I-Ming Jou

Tourniquet use in total knee arthroplasty: a meta-analysis

PurposeThe use of an intraoperative tourniquet for total knee arthroplasty (TKA) is a common practice. However, the effectiveness and safety are still questionable. A systematic review was conducted to examine that whether using a tourniquet in TKA was effective without increasing the risk of complications.MethodsA comprehensive literature search was done in PubMed Medicine, Embase, and other internet database. The review work and the following meta-analysis were processed to evaluate the role of tourniquet in TKA.ResultsEight randomized controlled trials and three high-quality prospective studies involving 634 knees and comparing TKA with and without the use of a tourniquet were included in this analysis. The results demonstrated that using a tourniquet could decrease the measured blood loss but could not decrease the calculated blood loss, which indicated actual blood loss. Patients managed with a tourniquet might have higher risks of thromboembolic complications. Using the tourniquet with late release after wound closure could shorten the operation time; whereas early release did not show this benefit.ConclusionsThe current evidence suggested that using tourniquet in TKA may save time but may not reduce the blood loss. Due to the higher risks of thromboembolic complications, we should use a tourniquet in TKA with caution.

Ultrasonography for diagnosing carpal tunnel syndrome: a meta-analysis of diagnostic test accuracy

Ultrasonography is widely used to diagnose carpal tunnel syndrome (CTS), a common peripheral neuropathy, but the reported diagnostic accuracy varies. This meta-analysis focused on the diagnostic test accuracy of ultrasonography for diagnosing CTS. Structured searches of PubMed for 1990-2010 were done and the data were extracted and meta-analyzed by pooling estimates of sensitivity, specificity, likelihood ratios and diagnostic odds ratios. Diagnostic performance was also judged by using a summary receiver operating characteristic curve. Twenty-eight trials involving 3995 wrists were included. A greater cross-sectional area (CSA) of the median nerve at the carpal tunnel inlet (CSA-I) and a greater flattening ratio at the level of the hamate were seen in CTS wrists than in control wrists. A CSA-I ≥9 mm(2) is the best single diagnostic criterion, with a diagnostic odds ratio of 40.4 (sensitivity 87.3%, specificity 83.3%).

Brief Report: Amelioration of collagen-induced arthritis in mice by lentivirus-mediated silencing of microRNA-223

OBJECTIVE MicroRNA (miRNA) plays a role in autoimmune diseases. MiRNA-223 (miR-223) is up-regulated in patients with rheumatoid arthritis (RA) and is involved in osteoclastogenesis, which contributes to erosive disease. The aim of this study was to test the feasibility of using lentiviral vectors expressing the miR-223 target sequence (miR-223T) to suppress miR-223 activity as a therapeutic strategy in a mouse model of collagen-induced arthritis (CIA). METHODS Levels of miR-223 in the synovial tissue of patients with RA or osteoarthritis (OA), as well as in the ankle joints of mice with CIA, were determined by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Lentiviral vectors expressing miR-223T (LVmiR-223T) or luciferase short hairpin RNA (LVshLuc) as a control vector were injected intraperitoneally into mice with CIA. Treatment responses and disease-related bone mineral density were monitored. Levels of nuclear factor 1A (NF-1A), a direct target of miR-223, and macrophage colony-stimulating factor receptor (M-CSFR), which is critical for osteoclastogenesis, were measured by immunohistochemistry and quantitative RT-PCR. Osteoclasts were assessed by tartrate-resistant acid phosphatase staining. RESULTS MiR-223 expression was significantly higher in the synovium of RA patients and in the ankle joints of mice with CIA as compared to OA patients and normal mice. LVmiR-223T treatment reduced the arthritis score, histologic score, miR-223 expression, osteoclastogenesis, and bone erosion in mice with CIA. Down-regulation of miR-223 with concomitant increases in NF-1A levels and decreases in M-CSFR levels was detected in the synovium of LVmiR-223T-treated mice. CONCLUSION This study is the first to demonstrate that lentivirus-mediated silencing of miR-223 can reduce disease severity of experimental arthritis. Furthermore, our results indicate that inhibition of miR-223 activity should be further explored as a therapeutic strategy in RA.

Two-stage cementless revision THR after infection. 5 recurrences in 40 cases followed 2.5-7 years

We revised 40 infected hip prostheses in 40 patients as a two-stage procedure, including intravenous and oral antibiotics, gentamicin beads, and delayed cementless implantation of porous-coated THR. The duration of antibiotic treatment was 8 weeks. The interval from resection to reimplantation was, on average, 48 (8-108) weeks. 39 patients were followed, on average, 4 (2.5-7) years. 5 patients had a recurrent infection. In patients who did not have a recurrent infection, the Harris hip score exceeded 80 in 32 patients. Radiographically, femoral component migration of 2-6 mm was noted in 3 cases. The recurrent infection rate, and the functional and radiographic results are comparable with those obtained using a two-stage procedure with antibiotic cement.

