Differential Cytotoxicity of Corticosteroids on Human Mesenchymal Stem Cells
Background Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have shown the deleterious effects of corticosteroids on chondrocytes, suggesting a potentiation of degenerative joint disease. Mesenchymal stem cel...
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Published in | Clinical orthopaedics and related research Vol. 473; no. 3; pp. 1155 - 1164 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Boston
Springer US
01.03.2015
Lippincott Williams & Wilkins Ovid Technologies |
Subjects | |
Online Access | Get full text |
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Abstract | Background
Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have shown the deleterious effects of corticosteroids on chondrocytes, suggesting a potentiation of degenerative joint disease. Mesenchymal stem cells (MSCs) are the direct progenitors of chondrocytes and other musculoskeletal tissue. Additionally, they serve an important antiinflammatory role, which can combat the chronic inflammatory state that mediates degenerative joint disease. Little is known about how corticosteroids interact with this regenerative and reparative cell population.
Questions/purposes
We asked: (1) Are corticosteroids cytotoxic to MSCs in a dose–response fashion? (2) Is there a differential effect in the level of cytotoxicity to MSCs between commercially available corticosteroid preparations?
Methods
Human MSCs were isolated and cultured from periarticular adipose tissue obtained from 20 patients undergoing primary THA. MSCs were exposed for 60 minutes to one of four commonly used corticosteroid preparations: betamethasone sodium phosphate-betamethasone acetate (6 mg/mL), dexamethasone sodium phosphate (4 mg/mL), methylprednisolone (40 mg/mL), or triamcinolone acetonide (40 mg/mL). Among the four preparations (treatment groups), cells were exposed to increasing concentrations of drugs according to the following titrations of the commercially available preparation: 0.0 (control solution of 1X phosphate buffered saline), 3.125, 6.25, 12.5, 25, 50, 75, and 100 % (undiluted commercial product). Cells were allowed to recover in standard culture media for 24 hours. After the recovery period, cell viability was measured using -(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) tetrazolium dye-based cellular viability assay and live-dead cell fluorescent staining. For the MTS assay, measurements were quantified in units of optical density (OD). ANOVA was performed at every experimental steroid concentration. When this global test was statistically significant, all pairwise comparisons were performed at that concentration with p values adjusted by the Tukey method to guard against Type I error.
Results
Exposure to corticosteroids decreased MSC viability in a curvilinear dose–response pattern. For betamethasone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.12) and decreased to 0.00 (SD, 0.00) at 25% steroid concentration. For dexamethasone, the mean MTS OD at 0% steroid concentration was 1.00 (SD, 0.07) and decreased to 0.00 (SD, 0.01) at 100% steroid concentration. For methylprednisolone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 100% steroid concentration. For triamcinolone, the mean MTS OD at 0% steroid concentration was 1.02 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 75% steroid concentration. There were large differences among commercially available preparations, and these differences were present at every concentration. In general, dexamethasone was most gentle on MSCs (average OD by steroid concentration: 0% = 1.00; 3.125% = 0.86; 6.25% = 0.74; 12.5% = 0.53; 25% = 0.30; 50% = 0.20; 75% = 0.09; 100% = 0.00, triamcinolone and methylprednisolone were intermediate (triamcinolone average OD by steroid concentration: 0% = 1.02; 3.125% = 0.82; 6.25% = 0.64; 12.5% = 0.45; 25% = 0.18; 50% = 0.03; 75% = 0.00; 100% = 0.00; methylprednisolone average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.54; 12.5% = 0.31; 25% = 0.12; 50% = 0.01; 75% = 0.00; 100% = 0.00), and betamethasone was most toxic (average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.27; 12.5% = 0.02; 25% = 0.00; 50% = 0.00; 75% = 0.00; 100% = 0.00). ANOVA testing showed p values less than 0.0001 at every tested concentration (with the exception of the 0% control solution; p = 0.204) with subsequent pairwise comparisons supporting the relationships described above. The outcomes were maintained after stratifying by age, sex, or indication for THA (osteoarthritis versus avascular necrosis).
