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Lin-Hsiu Weng

Bio: Lin-Hsiu Weng is an academic researcher from Chang Gung University. The author has contributed to research in topics: Osteoarthritis & Cartilage. The author has an hindex of 7, co-authored 8 publications receiving 421 citations.

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TL;DR: Extracorporeal shockwave therapy appeared to be more effective and safer than traditional conservative treatments in the management of patients with chronic patellar tendinopathy.
Abstract: BackgroundChronic patellar tendinopathy is an overuse syndrome with pathologic changes similar to tendinopathies of the shoulder, elbow, and heel. Extracorporeal shockwave was shown effective in many tendinopathies.HypothesisExtracorporeal shockwave therapy may be more effective than conservative treatment for chronic patellar tendinopathy.Study DesignRandomized controlled clinical trial; Level of evidence, 2.MethodsThis study consisted of 27 patients (30 knees) in the study group and 23 patients (24 knees) in the control group. In the study group, patients were treated with 1500 impulses of extracorporeal shockwave at 14 KV (equivalent to 0.18 mJ/mm 2 energy flux density) to the affected knee at a single session. Patients in the control group were treated with conservative treatments including nonsteroidal anti-inflammatory drugs, physiotherapy, exercise program, and the use of a knee strap. The evaluation parameters included pain score, Victorian Institute of Sports Assessment score, and ultrasonographi...

137 citations

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TL;DR: Interference with the cartilage- and bone-deleterious actions of Dkk-1 provides therapeutic potential for alleviating cartilage destruction and subchondral bone damage in OA knee joints.
Abstract: Objective Perturbation of Wnt signaling components reportedly regulates chondrocyte fate and joint disorders. The Wnt inhibitor Dkk-1 mediates remodeling of various tissue types. We undertook this study to examine whether control of Dkk-1 expression prevents joint deterioration in osteoarthritic (OA) knees. Methods Anterior cruciate ligament transection–and collagenase-induced OA in rat knees was treated with end-capped phosphorothioate Dkk-1 antisense oligonucleotide (Dkk-1–AS). Articular cartilage destruction, cartilage degradation markers, bone mineral density (BMD), and subchondral trabecular bone volume of injured knee joints were measured using Mankin scoring, enzyme-linked immunosorbent assay, dual x-ray absorptiometry, and histomorphometry. Dkk-1–responsive molecule expression and apoptotic cells in knee tissue were detected by quantitative reverse transcriptase–polymerase chain reaction, immunoblotting, and TUNEL staining. Results Up-regulated Dkk-1 expression was associated with increased Mankin score and with increased serum levels of cartilage oligomeric matrix protein and C-telopeptide of type II collagen (CTX-II) during OA development. Dkk-1–AS treatment alleviated OA-associated increases in Dkk-1 expression, Mankin score, cartilage fibrillation, and serum cartilage degradation markers. Dkk-1–AS also alleviated epiphyseal BMD loss and subchondral bone exposure associated with altered serum levels of osteocalcin and CTX-I. The treatment abrogated chondrocyte/osteoblast apoptosis and subchondral trabecular bone remodeling in OA. Dkk-1 knockdown increased levels of nuclear β-catenin and phosphorylated Ser473-Akt but attenuated expression of inflammatory factors (Toll-like receptor 4 [TLR-4], TLR-9, interleukin-1β, and tumor necrosis factor α), the apoptosis regulator Bax, matrix metalloproteinase 3, and RANKL in OA knee joints. Conclusion Interference with the cartilage- and bone-deleterious actions of Dkk-1 provides therapeutic potential for alleviating cartilage destruction and subchondral bone damage in OA knee joints.

109 citations

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TL;DR: It appears that VEGF modulates angiogenesis and osteogenesis in shockwave-promoted bone healing in rabbits.