T helper cells promote disease progression of osteoarthritis by inducing macrophage inflammatory protein-1γ

OBJECTIVE Immune cells are involved in the pathogenesis of osteoarthritis (OA). We examined the effects of T helper (Th) cells, which induce the expression of macrophage inflammatory protein (MIP-1γ), on the progression of OA. DESIGN Using anterior cruciate ligament-transection (ACLT), we induced OA in one hind-leg knee joint of B6 mice. The CD4(+) T cells from splenocytes and synovium were flow-cytometrically and immunochemically evaluated, respectively. The knee joints were histologically assessed for manifestations of OA. MIP-1γ levels and nuclear factor-κB (NF-κB) in the knee joints were measured using enzyme-linked immunosorbent and immunoblotting assays, respectively; osteoclastogenesis was detected by tartrate-resistant acid phosphatase (TRAP) staining. The inflammatory responses and MIP-1γ expression were examined using immunohistochemistry. RESULTS The number of CD4(+) T cells and the expression of interferon-γ (IFN-γ) increased during OA onset (30 days after ACLT) and then decreased at a later stage of OA (90 days after ACLT). Tissue damage induced by CD4(+) T cells was evident at the later stage. The activation of CD4(+) T cells induced the expression of MIP-1γ and NF-κB. The expression of MIP-1γ can be detected in synovium which CD4(+) T cells were infiltrated. The increased MIP-1γ expression caused an increase in the number of osteoclasts in joints. The regulation of CD4(+) T cells was accompanied by increased macrophage infiltration and matrix metalloproteinase (MMP)-9 expression. Histopathological examinations revealed that CD4(+) T cell knockout (CD4(-/-)) mice had less expression of MIP-1γ and slower cartilage degeneration than control mice had. CONCLUSIONS CD4(+) T cells were activated during the onset of OA, but cartilage damage was more prominent at a later stage. CD4(+) T cells were involved in the pathogenesis of OA: they induced MIP-1γ expression and subsequent osteoclast formation.

Intraarticular gene transfer of thrombospondin-1 suppresses the disease progression of experimental osteoarthritis

In osteoarthritis, angiogenesis, which occurs in the osteochondral junction and synovium, may accelerate inflammation and contribute to the severity of the disease. We used anterior cruciate ligament‐transection (ACLT) to investigate the therapeutic effect of an angiogenesis inhibitor, thrombospondin‐1 (TSP‐1), in a rat model of osteoarthritis. Osteoarthritis was induced in Wistar rats in the knee of one hind leg. After ACLT, AdTSP‐1 (adenoviral vector encoding mouse TSP‐1) was intraarticularly injected into the knee joints. Transgene expression, angiogenesis, and inflammatory responses in the knee joints were examined. They were also assessed morphologically, radiographically, and histologically for manifestations of disease. The levels of TSP‐1 peaked on day 3 and were substantially maintained for at least 9 days after AdTSP‐1 infection. Adenovirus‐mediated gene expression was detected in the synovial membrane and chondrocytes. TSP‐1 gene transfer induced transforming growth factor‐β (TGF‐β) production, but it reduced microvessel density, macrophage infiltration, and interleukin‐1β (IL‐1β) levels. Gross morphological and histopathological examinations revealed that rats treated with AdTSP‐1 had less severe osteoarthritis than controls. In vivo adenovirus‐mediated TSP‐1 gene transfer significantly reduced microvessel density, inflammation, and suppressed the progression of osteoarthritis. This study provides potential applications of TSP‐1 gene delivery for treating osteoarthritis. Published by Wiley Periodicals, Inc. J Orthop Res 28:1300–1306, 2010

Temporary drainage clamping after total knee arthroplasty: a meta-analysis of randomized controlled trials.

Drainage-clamping methods are thought to be effective in reducing blood loss after total knee arthroplasty (TKA). We conducted a systematic review to examine if these methods were effective without increasing the risk of complications. After a comprehensive search, 6 randomized controlled trials involving 603 knees and comparing clamping drainage and the immediate release of the drain after elective TKA were included in this analysis. The results demonstrated that drainage clamping could decrease the volume of drainage, but only clamping for no less than 4 hours could reduce the true blood loss. There was no significant difference between the 2 groups regarding blood transfusion, postoperative range of motion, incidence of thromboembolic events, and wound complications. The current evidence cannot confirm the advantage of clamping drainage after TKA.

Adenovirus-Mediated Kallistatin Gene Transfer Ameliorates Disease Progression in a Rat Model of Osteoarthritis Induced by Anterior Cruciate Ligament Transection