Conclusions
Commonly used intraarticular corticosteroids had a dose-dependent, profound, and differential effect on MSCs in this in vitro model, with betamethasone being the most toxic. Further studies are needed to assess if the in vitro effects of these agents translate into similar in vivo outcomes.
Clinical Relevance
Corticosteroids frequently are used by physicians to reduce inflammation in patients with musculoskeletal disorders, but these agents may hinder MSCs’ innate regenerative capacity in exchange for temporary analgesia. Our study suggests that choosing dexamethasone may result in less harmful effects when compared with other injectable steroids. |
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AbstractList | Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have shown the deleterious effects of corticosteroids on chondrocytes, suggesting a potentiation of degenerative joint disease. Mesenchymal stem cells (MSCs) are the direct progenitors of chondrocytes and other musculoskeletal tissue. Additionally, they serve an important antiinflammatory role, which can combat the chronic inflammatory state that mediates degenerative joint disease. Little is known about how corticosteroids interact with this regenerative and reparative cell population.
We asked: (1) Are corticosteroids cytotoxic to MSCs in a dose-response fashion? (2) Is there a differential effect in the level of cytotoxicity to MSCs between commercially available corticosteroid preparations?
Human MSCs were isolated and cultured from periarticular adipose tissue obtained from 20 patients undergoing primary THA. MSCs were exposed for 60 minutes to one of four commonly used corticosteroid preparations: betamethasone sodium phosphate-betamethasone acetate (6 mg/mL), dexamethasone sodium phosphate (4 mg/mL), methylprednisolone (40 mg/mL), or triamcinolone acetonide (40 mg/mL). Among the four preparations (treatment groups), cells were exposed to increasing concentrations of drugs according to the following titrations of the commercially available preparation: 0.0 (control solution of 1X phosphate buffered saline), 3.125, 6.25, 12.5, 25, 50, 75, and 100 % (undiluted commercial product). Cells were allowed to recover in standard culture media for 24 hours. After the recovery period, cell viability was measured using -(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) tetrazolium dye-based cellular viability assay and live-dead cell fluorescent staining. For the MTS assay, measurements were quantified in units of optical density (OD). ANOVA was performed at every experimental steroid concentration. When this global test was statistically significant, all pairwise comparisons were performed at that concentration with p values adjusted by the Tukey method to guard against Type I error.
Exposure to corticosteroids decreased MSC viability in a curvilinear dose-response pattern. For betamethasone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.12) and decreased to 0.00 (SD, 0.00) at 25% steroid concentration. For dexamethasone, the mean MTS OD at 0% steroid concentration was 1.00 (SD, 0.07) and decreased to 0.00 (SD, 0.01) at 100% steroid concentration. For methylprednisolone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 100% steroid concentration. For triamcinolone, the mean MTS OD at 0% steroid concentration was 1.02 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 75% steroid concentration. There were large differences among commercially available preparations, and these differences were present at every concentration. In general, dexamethasone was most gentle on MSCs (average OD by steroid concentration: 0% = 1.00; 3.125% = 0.86; 6.25% = 0.74; 12.5% = 0.53; 25% = 0.30; 50% = 0.20; 75% = 0.09; 100% = 0.00, triamcinolone and methylprednisolone were intermediate (triamcinolone average OD by steroid concentration: 0% = 1.02; 3.125% = 0.82; 6.25% = 0.64; 12.5% = 0.45; 25% = 0.18; 50% = 0.03; 75% = 0.00; 100% = 0.00; methylprednisolone average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.54; 12.5% = 0.31; 25% = 0.12; 50% = 0.01; 75% = 0.00; 100% = 0.00), and betamethasone was most toxic (average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.27; 12.5% = 0.02; 25% = 0.00; 50% = 0.00; 75% = 0.00; 100% = 0.00). ANOVA testing showed p values less than 0.0001 at every tested concentration (with the exception of the 0% control solution; p = 0.204) with subsequent pairwise comparisons supporting the relationships described above. The outcomes were maintained after stratifying by age, sex, or indication for THA (osteoarthritis versus avascular necrosis).
