Use of a Box-cut Osteotomy Preserving Collateral Ligaments in Costal Osteochondral Graft Reconstruction of Proximal Interphalangeal Joint Cartilage Defects.

We report two patients with reconstruction of osteochondral defects of the proximal interphalangeal joint (PIPJ) using a costal osteochondral graft (COG). A box-cut osteotomy was done at the end of the phalanx preserving the lateral cortices and the insertion of the collateral ligaments. A COG was harvested from the rib, moulded and press fit into the groove formed by the box-cut osteotomy. The COG was fixed with mini screws in the coronal plane (dorsal to palmar) and the fixation off-loaded with an external fixator. This technique maintained the collateral ligament in-situ and is useful in reconstruction of chondral defects of the PIPJ. Level of Evidence: Level V (Therapeutic).

Treatment for Brodie's abscess of the radius in an adolescent: A case report.

INTRODUCTION: Brodie's abscess is an uncommon type subacute osteomyelitis. It is typically localized in the metaphysis of tubular bones, particularly in the lower extremities. We herein report a rare case of the abscess appearing in the upper extremities. Furthermore, we successfully treated the large abscess without autogenous bone grafting. PRESENTATION OF CASE: 14-year-old female presented with pain and swelling on the right forearm. Plain radiograph and CT scan indicated a 10 cm longitudinal cortical bone hypertrophy and a well-defined radiolucent lesion in the diaphysis of the right radius. MRI demonstrated that the lesion was hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging inside as well as outside the bone marrow of the radius. Laboratory data showed no inflammatory response, but Staphylococcus aureus was detected by biopsy. We diagnosed Brodie's abscess of the radius, and performed definitive surgery. Infected bone marrow was curetted and a bony sequestrum inside the cortical bone was harvested. We did not use autogenous bone grafting, since the upper extremities are areas of unloaded bone. Postoperative administration of antibiotics was subsequently performed. One year after surgery, the patient was asymptomatic and there were no complications or signs of infection recurrence. CONCLUSION: We diagnosed and surgically treated a rare case of Brodie's abscess of the radius in an adolescent. An abscess with large cavity is usually treated by curettage and autogenous cancellous bone grafting. However, since the upper extremities are areas of unloaded bone, we successfully treated the abscess by debridement without bone grafting.

Double non-contiguous fractures in a patient with spondylo-epiphyseal dysplasia with spinal ankylosis treated with open and percutaneous spinal fixation technique: a case report.

BACKGROUND: Patients with ankylosing spines are susceptible to developing spinal fractures even with minor trauma and can develop early or late neurological injuries. These fractures require early and aggressive surgical management to enable spinal stability and/or neural decompression. Being highly unstable by nature, they require relatively long segment instrumentation and fusion, which can increase paravertebral soft tissue damage and perioperative bleeding. The purpose of this report is to describe a rare case of traumatic double fractures at the cervico-thoracic and thoraco-lumbar transition zones in ankylosing spine with spondylo-epiphyseal dysplasia (SED) of unknown cause, which were successfully treated with a combined open and percutaneous spinal fusion procedure. CASE PRESENTATION: A 46-year-old woman who was diagnosed with non-contiguous fractures in cervico-thoracic and thoraco-lumbar junction zones among multiple injuries sustained in a traffic accident was treated with hybrid techniques for posterior instrumentation with an open approach using a computed tomography (CT)-based navigation system and percutaneous pedicle-screwing method. She regained mobility to pre-admission levels and started walking on crutches 3 months postoperatively. Genetic testing for the cause of SED revealed no mutation in the COL2A1 or TRPVR4 genes. The union of fractured spine was confirmed on CT scan 1 year postoperatively. CONCLUSION: This is the first report of double spinal fractures in an ankylosing spine with genetically undetermined spondyloepiphyseal dysplasia. A long-segment posterior instrumentation procedure incorporating the invasive treatment of spinal fractures in ankylosing spondylitis or diffuse idiopathic hyperostosis was effective.

Quantification of pelvic tilt and rotation by width/height ratio of obturator foramina on anteroposterior radiographs.

