scholarly journals Du Huo Ji Sheng Tang relieves knee osteoarthritis via suppressing NLRP3/NF-κB inflammatory signals in rats

2020 ◽  
Vol 18 ◽  
pp. 205873922094262
Author(s):  
Wenjin Chen ◽  
Jianwei Wang ◽  
Zhen Hua ◽  
Yafeng Zhang
Keyword(s):  
Synovial Fluid ◽  
Knee Joint ◽  
Synovial Membrane ◽  
Dose Group ◽  
Serum Levels ◽  
Caspase 1 ◽  
Inflammatory Signals ◽  
Tnf Α ◽  
Swelling Volume ◽  
And Cartilage

Knee osteoarthritis (KOA) is a common chronic disease in the elderly and leads to a high rate of disability. Du Huo Ji Sheng Tang (DHJST), a Chinese traditional medicinal formula, is a classic prescription for the treatment of KOA. Here, we investigated whether DHJST could inhibit inflammation and treat KOA through suppressing NLRP3/nuclear factor (NF)-κB inflammatory signals in rats. The serum levels of interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor (TNF)-α, NLRP3, ASC, Caspase-1, p-NF-κB-P65, and p-IκBa were detected in healthy adults and patients with KOA before and after treatment. Sprague Dawley (SD) rats were divided into normal group, model group, diclofenac sodium group (5 mg/kg), DHJST high-dose group (1 g/kg), and DHJST low-dose group (0.5 g/kg). The right hind knee joint of the rats, except normal group, was injected with 4% papain (0.25 mL/kg) once every 7 days for three times. All rats were treated for 3 weeks. The swelling volume of right hind paw; five classification of inflammatory cells in synovial fluid; pathological changes of the knee-joint synovial membrane and cartilage; levels of IL-1β, IL-6, and TNF-α in serum and knee-joint synovial fluid; and the expressions of NLRP3/NF-κB inflammatory signals in the knee-joint synovial membrane were detected. The serum levels of IL-1β, IL-6, IL-10, TNF-α, NLRP3, ASC, Caspase-1, p-NF-κB-P65, and p-IκBa in KOA patients treated with DHJST were significantly decreased. The KOA rats treated with DHJST showed significant decreases in swelling volume of right hind paws; the percentage of leukocyte, lymphocyte, neutrophil, and eosinophils in synovial fluid; the levels of IL-1β, IL-6, and TNF-α in serum and knee-joint synovial fluid; and the expressions of NLRP3 ASC, Caspase-1, IL-1β, p-NF-κB-P65, and p-IκBa in the knee-joint synovial membrane, and showed an alleviation in pathological changes of the knee-joint synovial membrane and cartilage. Our data provide the first evidence that DHJST relieves KOA via suppressing NLRP3/NF-κB inflammatory signals in rats

scholarly journals Hyaluronic acid synthesis, degradation, and crosslinking in equine osteoarthritis: TNF-α-TSG-6-mediated HC-HA formation

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Diana C. Fasanello ◽  
Jin Su ◽  
Siyu Deng ◽  
Rose Yin ◽  
Marshall J. Colville ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hyaluronic Acid ◽  
Synovial Fluid ◽  
Complex Formation ◽  
Synovial Membrane ◽  
Fluid Composition ◽  
Fluid Viscosity ◽  
Tnf Α ◽  
Ha Synthase ◽  
And Cartilage