Commonly used intraarticular corticosteroids had a dose-dependent, profound, and differential effect on MSCs in this in vitro model, with betamethasone being the most toxic. Further studies are needed to assess if the in vitro effects of these agents translate into similar in vivo outcomes.
Corticosteroids frequently are used by physicians to reduce inflammation in patients with musculoskeletal disorders, but these agents may hinder MSCs' innate regenerative capacity in exchange for temporary analgesia. Our study suggests that choosing dexamethasone may result in less harmful effects when compared with other injectable steroids. Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have shown the deleterious effects of corticosteroids on chondrocytes, suggesting a potentiation of degenerative joint disease. Mesenchymal stem cells (MSCs) are the direct progenitors of chondrocytes and other musculoskeletal tissue. Additionally, they serve an important antiinflammatory role, which can combat the chronic inflammatory state that mediates degenerative joint disease. Little is known about how corticosteroids interact with this regenerative and reparative cell population. We asked: (1) Are corticosteroids cytotoxic to MSCs in a dose-response fashion? (2) Is there a differential effect in the level of cytotoxicity to MSCs between commercially available corticosteroid preparations? Human MSCs were isolated and cultured from periarticular adipose tissue obtained from 20 patients undergoing primary THA. MSCs were exposed for 60 minutes to one of four commonly used corticosteroid preparations: betamethasone sodium phosphate-betamethasone acetate (6 mg/mL), dexamethasone sodium phosphate (4 mg/mL), methylprednisolone (40 mg/mL), or triamcinolone acetonide (40 mg/mL). Among the four preparations (treatment groups), cells were exposed to increasing concentrations of drugs according to the following titrations of the commercially available preparation: 0.0 (control solution of 1X phosphate buffered saline), 3.125, 6.25, 12.5, 25, 50, 75, and 100 % (undiluted commercial product). Cells were allowed to recover in standard culture media for 24 hours. After the recovery period, cell viability was measured using -(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) tetrazolium dye-based cellular viability assay and live-dead cell fluorescent staining. For the MTS assay, measurements were quantified in units of optical density (OD). ANOVA was performed at every experimental steroid concentration. When this global test was statistically significant, all pairwise comparisons were performed at that concentration with p values adjusted by the Tukey method to guard against Type I error. Exposure to corticosteroids decreased MSC viability in a curvilinear dose-response pattern. For betamethasone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.12) and decreased to 0.00 (SD, 0.00) at 25% steroid concentration. For dexamethasone, the mean MTS OD at 0% steroid concentration was 1.00 (SD, 0.07) and decreased to 0.00 (SD, 0.01) at 100% steroid concentration. For methylprednisolone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 100% steroid concentration. For triamcinolone, the mean MTS OD at 0% steroid concentration was 1.02 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 75% steroid concentration. There were large differences among commercially available preparations, and these differences were present at every concentration. In general, dexamethasone was most gentle on MSCs (average OD by steroid concentration: 0% = 1.00; 3.125% = 0.86; 6.25% = 0.74; 12.5% = 0.53; 25% = 0.30; 50% = 0.20; 75% = 0.09; 100% = 0.00, triamcinolone and methylprednisolone were intermediate (triamcinolone average OD by steroid concentration: 0% = 1.02; 3.125% = 0.82; 6.25% = 0.64; 12.5% = 0.45; 25% = 0.18; 50% = 0.03; 75% = 0.00; 100% = 