59 citations

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TL;DR: Dkk-1 promoted angiogenic and cartilage degradation activities in synovial fibroblasts, which acceleratedsynovial angiogenesis and cart tissue destruction in osteoarthritic joints.
Abstract: Objective Synovial hypervascularity is a prominent pathologic feature in osteoarthritic (OA) joints. Wnt inhibitor Dkk-1 contributes to joint remodeling. We undertook this study to investigate whether Dkk-1 regulates cartilage destruction activities in OA synovial fibroblasts. Methods Synovial tissues were harvested from knees of patients with OA and from injured knees of non-OA patients who underwent arthroscopy. Expression of Dkk-1, angiogenic factors (stromal cell–derived factor 1 and colony-stimulating factor 1), and cartilage proteinases (ADAMTS-5 and matrix metalloproteinase 3 [MMP-3]) as well as vascularity in synovium and synovial fluid were quantified using enzyme-linked immunosorbent assay, reverse transcription–polymerase chain reaction, and histomorphometry. Synovial fibroblasts were treated with interleukin-1β (IL-1β), anti–Dkk-1 antibody, and RNA interference to characterize their angiogenic activity. Rats with OA knees were administered Dkk-1 antisense oligonucleotide to verify synovial angiogenesis and cartilage integrity. Results OA synovium exhibited increased vascularity and expression of angiogenic factors and proteinases in association with up-regulated Dkk-1 levels. Neutralizing Dkk-1 reduced the inhibitory effects of OA synovial fluid on aggrecan expression in chondrocyte cultures. IL-1β induction of Dkk-1 increased expression of hypoxia-inducible factor 1α (HIF-1α), angiogenic factors, ADAMTS-5, and MMP-3 in synovial fibroblasts and promoted angiogenesis in vascular endothelial cells. Knockdown of HIF-1α decreased Dkk-1 enhancement of angiogenic factor expression. Stabilization of glycogen synthase kinase 3β phosphorylated at Ser9, β-catenin, T cell factor 4, and ERK signaling attenuated Dkk-1 up-regulation of angiogenic factor and proteinase expression in synovial fibroblasts. In vivo, Dkk-1 interference reduced the expression of angiogenic factors and proteinases and ameliorated synovial vascularity and cartilage deterioration in knees of rats with OA. Conclusion Dkk-1 promoted angiogenic and cartilage degradation activities in synovial fibroblasts, which accelerated synovial angiogenesis and cartilage destruction. Dkk-1 blockade has therapeutic potential for reducing OA-induced synovitis and joint deterioration.

47 citations

Journal ArticleDOI
TL;DR: Extracorporeal shockwave therapy shows chondroprotective effect associated with improvement in subchondral bone remodeling in the initiation of ACLT OA knee model in rats.
Abstract: Purpose This study investigated the effects of extracorporeal shockwave therapy (ESWT) on the subchondral bone and articular cartilage in the initiation of osteoarthritis of the knee in rats.

46 citations


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TL;DR: The apparent paradoxical observations that OA is associated with both increased remodelling and osteopenia, as well as decreased remodlling and sclerosis, are consistent with the spatial and temporal separation of these processes during joint degeneration.
Abstract: The classical view of the pathogenesis of osteoarthritis (OA) is that subchondral sclerosis is associated with, and perhaps causes, age-related joint degeneration. Recent observations have demonstrated that OA is associated with early loss of bone owing to increased bone remodelling, followed by slow turnover leading to densification of the subchondral plate and complete loss of cartilage. Subchondral densification is a late event in OA that involves only the subchondral plate and calcified cartilage; the subchondral cancellous bone beneath the subchondral plate may remain osteopenic. In experimental models, inducing subchondral sclerosis without allowing the prior stage of increased bone remodelling to occur does not lead to progressive OA. Therefore, both early-stage increased remodelling and bone loss, and the late-stage slow remodelling and subchondral densification are important components of the pathogenetic process that leads to OA. The apparent paradoxical observations that OA is associated with both increased remodelling and osteopenia, as well as decreased remodelling and sclerosis, are consistent with the spatial and temporal separation of these processes during joint degeneration. This Review provides an overview of current knowledge on OA and discusses the role of subchondral bone in the initiation and progression of OA. A hypothetical model of OA pathogenesis is proposed.

651 citations

Journal ArticleDOI
TL;DR: Several molecular signaling pathways such as bone morphogenetic proteins and Wnts are hypothesized to have a role in OA and can activate cellular and molecular processes in both cartilage and bone cells, which could lead to the development of specific therapeutics or treatment strategies.
Abstract: Osteoarthritis (OA) refers to a group of mechanically-induced joint disorders to which both genetic and acquired factors contribute. Current pathophysiological concepts focus on OA as a disease of the whole joint. Within these models, the functional unit formed by the articular cartilage and the subchondral bone seems to be of particular interest. Cartilage and bone receive and dissipate the stress associated with movement and loading, and are therefore continuously challenged biomechanically. Recent data support the view that cartilage and bone can communicate over the calcified tissue barrier; vessels reach out from bone into the cartilage zone, patches of uncalcified cartilage are in contact with bone, and microcracks and fissures further facilitate transfer of molecules. Several molecular signaling pathways such as bone morphogenetic proteins and Wnts are hypothesized to have a role in OA and can activate cellular and molecular processes in both cartilage and bone cells. In addition, intracellular activation of different kinase cascades seems to be involved in the molecular crosstalk between cartilage and bone cells. Further research is required to integrate these different elements into a comprehensive approach that will increase our understanding of the disease processes in OA, and that could lead to the development of specific therapeutics or treatment strategies.