Abstract Background TNF-α-stimulated gene 6 (TSG-6) protein, a TNF-α-responsive hyaladherin, possesses enzymatic activity that can catalyze covalent crosslinks of the polysaccharide hyaluronic acid (HA) to another protein to form heavy chain-hyaluronic acid (HC-HA) complexes in pathological conditions such as osteoarthritis (OA). Here, we examined HA synthase and inflammatory gene expression; synovial fluid HA, TNF-α, and viscosity; and TSG-6-mediated HC-HA complex formation in an equine OA model. The objectives of this study were to (1) evaluate the TNF-α-TSG-6-HC-HA signaling pathway across multiple joint tissues, including synovial membrane, cartilage, and synovial fluid, and (2) determine the impact of OA on synovial fluid composition and biophysical properties. Methods HA and inflammatory cytokine concentrations (TNF-α, IL-1β, CCL2, 3, 5, and 11) were analyzed in synovial fluid from 63 OA and 25 control joints, and HA synthase (HAS1-3), TSG-6, and hyaluronan-degrading enzyme (HYAL2, HEXA) gene expression was measured in synovial membrane and cartilage. HA molecular weight (MW) distributions were determined using agarose gel electrophoresis and solid-state nanopore measurements, and HC-HA complex formation was detected via immunoblotting and immunofluorescence. SEC-MALS was used to evaluate TSG-6-mediated HA crosslinking, and synovial fluid and HA solution viscosities were analyzed using multiple particle-tracking microrheology and microfluidic measurements, respectively. Results TNF-α concentrations were greater in OA synovial fluid, and TSG6 expression was upregulated in OA synovial membrane and cartilage. TSG-6-mediated HC-HA complex formation was greater in OA synovial fluid and tissues than controls, and HC-HA was localized to both synovial membrane and superficial zone chondrocytes in OA joints. SEC-MALS demonstrated macromolecular aggregation of low MW HA in the presence of TSG-6 and inter-α-inhibitor with concurrent increases in viscosity. Conclusions Synovial fluid TNF-α concentrations, synovial membrane and cartilage TSG6 gene expression, and HC-HA complex formation were increased in equine OA. Despite the ability of TSG-6 to induce macromolecular aggregation of low MW HA with resultant increases in the viscosity of low MW HA solutions in vitro, HA concentration was the primary determinant of synovial fluid viscosity rather than HA MW or HC-HA crosslinking. The TNF-α-TSG-6-HC-HA pathway may represent a potential therapeutic target in OA.

scholarly journals The role of oxidative and nitrosative stress in the pathology of osteoarthritis: Novel candidate biomarkers for quantification of degenerative changes in the knee joint

2018 ◽  
Vol 10 (2) ◽  
Author(s):  
Alexander Franz ◽  
Laura Joseph ◽  
Constantin Mayer ◽  
Jan-Frieder Harmsen ◽  
Holger Schrumpf ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Synovial Fluid ◽  
Knee Joint ◽  
Human Serum ◽  
Synovial Membrane ◽  
Nitrosative Stress ◽  
Control Groups ◽  
Oxidative And Nitrosative Stress ◽  
And Oxidative Stress

Osteoarthritis (OA) is the most frequently diagnosed joint disorder worldwide with increasing prevalence and crucial impact on the quality of life of affected patients through chronic pain, decreasing mobility and invalidity. Although some risk factors, such as age, obesity and previous joint injury are well established, the exact pathogenesis of OA on a cellular and molecular level remains less understood. Today, the role of nitrosative and oxidative stress has not been investigated conclusively in the pathogenesis of OA yet. Therefore, the objective of this study was to identify biological substances for oxidative and nitrosative stress, which mirror the degenerative processes in an osteoarthritic joint. 69 patients suffering from a diagnosed knee pain participated in this study. Based on the orthopedic diagnosis, patients were classified into an osteoarthritis group (OAG, n=24) or in one of two control groups (meniscopathy, CG1, n=11; anterior cruciate ligament rupture, CG2, n=34). Independently from the study protocol, all patients underwent an invasive surgical intervention which was used to collect samples from the synovial membrane, synovial fluid and human serum. Synovial biopsies were analyzed histopathologically for synovitis (Krenn-Score) and immunohistochemically for detection of end products of oxidative (8-isoprostane F2α) and nitrosative (3-nitrotyrosine) stress. Additionally, the fluid samples were analyzed for 8-isoprostane F2α and 3-nitrotyrosine by competitive ELISA method. The analyzation of inflammation in synovial biopsies revealed a slight synovitis in all three investigated groups. Detectable concentrations of 3-nitrotyrosine were reported in all three investigated groups without showing any significant differences between the synovial biopsies, fluid or human serum. In contrast, significant increased concentrations of 8-isoprostane F2α were detected in OAG compared to both control groups. Furthermore, our data showed a significant correlation between the histopathological synovitis and oxidative stress in OAG (r=0.728, P<0.01). There were no significant differences between the concentrations of 8-isoprostane F2α in synovial fluid and human serum. The findings of the current study support the hypothesis that oxidative and nitrosative stress are components of the multi-factory pathophysiological formation of OA. It seems reasonable that an inflammatory process in the synovial membrane triggers the generation of oxidative and nitrosative acting substances which can lead to a further degradation of the articular cartilage. Based on correlations between the observed degree of inflammation and investigated biomarkers, especially 8-isoprostane F2α seems to be a novel candidate biomarker for OA. However, due to the finding that also both control groups showed increased concentrations of selected biomarkers, future studies have to validate the diagnostic potential of these biomarkers in OA and in related conditions of the knee joint.