0.00; methylprednisolone average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.54; 12.5% = 0.31; 25% = 0.12; 50% = 0.01; 75% = 0.00; 100% = 0.00), and betamethasone was most toxic (average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.27; 12.5% = 0.02; 25% = 0.00; 50% = 0.00; 75% = 0.00; 100% = 0.00). ANOVA testing showed p values less than 0.0001 at every tested concentration (with the exception of the 0% control solution; p = 0.204) with subsequent pairwise comparisons supporting the relationships described above. The outcomes were maintained after stratifying by age, sex, or indication for THA (osteoarthritis versus avascular necrosis). Commonly used intraarticular corticosteroids had a dose-dependent, profound, and differential effect on MSCs in this in vitro model, with betamethasone being the most toxic. Further studies are needed to assess if the in vitro effects of these agents translate into similar in vivo outcomes. Corticosteroids frequently are used by physicians to reduce inflammation in patients with musculoskeletal disorders, but these agents may hinder MSCs' innate regenerative capacity in exchange for temporary analgesia. Our study suggests that choosing dexamethasone may result in less harmful effects when compared with other injectable steroids. Background Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have shown the deleterious effects of corticosteroids on chondrocytes, suggesting a potentiation of degenerative joint disease. Mesenchymal stem cells (MSCs) are the direct progenitors of chondrocytes and other musculoskeletal tissue. Additionally, they serve an important antiinflammatory role, which can combat the chronic inflammatory state that mediates degenerative joint disease. Little is known about how corticosteroids interact with this regenerative and reparative cell population. Questions/purposes We asked: (1) Are corticosteroids cytotoxic to MSCs in a dose–response fashion? (2) Is there a differential effect in the level of cytotoxicity to MSCs between commercially available corticosteroid preparations? Methods Human MSCs were isolated and cultured from periarticular adipose tissue obtained from 20 patients undergoing primary THA. MSCs were exposed for 60 minutes to one of four commonly used corticosteroid preparations: betamethasone sodium phosphate-betamethasone acetate (6 mg/mL), dexamethasone sodium phosphate (4 mg/mL), methylprednisolone (40 mg/mL), or triamcinolone acetonide (40 mg/mL). Among the four preparations (treatment groups), cells were exposed to increasing concentrations of drugs according to the following titrations of the commercially available preparation: 0.0 (control solution of 1X phosphate buffered saline), 3.125, 6.25, 12.5, 25, 50, 75, and 100 % (undiluted commercial product). Cells were allowed to recover in standard culture media for 24 hours. After the recovery period, cell viability was measured using -(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) tetrazolium dye-based cellular viability assay and live-dead cell fluorescent staining. For the MTS assay, measurements were quantified in units of optical density (OD). ANOVA was performed at every experimental steroid concentration. When this global test was statistically significant, all pairwise comparisons were performed at that concentration with p values adjusted by the Tukey method to guard against Type I error. Results Exposure to corticosteroids decreased MSC viability in a curvilinear dose–response pattern. For betamethasone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.12) and decreased to 0.00 (SD, 0.00) at 25% steroid concentration. For dexamethasone, the mean MTS OD at 0% steroid concentration was 1.00 (SD, 0.07) and decreased to 0.00 (SD, 0.01) at 100% steroid concentration. For methylprednisolone, the mean MTS OD at 0% steroid concentration was 1.03 