OBJECTIVE: Compared to sagittal pelvic tilt, only a few studies have examined axial rotation on anteroposterior radiographs. We therefore quantified 3-D pelvic rotation using the width and height ratio of the obturator foramina under the various pelvic tilts. METHODS: Using CT reconstructions of 10 healthy pelvises, anterior pelvic planes (APPs) were rotated by 20° in 5° increments on the axial plane with various degrees of sagittal pelvic tilt. The correlation between the pelvic rotation angle and the width ratio (WR) in the axial plane and the height/width ratio (H/W) in the sagittal plane were examined. RESULTS: Axial pelvic rotation and WR showed a high linear correlation regardless of the sagittal tilt, with the correlation coefficient ranging from 0.93 to 0.98 in males and 0.87 to 0.95 in females. The angle that resulted in a WR of 1:2 was approximately 13° in males and 18° in females. H/W also showed a linear regression with sagittal tilt. Axial rotation was determined by the following equation incorporating pelvic tilts; axial rotation (male:female) = (19.9:24.2) + (2.1:3.6) × Hright/Wright + (0.9:1.5) × Hleft/Wleft - (23.2:25.1) × WR. CONCLUSIONS: Pelvic tilt and rotation could be quantified by the equation using width and height ratios of the obturator foramina on a plain anteroposterior radiograph. Width and height ratios of the obturator foramina proved to be useful parameters in clinical practice for understanding pelvic rotation.

Pelvic tilt and movement during total hip arthroplasty in the lateral decubitus position.

OBJECTIVES: Total hip arthroplasty (THA) is often performed in the lateral decubitus (lateral) position. In this position, the pelvis may have various degrees of tilt leading to implant malposition. We sought to quantify the pelvic tilt in lateral position and further pelvic movement during surgery. METHODS: In 95 cases with primary THA, three-dimensional pelvic tilts were quantified by superimposing images reconstructed from CT data onto antero-posterior radiographs taken in lateral position at set-up and after cup placement. Pelvises were fixed with a device compressing anterior superior iliac spines and sacrum. RESULTS: Various degrees of pelvic tilt occurred compared to the supine position; sagittal: -3.1° (-25.5° to 10.2°), axial: 3.9° (-8.4° to 17°), coronal: 0.9° (-11.9° to 13.2°). Absolute changes more than 5° were observed 43%, 47%, and 12% in the sagittal, axial, and coronal planes, respectively. The more preoperative posterior pelvic tilt resulted in the more change in the sagittal plane. Further pelvic movement of about 3° in three planes were observed ranging from -11° to 20° after cup placement. CONCLUSION: This study showed various pelvic tilt and movement during THA. As pelvic tilt directly alters the cup orientation, its changes should be well understood. Improved tools for positioning and holding the pelvis are required.

CCAAT/enhancer-binding protein ß promotes receptor activator of nuclear factor-kappa-B ligand (RANKL) expression and osteoclast formation in the synovium in rheumatoid arthritis.

INTRODUCTION: CCAAT/enhancer-binding protein ß (C/EBPß) is a transcription factor that is activated in the synovium in rheumatoid arthritis (RA) and promotes expression of various matrix metalloproteinases. In this study, we examined whether C/EBPß mediates the expression of receptor activator of nuclear factor-kappa-B ligand (RANKL) and drives osteoclast formation in primary fibroblast-like synoviocytes (FLS) from RA patients. The cooperation of C/EBPß and activation transcription factor-4 (ATF4) in the regulation of the RANKL promoter was also investigated. METHODS: Immunofluorescence staining was performed for C/EBPß, RANKL, and ATF4 in synovium from RA patients. Adenovirus expression vectors for two major isoforms, C/EBPß-liver-enriched activator protein (LAP) and - liver-enriched inhibitory protein (LIP), or small interfering RNA for C/EBPß, were used to manipulate C/EBPß expression in RA-FLS. RA-FLS over-expressing C/EBPß were co-cultured with peripheral blood mononuclear cells (PBMCs) to test osteoclast formation by tartrate-resistant acid phosphatase (TRAP) staining. A promoter assay for RANKL, a chromatin immunoprecipitation (ChIP) assay and an immunoprecipitation (IP) assay were also performed. RESULTS: Immunofluorescence staining showed colocalization of C/EBPß, ATF4 and RANKL in RA synovium. Western blotting revealed the expression of C/EBPß-LAP and -LIP in RA-FLS. Over-expression of either C/EBPß-LAP or -LIP significantly increased the expression of RANKL mRNA, while C/EBPß-LIP down-regulated osteoprotegerin (OPG) mRNA. The RANKL/OPG mRNA ratio was significantly increased by C/EBPß-LIP over-expression. Knockdown of C/EBPß with siRNA decreased the expression of RANKL mRNA. The number of TRAP-positive multinucleated cells was increased in co-cultures of PBMCs and FLS over-expressing either C/EBPß-LAP or -LIP, but was more significant with LIP. C/EBPß-LIP does not have a transactivation domain. However, promoter assays showed that C/EBPß-LIP and ATF4 synergistically transactivate the RANKL promoter. ChIP and IP assays revealed the cooperative binding of C/EBPß and ATF4 on the RANKL promoter. CONCLUSIONS: We demonstrated that C/EBPß, especially C/EBPß-LIP in cooperation with ATF4, is involved in osteoclast formation by regulating RANKL expression in RA-FLS. These findings suggest that C/EBPß plays a crucial role in bone destruction in RA joints.