scholarly journals Trifluorobenzamidine prevents allergic rhinitis by regulating IgE, IL-4 and IL-5 in T-cells

2020 ◽  
Vol 19 (5) ◽  
pp. 1023-1029
Author(s):  
Yongbo Zhang ◽  
Zhuo Wu ◽  
Yihui Yang ◽  
Lu Ding
Keyword(s):  
Allergic Rhinitis ◽  
Serum Levels ◽  
Eosinophil Infiltration ◽  
Spleen Weight ◽  
Caspase 1 ◽  
Tnf Α ◽  
Cytokine Levels ◽  
Enzymelinked Immunosorbent Assay ◽  
Inhibitory Potential ◽  
New Treatment

Purpose: To investigate the effect of trifluorobenzamidine (TBI) on a mouse model of ovalbumin (OVA)- induced allergic rhinitis. Methods: Allergic rhinitis was established in mice via sensitization on days 1, 5 and 14 through intraperitoneal injection of OVA (100 μg) in PBS. On day 15, the mice were subjected to intranasal exposure to OVA (1.5 mg dissolved in PBS). Prior to 10 days of intranasal exposure to OVA, the micewere treated with TBI at doses of 5, 10 and 20 μg/kg. Cytokine levels were determined using enzymelinked immunosorbent assay (ELISA) kits, while cyclooxygenase (COX)-2 and caspase-1 activity were assayed with western blotting. Results: Treatment with TBI significantly (p < 0.05) reduced OVA-mediated increases in nasal rub scores, and decreased serum levels of IgE, TNF-α, thymic stromal lymphopoietin (TSLP), IL-1β and histamine in mice. It also significantly regulated spleen weight and IL-4 secretion (p < 0.05) in OVAadministered mice. TBI significantly downregulated the expressions of IL-5, IL-13, TNFα, TSLP, IL-1β and IL-6 (p < 0.05). Administration of TBI caused a marked reduction in OVA-mediated increase in caspase-1 activity in mice intranasal tissues, and also significantly reduced OVA-induced excessive production of MIP-2 and ICAM-1 (p < 0.05). Moreover, TBI prevented OVA-induced infiltration of eosinophils and mast cells into intranasal tissues (p < 0.05). Conclusion: TBI reduces levels of IgE and various pro-inflammatory cytokines in OVA-administered mice. It also regulates Th1:Th2 ratio, inhibited activity of caspase-1, suppressed mast cell/eosinophil infiltration and reduced ICAM-1 and MIP-2 levels. Therefore, TBI possesses inhibitory potential against rhinitis allergy, and thus can potentially be developed as a new treatment strategy for asthma. Keywords: Trifluorobenzamidine, Anti-inflammation, Allergic rhinitis, Cytokines, Caspase-1, Itching

scholarly journals Comparison of serum and synovial fluid IL-1β, IL-18, TNF-α and Caspase-1 levels between OA knee patients taking Colchicine vs NSAIDS

2018 ◽  
Vol 26 ◽  
pp. S307
Author(s):  
R.R. Sahoo ◽  
U. Dhakad ◽  
R. Srivastava ◽  
M. Singh ◽  
S.K. Das
Keyword(s):  
Synovial Fluid ◽  
Caspase 1 ◽  
Tnf Α

scholarly journals Myrtenal and β-caryophyllene oxide screened from Liquidambaris Fructus suppress NLRP3 inflammasome components in rheumatoid arthritis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wen-xuan Li ◽  
Ping Qian ◽  
Yi-tong Guo ◽  
Li Gu ◽  
Jessore Jurat ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Molecular Docking ◽  
Nlrp3 Inflammasome ◽  
Network Pharmacology ◽  
Caryophyllene Oxide ◽  
Active Ingredients ◽  
Caspase 1 ◽  
Tnf Α ◽  
Cartilage Erosion ◽  
And Cartilage