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 100% steroid concentration. For triamcinolone, the mean MTS OD at 0% steroid concentration was 1.02 (SD, 0.09) and decreased to 0.00 (SD, 0.00) at 75% steroid concentration. There were large differences among commercially available preparations, and these differences were present at every concentration. In general, dexamethasone was most gentle on MSCs (average OD by steroid concentration: 0% = 1.00; 3.125% = 0.86; 6.25% = 0.74; 12.5% = 0.53; 25% = 0.30; 50% = 0.20; 75% = 0.09; 100% = 0.00, triamcinolone and methylprednisolone were intermediate (triamcinolone average OD by steroid concentration: 0% = 1.02; 3.125% = 0.82; 6.25% = 0.64; 12.5% = 0.45; 25% = 0.18; 50% = 0.03; 75% = 0.00; 100% = 0.00; methylprednisolone average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.54; 12.5% = 0.31; 25% = 0.12; 50% = 0.01; 75% = 0.00; 100% = 0.00), and betamethasone was most toxic (average OD by steroid concentration: 0% = 1.03; 3.125% = 0.74; 6.25% = 0.27; 12.5% = 0.02; 25% = 0.00; 50% = 0.00; 75% = 0.00; 100% = 0.00). ANOVA testing showed p values less than 0.0001 at every tested concentration (with the exception of the 0% control solution; p = 0.204) with subsequent pairwise comparisons supporting the relationships described above. The outcomes were maintained after stratifying by age, sex, or indication for THA (osteoarthritis versus avascular necrosis). Conclusions Commonly used intraarticular corticosteroids had a dose-dependent, profound, and differential effect on MSCs in this in vitro model, with betamethasone being the most toxic. Further studies are needed to assess if the in vitro effects of these agents translate into similar in vivo outcomes. Clinical Relevance Corticosteroids frequently are used by physicians to reduce inflammation in patients with musculoskeletal disorders, but these agents may hinder MSCs’ innate regenerative capacity in exchange for temporary analgesia. Our study suggests that choosing dexamethasone may result in less harmful effects when compared with other injectable steroids. |
Author | Wagner, Eric R. Wyles, Saranya P. Wyles, Cody C. Houdek, Matthew T. Sierra, Rafael J. Behfar, Atta |
Author_xml | – sequence: 1 givenname: Cody C. surname: Wyles fullname: Wyles, Cody C. organization: Mayo Medical School, Mayo Clinic – sequence: 2 givenname: Matthew T. surname: Houdek fullname: Houdek, Matthew T. organization: Department of Orthopaedic Surgery, Mayo Clinic – sequence: 3 givenname: Saranya P. surname: Wyles fullname: Wyles, Saranya P. organization: Mayo Medical School, Mayo Clinic – sequence: 4 givenname: Eric R. surname: Wagner fullname: Wagner, Eric R. organization: Department of Orthopaedic Surgery, Mayo Clinic – sequence: 5 givenname: Atta surname: Behfar fullname: Behfar, Atta organization: Center for Regenerative Medicine and Division of Cardiovascular Disease, Mayo Clinic – sequence: 6 givenname: Rafael J. surname: Sierra fullname: Sierra, Rafael J. email: sierra.rafael@mayo.edu organization: Department of Orthopaedic Surgery, Mayo Clinic |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25187334$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.1080/17453674.1997.11744766 10.2106/00004623-196648070-00012 |
ContentType | Journal Article |
Copyright | The Association of Bone and Joint Surgeons® 2014 The Association of Bone and Joint Surgeons 2015 |
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Keywords | Average Optical Density Avascular Necrosis Triamcinolone Betamethasone Triamcinolone Acetonide |
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PublicationTitle | Clinical orthopaedics and related research |