CCAAT/enhancer binding protein ß regulates expression of Indian hedgehog during chondrocytes differentiation.

BACKGROUND: CCAAT/enhancer binding protein ß (C/EBPß) is a transcription factor that promotes hypertrophic differentiation of chondrocytes. Indian hedgehog (Ihh) also stimulates the hypertrophic transition of chondrocytes. Furthermore, runt-related transcription factor-2 (RUNX2) was reported to regulate chondrocyte maturation during skeletal development and to directly regulate transcriptional activity of Ihh. In this study, we investigated whether the interaction of C/EBPß and RUNX2 regulates the expression of Ihh during chondrocyte differentiation. METHODOLOGY/RESULTS: Immunohistochemistry of embryonic growth plate revealed that both C/EBPß and Ihh were strongly expressed in pre-hypertrophic and hypertrophic chondrocytes. Overexpression of C/EBPß by adenovirus vector in ATDC5 cells caused marked stimulation of Ihh and Runx2. Conversely, knockdown of C/EBPß by lentivirus expressing shRNA significantly repressed Ihh and Runx2 in ATDC5 cells. A reporter assay revealed that C/EBPß stimulated transcriptional activity of Ihh. Deletion and mutation analysis showed that the C/EBPß responsive element was located between -214 and -210 bp in the Ihh promoter. An electrophoretic mobility shift assay (EMSA) and a chromatin immunoprecipitation (ChIP) assay also revealed the direct binding of C/EBPß to this region. Moreover, reporter assays demonstrated that RUNX2 failed to stimulate the transcriptional activity of the Ihh promoter harboring a mutation at the C/EBPß binding site. EMSA and ChIP assays showed that RUNX2 interacted to this element with C/EBPß. Immunoprecipitation revealed that RUNX2 and C/EBPß formed heterodimer complex with each other in the nuclei of chondrocytes. These data suggested that the C/EBPß binding element is also important for RUNX2 to regulate the expression of Ihh. Ex vivo organ culture of mouse limbs transfected with C/EBPß showed that the expression of Ihh and RUNX2 was increased upon ectopic C/EBPß expression. CONCLUSIONS: C/EBPß and RUNX2 cooperatively stimulate expression of Ihh through direct interactions with a C/EBPß binding element, which further promotes hypertrophic differentiation of chondrocytes during the chondrocyte differentiation process.

CCAAT/enhancer-binding protein ß regulates the repression of type II collagen expression during the differentiation from proliferative to hypertrophic chondrocytes.

CCAAT/enhancer-binding protein ß (C/EBPß) is a transcription factor that promotes hypertrophic differentiation by stimulating type X collagen and matrix metalloproteinase 13 during chondrocyte differentiation. However, the effect of C/EBPß on proliferative chondrocytes is unclear. Here, we investigated whether C/EBPß represses type II collagen (COL2A1) expression and is involved in the regulation of sex-determining region Y-type high mobility group box 9 (SOX9), a crucial factor for transactivation of Col2a1. Endogenous expression of C/EBPß in the embryonic growth plate and differentiated ATDC5 cells were opposite to those of COL2A1 and SOX9. Overexpression of C/EBPß by adenovirus vector in ATDC5 cells caused marked repression of Col2a1. The expression of Sox9 mRNA and nuclear protein was also repressed, resulting in decreased binding of SOX9 to the Col2a1 enhancer as shown by a ChIP assay. Knockdown of C/EBPß by lentivirus expressing shRNA caused significant stimulation of these genes in ATDC5 cells. Reporter assays demonstrated that C/EBPß repressed transcriptional activity of Col2a1. Deletion and mutation analysis showed that the C/EBPß core responsive element was located between +2144 and +2152 bp within the Col2a1 enhancer. EMSA and ChIP assays also revealed that C/EBPß directly bound to this region. Ex vivo organ cultures of mouse limbs transfected with C/EBPß showed that the expression of COL2A1 and SOX9 was reduced upon ectopic C/EBPß expression. Together, these results indicated that C/EBPß represses the transcriptional activity of Col2a1 both directly and indirectly through modulation of Sox9 expression. This consequently promotes the phenotypic conversion from proliferative to hypertrophic chondrocytes during chondrocyte differentiation.