Abstract Background Liquidambaris Fructus (LF) is the infructescence of Liquidambar formosana. In Traditional Chinese Medicine, LF has been used to treat joint pain, a common symptom of arthritis and rheumatism; however, a lack of pharmacological evidence has limited its applications in modern clinics. Therefore, this study aims to explore the protective effect of LF on rheumatoid arthritis (RA) and to identify its active ingredients. Methods Rats with adjuvant-induced arthritis (AIA) were divided into 4 groups and administered petroleum ether extract of LF (PEL), ethyl acetate extract of LF (EEL), water extract of LF (WEL), or piroxicam (PIR) respectively for 3 weeks. Two additional groups were used as normal control (NC) and model control (MC) and administered distilled water as a placebo. The clinical scores for arthritis, bone surface, synovial inflammation and cartilage erosion were used to evaluate the therapeutic efficacy of each treatment. The serum IL-1β and TNF-α level and the expression of NLRP3, IL-1β and caspase-1 p20 in the synovial tissue of AIA rats were evaluated by ELISA and Western blot. The active ingredients of LF were investigated using network pharmacology and molecular docking methods, and their inhibition of NLRP3 inflammasome activation was verified in the human rheumatoid arthritis fibroblast-like synovial cells (RA-FLS) model. Results PEL could alleviate paw swelling, bone and joint destruction, synovial inflammation and cartilage erosion in the AIA rats, with significantly superior efficacy to that of EEL and WEL. PEL reduced IL-1β and TNF-α serum levels, and attenuated the upregulation of NLRP3, IL-1β and caspase-1 p20 expression in the synovial tissue of AIA rats. Network pharmacology and molecular docking results indicated that myrtenal and β-caryophyllene oxide were the main two active ingredients of PEL, and these two compounds showed significant inhibition on TNF-α, NLRP3, IL-1β and caspase-1 p20 expression in RA-FLS. Conclusions Myrtenal and β-caryophyllene oxide screened from PEL could suppress the activation of NLRP3 inflammasome, thereby alleviating RA symptoms.

Expression of caspase activation recruitment and pyrin domain levels of apoptosis-associated speck-like protein complex in the pancreas of rats subjected to experimental pancreatitis

2013 ◽  
Vol 33 (9) ◽  
pp. 940-948 ◽  
Author(s):  
R Aruna ◽  
A Geetha ◽  
P Suguna
Keyword(s):  
Mrna Expression ◽  
Messenger Rna ◽  
Experimental Period ◽  
Serum Levels ◽  
Activity Levels ◽  
Caspase Activation ◽  
Caspase 1 ◽  
Pyrin Domain ◽  
Tnf Α ◽  
Factor Α

The present study investigated the effect of rutin, a natural flavonoid, on the expression of caspase activation recruitment domain (CARD) and pyrin domain (PYD) of apoptosis-associated speck-like protein (ASC), a mediator of inflammation, in the pancreas of rats administered with ethanol (EtOH) and high-fat diet (HFD). Pancreatitis was induced in male albino Wistar rats by administering EtOH (8–12 g/kg/day) and HFD (22% fat) for 90 days. In addition, rats also received 100 mg rutin/kg body weight orally from 31st day till the experimental period. Serum levels of cytokines, interleukin 18 (IL-18) and IL-6; activity levels of caspase-1 and myeloperoxidase (MPO); messenger RNA (mRNA) expression of tumor necrosis factor α (TNF-α), caspase-1, CARD and PYD of ASC; and histological changes in pancreas were assessed. We observed a significant elevation in serum IL-18, IL-6, caspase-1 and MPO activities, mRNA expression of PYD, TNF-α and caspase-1 in the pancreas of rats administered with EtOH and HFD. Rutin administration along with EtOH and HFD significantly upregulated the mRNA expression of CARD and downregulated PYD, caspase-1, and TNF-α expressions. Rutin supplementation was also found to reduce IL-18 and IL-6 levels; and inflammatory changes in tissue architecture were evidenced by histological observations. The anti-inflammatory activity of rutin might be due to its effect on modulating the expression of ASC complex that mediates inflammation.