536 citations

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TL;DR: Treatment of patients with chronic lateral epicondylitis with PRP reduces pain and increases function significantly, exceeding the effect of corticosteroid injection even after a follow-up of 2 years.
Abstract: Background: Platelet-rich plasma (PRP) has been shown to be a general stimulation for repair and 1-year results showed promising success percentages. Purpose: This trial was undertaken to determine the effectiveness of PRP compared with corticosteroid injections in patients with chronic lateral epicondylitis with a 2-year follow-up. Study Design: Randomized controlled trial; Level of evidence, 1. Methods: The trial was conducted in 2 Dutch teaching hospitals. One hundred patients with chronic lateral epicondylitis were randomly assigned to a leukocyte-enriched PRP group (n = 51) or the corticosteroid group (n = 49). Randomization and allocation to the trial group were carried out by a central computer system. Patients received either a corticosteroid injection or an autologous platelet concentrate injection through a peppering needling technique. The primary analysis included visual analog scale (VAS) pain scores and Disabilities of the Arm, Shoulder and Hand (DASH) outcome scores. Results: The PRP group was more often successfully treated than the corticosteroid group (P\.0001). Success was defined as a reduction of 25% on VAS or DASH scores without a reintervention after 2 years. When baseline VAS and DASH scores were compared with the scores at 2-year follow-up, both groups significantly improved across time (intention-to-treat principle). However, the DASH scores of the corticosteroid group returned to baseline levels, while those of the PRP group significantly improved (as-treated principle). There were no complications related to the use of PRP. Conclusion: Treatment of patients with chronic lateral epicondylitis with PRP reduces pain and increases function significantly, exceeding the effect of corticosteroid injection even after a follow-up of 2 years. Future decisions for application of PRP for lateral epicondylitis should be confirmed by further follow-up from this trial and should take into account possible costs and harms as well as benefits.

508 citations

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TL;DR: The overview of the existing approaches in evaluation and interpretation of IHC data can be used in bone tissue research and for either better understanding of existing scoring systems or developing a new one.
Abstract: Immunohistochemistry (IHC) is a well-established, widely accepted method in both clinical and experimental parts of medical science. It allows receiving valuable information about any process in any tissue, and especially in bone. Each year the amount of data, received by IHC, grows in geometric progression. But the lack of standardization, especially on the post-analytical stage (interpreting and reporting of results), makes the comparison of the results of different studies impossible. Comprehensive PubMED literature search with a combination of search words “immunohistochemistry” and “scoring system” was performed and 773 articles describing IHC results were identified. After further manual analysis 120 articles were selected for detailed evaluation of used approaches. Six major approaches to the interpretation and presentation of IHC analysis results were identified, analyzed and described. The overview of the existing approaches in evaluation and interpretation of IHC data, which are provided in the article, can be used in bone tissue research and for either better understanding of existing scoring systems or developing a new one. Standard multiparametric, semiquantitative IHC scoring systems should simplify and clarify the process of interpretation and reporting of received data. The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_221

445 citations

Journal ArticleDOI
TL;DR: The results indicate that osteoblast-derived VEGF plays critical roles at several stages in the repair process, and provides a basis for clinical strategies to improve bone regeneration and treat defects in bone healing.
Abstract: Osteoblast-derived VEGF is important for bone development and postnatal bone homeostasis. Previous studies have demonstrated that VEGF affects bone repair and regeneration; however, the cellular mechanisms by which it works are not fully understood. In this study, we investigated the functions of osteoblast-derived VEGF in healing of a bone defect. The results indicate that osteoblast-derived VEGF plays critical roles at several stages in the repair process. Using transgenic mice with osteoblast-specific deletion of Vegfa, we demonstrated that VEGF promoted macrophage recruitment and angiogenic responses in the inflammation phase, and optimal levels of VEGF were required for coupling of angiogenesis and osteogenesis in areas where repair occurs by intramembranous ossification. VEGF likely functions as a paracrine factor in this process because deletion of Vegfr2 in osteoblastic lineage cells enhanced osteoblastic maturation and mineralization. Furthermore, osteoblast- and hypertrophic chondrocyte-derived VEGF stimulated recruitment of blood vessels and osteoclasts and promoted cartilage resorption at the repair site during the periosteal endochondral ossification stage. Finally, osteoblast-derived VEGF stimulated osteoclast formation in the final remodeling phase of the repair process. These findings provide a basis for clinical strategies to improve bone regeneration and treat defects in bone healing.

388 citations