CCAAT/enhancer binding protein ß regulates expression of matrix metalloproteinase-3 in arthritis.

OBJECTIVES: To investigate whether CCAAT/enhancer binding protein ß (C/EBPß) mediates the expression of matrix metalloproteinase-3 (MMP-3) and aggrecanases in arthritis. METHODS: Localisation of C/EBPß and MMP-3 in synovium and cartilage from patients with rheumatoid arthritis and osteoarthritis was determined by immunohistochemistry. Cell lines SW982, C28/I2 and human fibroblast-like synoviocytes stimulated by interleukin 1ß (IL-1ß) were subjected to western blotting and quantitative PCR. Overexpression of C/EBPß by adenovirus was performed in cells and organ culture of normal cartilage. Knockdown of C/EBPß by small interference RNA was performed in cells. Activity of the human MMP-3 and aggrecanase-2 ADAMTS-5 (a disintegrin and metalloproteinase with thrombospondin motifs) promoters was analysed by a luciferase assay. To determine whether C/EBPß directly binds to the MMP-3 or ADAMTS-5 promoter,a chromatin immunoprecipitation assay was performed. RESULTS: Immunohistochemistry showed that C/EBPß and MMP-3 were co-localised in arthritic synovium and cartilage. Western blots revealed increased C/EBPß expression in cells treated with IL-1ß. Expression of MMP-3, MMP-13 and ADAMTS-5 mRNA was significantly increased by the overexpression of C/EBPß. C/EBPß stimulated MMP-3 expression and induced matrix degradation in cartilage explants. C/EBPß knockdown reduced MMP-3 and ADAMTS-5 expression. C/EBPß stimulated the 2011 bp MMP-3 promoter and the 1768 bp ADAMTS-5 promoter in a dose-dependent manner. Deletion and mutation analysis of the MMP-3 promoter showed that the C/EBPß core responsive element was located between -108 bp and -100 bp. The chromatin immunoprecipitation assay showed that C/EBPß was directly bound to MMP-3 and ADAMTS-5 promoters. CONCLUSIONS: These data demonstrate that C/EBPß is involved in expression of MMP-3 and ADAMTS-5 in arthritic synovium and cartilage.

[Partial electrical reset of CT irradiation on implantable cardiac devices: relationship between reset and tube voltage, tube current, and rotation time].

The aim of this study was to investigate the relationship between partial electrical reset (PER) and CT scan parameters (tube voltage, tube current, rotation time, and product of tube current and rotation time in mAs). A cardiac resynchronization therapy pacemaker (Insync 8040, Medtronic Inc., Tokyo) and 320 area detector CT scanner (Aquilion ONE, Toshiba medical systems, Otawara, Japan) with volume scan were used. The pacemaker was put in DDD mode. The PERs were interpreted using both the programmer's wave forms and error messages. The exposure was repeated 5 times per CT setting. The pacemaker was placed on the anterior wall and upper side of a chest phantom. Each CT scan was performed using the following parameters: tube voltage of 80, 100, 120, and 135 kV; tube current of 50-550 mA; and rotation time of 0.35-1.5 s. PERs were observed at 100, 120, and 135 kV, and more PERs were observed as the tube voltage increased. The PER tube current decreased as the rotation time was increased. In contrast, the PER tube current and rotation time product (mAs) increased as the rotation time was increased. More specifically, the radiation dose rate was the affected factor of the PERs. To avoid PER of pacemakers, CT scan parameters with lower radiation dose rates (low rather than high tube current and rotational time) is recommended. In conclusion, our results will help with CT scans of patients who have implantable cardiac devices (included pacemakers and cardioverter defibrillators).