scholarly journals Caspase-1-Inhibitor AC-YVAD-CMK Inhibits Pyroptosis and Ameliorates Acute Kidney Injury in a Model of Sepsis

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Mei Yang ◽  
Jin-tao Fang ◽  
Ni-shang Zhang ◽  
Long-jiang Qin ◽  
Yang-yang Zhuang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cecal Ligation ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Serum Levels ◽  
Interleukin 18 ◽  
Tissue Samples ◽  
Caspase 1 ◽  
Tnf Α ◽  
Histologic Changes

Objective. To observe the protective effect of AC-YVAD-CMK on sepsis-induced acute kidney injury in mice and to explore its possible mechanisms primarily. Methods. Eighteen male C57BL/6 mice were randomly divided into sham-operated group (Control), cecal ligation and puncture group (CLP), and CLP model treated with AC-YVAD-CMK group (AC-YVAD-CMK) ( n = 6 in each group). Mice were sacrificed at 24 h after operation, and blood and kidney tissue samples were collected for analyses. Histologic changes were determined microscopically following HE staining. The expression of Ly-6B and CD68 was investigated using immunohistochemistry. Serum concentrations of creatinine (sCR) and blood urea nitrogen (BUN) were measured. Serum levels of interleukin-1β (IL-1β), interleukin-18 (IL-18), TNF-α, and interleukin-6 (IL-6) were determined by ELISA. The expressions of Caspas-1, NLRP-1, IL-1β, and IL-18 in renal tissues were investigated using Western blot. Immunofluorescence staining was used to detect the expression of GSDMD protein in renal tissues. Results. AC-YVAD-CMK treatment significantly alleviates sepsis-induced acute kidney injury, with decreased histological injury in renal tissues, suppresses the accumulation of neutrophils and macrophages in renal tissues, and decreased sCR and BUN level ( P < 0.05 ). Attenuation of sepsis-induced acute kidney injury was due to the prohibited production of inflammatory cytokines and decrease expression of Caspas-1, NLRP-1, IL-1β, and IL-18 in renal tissues. In addition, AC-YVAD-CMK treatment significantly reduced the expression of GSDMD in renal tissues compared to those observed in controls ( P < 0.05 ). Conclusions. We demonstrated a marked renoprotective effect of caspase-1-inhibitor AC-YVAD-CMK in a rat model of sepsis by inhibition of pyroptosis.

scholarly journals The Protective Effect of Dietary Administration of Puerarin on Canine Osteoarthritis Model With Anterior Cruciate Ligament Transected

2020 ◽  
Author(s):  
Tianwen Ma ◽  
Yajing Wen ◽  
Xiaopeng Song ◽  
Hailong Hu ◽  
Yue Li ◽  
...  
Keyword(s):  
Anterior Cruciate Ligament ◽  
Synovial Fluid ◽  
Protective Effect ◽  
Cruciate Ligament ◽  
Cartilage Degradation ◽  
Inflammatory Factor ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Anterior Cruciate ◽  
And Cartilage

Abstract BackgroundLameness caused by osteoarthritis (OA) is one of the main causes of disability in elderly dogs. Non-steroidal anti-inflammatory drugs (NSAIDs) are important tools in the treatment of canine OA. In recent years, due to the many side effects of NSAIDs, patients cannot tolerate or do not want to take the risk of NSAIDs. People are becoming more and more interested in new treatments for canine OA, and so-called nutritional supplements have emerged. Puerarin has a wide range of pharmacological activities and is often used as a clinical prescription drug and dietary supplement in China. However, the effect of puerarin on canine OA has not been evaluated. Therefore, the purpose of this study is to evaluate the anti-inflammatory and anti-cartilage degradation effects of puerarin in a canine OA model induced by anterior cruciate ligament transection (ACLT), and to detect the serum inflammatory factor interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) levels and cartilage degradation biomarker C-terminal telopeptides of collagen type II (CTX-II), cartilage oligomeric matrix protein (COMP) and chondroitin sulfate 846 epitope (CS 846) levels in serum and synovial fluid at different periods of puerarin administration. ResultsEight weeks after the administration, the veterinarian performed clinical and imaging evaluations to comprehensively evaluate the protective effect of puerarin on canine OA. Daily oral administration of 20 mg/kg puerarin can significantly inhibit the expression of IL-1β, IL-6 and TNF-α in serum within 8 weeks (P < 0.05), and its anti-inflammatory effect is similar to oral celecoxib (negative control group). Puerarin has a certain protective effect on articular cartilage and can reduce the level of biomarkers CTX-II, COMP and CS 846 in serum and synovial fluid in the early stage of OA (P < 0.05). In addition, the clinical scores and radiographs scores were significantly reduced after 8 weeks of puerarin treatment (P < 0.05). ConclusionsCanine OA cartilage may be mediated through anti-inflammatory, anti-metabolism and anabolic effects, and strongly down-regulate the inflammatory factors IL-1β, IL-6 and TNF-α and cartilage degradation biomarkers CTX-II, COMP and CS 846 are related, providing a good alternative therapy for OA.