In osteoarthritis (OA), inflammation and apoptosis are two important factors contributing to disease progression. As kallistatin can suppress inflammatory responses and reduce cell apoptosis, we investigated the therapeutic effect of kallistatin gene transfer in the rat model of OA by anterior cruciate ligament transection (ACLT). OA was induced in Wistar rats by ACLT in the knee of one hind limb. Adenoviral vector encoding human kallistatin (AdHKBP) was injected intraarticularly into the knee joints after ACLT. The viral effect on tissue was evaluated. The inflammatory responses and transgene expression were determined by immunoblot analysis, enzyme-linked immunosorbent assay, and immunohistochemistry. Apoptosis of chondrocytes was quantified by TUNEL assay. The effects of kallistatin in combination with hyaluronic acid (HA) on the medial femoral condyles and synovia were also assessed histologically. Inflammation trigged by the vectors was limited. Expression of human kallistatin after intraarticular injection was identified. Kallistatin gene transfer reduced the levels of interleukin-1beta and tumor necrosis factor-alpha in joints. Examination of gross morphology revealed that rats treated with AdHKBP had reduced severity of OA compared with control rats treated with adenoviral vector encoding green fluorescent protein (AdGFP). The protective effect of kallistatin on cartilage was accompanied by a decrease in apoptotic cells. Intraarticular administration of AdHKBP, when in conjunction with HA, significantly improved knee joint histologic scores. These results suggest that local administration of adenoviral vectors encoding kallistatin significantly suppressed OA progression, accompanied by reduction of inflammatory response and apoptosis. Thus, kallistatin gene therapy may be a potential treatment for OA.

Spinal somatosensory evoked potential to evaluate neurophysiologic changes associated with postlaminotomy fibrosis: an experimental study.

Study Design. We evaluated electrophysiologic changes of the cauda equina after lumbar laminotomy in rats. Objective. To clarify immediate and long-term electrophysiologic and neurologic responses in an experimental postlaminotomy animal fibrosis model. Summary of Background Data. Postspinal surgery-induced epidural fibrosis is assessed using either Gadolinium- enhanced magnetic resonance imaging (MRI) or intraoperative observations. In experimental animal models mimicking this complication, many approaches are used: advanced imaging (computed tomography, CT; and MRI), functional observations, biomechanical techniques, and histologic examinations. However, no study has reported the substantial neurophysiologic changes of the cauda equina in such a model. Methods. Rats were given a sham operation (laminar exposure only), a left L5 hemilaminotomy alone, or a left L5 hemilaminotomy with extradural topical collagen. Mixed-nerve-elicited somatosensory-evoked potentials (M-SSEPs) and dermatomal (D)-SSEPs were recorded at the thoracolumbar junction after percutaneous stimulation of the posterior tibial nerve at the bilateral medial ankles and the L5 dermatomal field, respectively. Potentials recorded on the operated and nonoperated sides before surgery and then 30 minutes, 2 weeks, and 1, 2, and 3 months after surgery were compared. Walking track and thermal hyperalgesia test results and a final histologic analysis of perineural fibrosis were correlated. Results. Electrical stimulation yielded reproducible responses in all rats on all tests. Preoperative and postoperative measurements showed no statistically significant differences in M-SSEP or D-SSEP. Postoperative D-SSEPs in both experimental groups showed significant reductions in relative amplitude, but the M-SSEPs of all groups and D-SSEPs of the control groups remained constant. Conclusion. SSEP is valuable for detecting electrophysiologic changes after laminotomy fibrosis, but acceptable accuracy requires proper stimulation and recording settings. D-SSEP monitoring provided reliable, useful information about the functional integrity of the cauda equina in this animal model. We recommend D-SSEP monitoring as a supplemental tool for quantifying the effect of postlaminotomy fibrosis on neuropathy.

Amelioration of collagen-induced arthritis in rats by adenovirus-mediated PTEN gene transfer.

OBJECTIVE The phosphatidylinositol 3-kinase (PI 3-kinase)/Akt pathway is known to be activated in rheumatoid arthritis (RA) synovial tissue, which impacts cell growth, proliferation, survival, and migration. Phosphatase and tensin homolog deleted from chromosome 10 (PTEN) functions as a negative regulator of PI 3-kinase signaling, thus blocking Akt activation. The aim of this study was to examine the effect of PTEN gene transfer in rats with collagen-induced arthritis (CIA). METHODS Adenoviral vectors encoding human PTEN (AdPTEN) or beta-galactosidase (AdLacZ) were injected intraarticularly into rats with CIA, and their treatment responses were monitored by measures of clinical, radiographic, and histologic changes. The expression of phosphorylated Akt, total Akt, vascular endothelial growth factor (VEGF), proinflammatory cytokines, and chemokines, as well as the extent of microvessel density in the ankle joints were determined. RESULTS AdPTEN treatment reduced Akt phosphorylation and decreased VEGF production in human RA synovial fibroblasts. Compared with AdLacZ treatment of the rats with CIA, AdPTEN treatment significantly reduced ankle circumference, articular index scores, radiography scores, and histology scores, and also decreased microvessel density and levels of VEGF and interleukin-1beta. Furthermore, PTEN gene transfer led to down-regulation of Akt activation and increased apoptosis in the ankle joints. CONCLUSION This study is the first to demonstrate the in vivo effect of intraarticular gene delivery of PTEN on amelioration of arthritis symptoms in rats with CIA, which involved antiangiogenic, antiproliferative, and antiinflammatory effects of PTEN via inhibition of the PI 3-kinase/Akt signaling pathway. Our findings also implicate the PI 3-kinase/Akt pathway as a therapeutic target for the treatment of RA or other inflammatory diseases.