction of both cytokine in a dose-dependent fashion, although there was no detectable level of TNF-alpha in the supernatant from coculture. In addition, coculture of RA-NLCs and monocytes without direct cell contact did not induce cytokine production. To determine IL-6 producing cells, RA-NLCs and monocytes were separated into each fraction after coculture for 24 h. Cocultured RA-NLCs contained approximately 80 times higher IL-6 mRNA than the RA-NLCs cultured alone. The levels of IL-8 were also much higher (about 900 times) in the supernatant from coculture than in those from cultures of RA-NLCs alone. Cocultured RA-NLCs expressed IL-8 mRNA about 620 times higher than those cultured alone. These results indicate that NLCs produce high levels of IL-6 and IL-8 after cell-cell interaction with monocytes/macrophages via membrane-bound TNF-alpha, and that activation of NLCs by monocytes/macrophages may be involved in the pathogenesis of RA through maintenance of synovial inflammation.

Journal Article↗
PubMed2005

Gait analysis system for assessment of dynamic loading axis of the knee.

The purpose of this study was (1) to demonstrate a computer-assisted gait analysis system that can visualize the locus of the dynamic loading axis on the proximal tibia joint surface, and (2) to assess the accuracy of this system in a patient with bilateral knee osteoarthritis (OA). This system uses force plate data, CT skeletal structure data and motion capture data obtained from an infrared position sensor. The relative positions between bones and markers were used to calculate skeletal model movement based on movement of the markers. The locus of the dynamic loading axis on the knee joint was defined as the point on the proximal tibia joint surface that intersected with the loading axis of the lower limb, which passed through the centre of the femoral head and the centroid of multiple points surrounded by the distal tibia joint surface contour. To assess the accuracy of this system, open MRI was used to evaluate positions of skin markers against bones in six healthy volunteers. The locus in a patient was affected by differences between the varus knee with medial compartment OA on the non-operative side and the knee treated with high tibial osteotomy (HTO) on the opposite side. At knee flexion angles of 0 degrees, 15 degrees and 30 degrees, the mean value of measurement error for point locations on the locus was within 5.6% of joint width in the lateral direction (JWLD) on the proximal tibia joint. This system can provide clinically useful information for evaluation of the dynamic loading axis on the knee joint surface.

Aged↗
PubMed2005

Change in the locus of dynamic loading axis on the knee joint after high tibial osteotomy.

The purpose of this study was to visualise the locus of the dynamic loading axis on the knee joint, and to evaluate changes in this locus during gait after high tibial osteotomy (HTO) in three patients who underwent HTO for medial compartment osteoarthritis (OA) of a varus knee. The bone structure of the lower limb and the relative position of skin markers were acquired from CT images. Motion capture data was acquired using spherical skin markers. Skeletal model movement during gait was calculated based on the movement of the markers. The locus of the dynamic loading axis on the knee joint was defined as the point on the proximal tibia joint surface that intersected with the loading axis of the lower limb, which passed through the centre of the femoral head and the centroid of multiple points surrounded by the distal tibia joint surface contour. This system was able to visualise the locus of the dynamic loading axis on the knee joint and not only lateral but also anterior-posterior direction movement. After HTO, the locus shifted from a medial and posterior area of the medial joint edge of the knee to a central area of the knee joint surface. This indicates that HTO shifted the dynamic loading axis. Lateral movement of the dynamic loading axis in the early stance phase of gait was reduced within a year after HTO.

Aged↗
PubMed2005

A new biotechnology for articular cartilage repair: subchondral implantation of a composite of interconnected porous hydroxyapatite, synthetic polymer (PLA-PEG), and bone morphogenetic protein-2 (rhBMP-2).

OBJECTIVE: Articular cartilage repair remains a major obstacle in tissue engineering. We recently developed a novel tool for articular cartilage repair, consisting of a triple composite of an interconnected porous hydroxyapatite (IP-CHA), recombinant human bone morphogenetic protein-2 (rhBMP-2), and a synthetic biodegradable polymer [poly-d,l-lactic acid/polyethylene glycol (PLA-PEG)] as a carrier for rhBMP-2. In the present study, we evaluated the capacity of the triple composite to induce the regeneration of articular cartilage. METHODS: Full-thickness cartilage defects were created in the trochlear groove of 52 New Zealand White rabbits. Sixteen defects were filled with the bone morphogenetic protein (BMP)/PLA-PEG/IP-CHA composite (group I), 12 with PLA-PEG/IP-CHA (group II), 12 with IP-CHA alone (group III), and 12 were left empty (group IV). The animals were killed 1, 3, and 6 weeks after surgery, and the gross appearance of the defect sites was assessed. The harvested tissues were examined radiographically and histologically. RESULTS: One week after implantation with the BMP/PLA-PEG/IP-CHA composite (group I), vigorous repair had occurred in the subchondral defect. It contained an agglomeration of mesenchymal cells which had migrated from the surrounding bone marrow either directly, or indirectly via the interconnecting pores of the IP-CHA scaffold. At 6 weeks, these defects were completely repaired. The regenerated cartilage manifested a hyaline-like appearance, with a mature matrix and a columnar organization of chondrocytes. CONCLUSIONS: The triple composite of rhBMP-2, PLA-PEG, and IP-CHA promotes the repair of full-thickness articular cartilage defects within as short a period as 3 weeks in the rabbit model. Hence, this novel cell-free implant biotechnology could mark a new development in the field of articular cartilage repair.

Animals↗
PubMed2005

In vivo three-dimensional wrist motion analysis using magnetic resonance imaging and volume-based registration.

This study represents a new attempt to non-invasively analyze three-dimensional motions of the wrist in vivo. A volume-based registration method using magnetic resonance imaging (MRI) was developed to avoid radiation exposure. The primary aim was to evaluate the accuracy of volume-based registration and compare it with surface-based registration. The secondary aim was to evaluate contributions of the scaphoid and lunate to global wrist motion during flexion-extension motion (FEM), radio-ulnar deviation (RUD) and radial-extension/ulnoflexion, "dart-throwing" motion (DTM) in the right wrists of 12 healthy volunteers. Volume-based registration displayed a mean rotation error of 1.29 degrees +/-1.03 degrees and a mean translation error of 0.21+/-0.25 mm and was significantly more accurate than surface-based registration in rotation. Different patterns of contribution of the scaphoid and lunate were identified for FEM, RUD, and DTM. The scaphoid contributes predominantly in the radiocarpal joint during FEM, in the midcarpal joint during RUD and almost equally between these joints during DTM. The lunate contributes almost equally in both joints during FEM and predominantly in the midcarpal joint during RUD and DTM.

Biomechanical Phenomena↗
PubMed2005

Estimation of dislocation after total hip arthroplasty by 4-dimensional.

We constructed a 4-dimensional musculoskeletal model for patients who have undergone total hip arthroplasty (THA), which aimed to simulate the movement of the patient's inner body structure and estimate the complications that can arise with THA. The model reflects patient-specific characteristics of the bone geometry, implant alignment and hip movement. In order to estimate the direction of the muscle force and the length of the muscles, we developed a string-type muscle model that represents the route of the muscles. The strings expand and contract according to the movement of the origin and insertion location of the muscle. We developed models for the seven muscles related to movement of the hip joint. By using this model, clinicians will be able to predict the possibility of dislocation or recognize the actual causes of dislocation, as well as any possible influences the muscle may have on dislocation.

Arthroplasty, Replacement, Hip↗