scholarly journals Device-Based Enrichment of Knee Joint Synovial Cells to Drive MSC Chondrogenesis Without Prior Culture Expansion In Vitro: A Step Closer to 1-Stage Orthopaedic Procedures

2021 ◽  
pp. 036354652110551
Author(s):  
Ala Altaie ◽  
Thomas G. Baboolal ◽  
Owen Wall ◽  
Hemant Pandit ◽  
Elena Jones ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Knee Joint ◽  
Cartilage Repair ◽  
Synovial Membrane ◽  
M2 Macrophage ◽  
Two Samples ◽  
Before And After ◽  
Joint Repair ◽  
Device Use

Background: Synovial fluid (SF) mesenchymal stem cells (MSCs) are derived from the synovial membrane and have cartilage repair potential. Their current use in clinical practice is largely exploratory. As their numbers tend to be small, therapeutic procedures using MSCs typically require culture expansion. Previous reports indicate that the stem cell–mobilizing device (STEM device) intraoperatively increases SF-MSCs. Purpose: This study evaluated the chondrogenic potential of non–culture expanded synovium-mobilized MSCs and SF-microfragments obtained after enrichment using the STEM device and ascertained if device-mediated synovial membrane manipulation facilitated ongoing MSC release. Study Design: Controlled laboratory study. Methods: Two samples of aspiration fluid were collected intraoperatively before and after STEM device utilization from patients (n = 16) undergoing diagnostic or therapeutic knee arthroscopy. Human knee synovium (n = 5) was collected during total knee replacement, and a suspended culture was performed to assess the effect of the STEM device on ongoing MSC release. Colony forming unit–fibroblastic assays were used to determine the number of MSCs. Additionally, cytometric characterization of stromal and immune cells and chondrogenesis differentiation assay were performed without culture expansion. Filtered platelet concentrates were prepared using the HemaTrate system. Results: After STEM device use, a significant increase was evident in SF-MSCs ( P = .03) and synovial fluid–resident synovial tissue microfragments ( P = .03). In vitro–suspended synovium released significantly more MSCs following STEM device use than nonstimulated synovium ( P = .01). The STEM device–released total cellular fraction produced greater in vitro chondrogenesis with significantly more glycosaminoglycans (GAGs; P < .0001) when compared with non–STEM device synovial fluid material. Nonexpanded SF-MSCs and SF-microfragments combined with autologous filtered platelet concentrate produced significantly more GAGs than the complete chondrogenic media ( P < .0001). The STEM device–mobilized cells contained more M2 macrophage cells and fewer M1 cells. Conclusion: Non–culture expanded SF-MSCs and SF-microfragments had the potential to undergo chondrogenesis without culture expansion, which can be augmented using the STEM device with increased MSC release from manipulated synovium for several days. Although preliminary, these findings offer proof of concept toward manipulation of the knee joint environment to facilitate endogenous repair responses. Clinical Relevance: Although numbers were small, this study highlights 3 factors relevant to 1-stage joint repair using the STEM device: increased SF-MSCs and SF-microfragments and prolonged synovial release of MSCs. Joint repair strategies involving endogenous MSCs for cartilage repair without the need for culture expansion in a 1-stage procedure may be possible.

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