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References | DragooJLDanialCMBraunHJPouliotMAKimHJThe chondrotoxicity of single-dose corticosteroidsKnee Surg Sports Traumatol Arthrosc.201220180918142218692110.1007/s00167-011-1820-6 RaynauldJPBuckland-WrightCWardRChoquetteDHaraouiBMartel-PelletierJUthmanIKhyVTremblayJLBertrandCPelletierJPSafety and efficacy of long-term intraarticular steroid injections in osteoarthritis of the knee: a randomized, double-blind, placebo-controlled trialArthritis Rheum.2003483703771:CAS:528:DC%2BD3sXhslKktrc%3D1257184510.1002/art.10777 BreuAEcklSZinkWKujatRAngelePCytotoxicity of local anesthetics on human mesenchymal stem cells in vitroArthroscopy.201329167616842399314510.1016/j.arthro.2013.06.018 Papacrhistou G [sic], Anagnostou S, Katsorhis T. The effect of intraarticular hydrocortisone injection on the articular cartilage of rabbits. Acta Orthop Scand Suppl. 1997;275:132–134. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R, Wells G. Intraarticular corticosteroid for treatment of osteoarthritis of the knee. Cochrane Database Syst Rev. 2006:CD005328. MankinHJCongerKAThe acute effects of intra-articular hydrocortisone on articular cartilage in rabbitsJ Bone Joint Surg Am.196648138313881:CAS:528:DyaF2sXjsFWktQ%3D%3D5921793 RahnamaRWangMDangACKimHTKuoACCytotoxicity of local anesthetics on human mesenchymal stem cellsJ Bone Joint Surg Am.2013951321372332496010.2106/JBJS.K.01291 SuriPMorgenrothDCHunterDJEpidemiology of osteoarthritis and associated comorbiditiesPM R.201245 supplS10S192263268710.1016/j.pmrj.2012.01.007 Crespo-DiazRBehfarAButlerGWPadleyDJSarrMGBartunekJDietzABTerzicAPlatelet lysate consisting of a natural repair proteome supports human mesenchymal stem cell proliferation and chromosomal stabilityCell Transplant.2011207978112109240610.3727/096368910X543376 Tukey JW. The Problem of Multiple Comparisons. In Braun HI, ed. The Collected Works of John W. Tukey. Vol 8. New York, NY: Chapman & Hall; 1994:1–560. SyedHMGreenLBianskiBJobeCMWongworawatMDBupivacaine and triamcinolone may be toxic to human chondrocytes: a pilot studyClin Orthop Relat Res.20114692941294731715242138421110.1007/s11999-011-1834-x DavisDCyriacMGeDYouZSavoieFHIn vitro cytotoxic effects of benzalkonium chloride in corticosteroid injection suspensionJ Bone Joint Surg Am.2010921291372004810510.2106/JBJS.H.01561 NakazawaFMatsunoHYudohKWatanabeYKatayamaRKimuraTCorticosteroid treatment induces chondrocyte apoptosis in an experimental arthritis model and in chondrocyte culturesClin Exp Rheumatol.2002207737811:STN:280:DC%2BD3s%2Fgt1Omtw%3D%3D12508768 BjordalJMJohnsonMILopes-MartinsRABogenBChowRLjunggrenAEShort-term efficacy of physical interventions in osteoarthritic knee pain: a systematic review and meta-analysis of randomised placebo-controlled trialsBMC Musculoskelet Disord.200785119315961758744610.1186/1471-2474-8-51 CelesteCIonescuMRobin PooleALavertySRepeated intraarticular injections of triamcinolone acetonide alter cartilage matrix metabolism measured by biomarkers in synovial fluidJ Orthop Res.2005236026101:CAS:528:DC%2BD2MXktVOjtL4%3D1588548110.1016/j.orthres.2004.10.003 BjordalJMKlovningALjunggrenAESlordalLShort-term efficacy of pharmacotherapeutic interventions in osteoarthritic knee pain: a meta-analysis of randomised placebo-controlled trialsEur J Pain.2007111251381:CAS:528:DC%2BD28Xht1Kgu73P1668224010.1016/j.ejpain.2006.02.013 MoritoTMunetaTHaraKJuYJMochizukiTMakinoHUmezawaASekiyaISynovial fluid-derived mesenchymal stem cells increase after intra-articular ligament injury in humansRheumatology (Oxford).200847113711431:STN:280:DC%2BD1cvlsVGitA%3D%3D1839089410.1093/rheumatology/ken114 SkedrosJGHuntKJPittsTCVariations in corticosteroid/anesthetic injections for painful shoulder conditions: comparisons among orthopaedic surgeons, rheumatologists, and physical medicine and primary-care physiciansBMC Musculoskelet Disord.200786319508741761790010.1186/1471-2474-8-63 LawrenceRCFelsonDTHelmickCGArnoldLMChoiHDeyoRAGabrielSHirschRHochbergMCHunderGGJordanJMKatzJNKremersHMWolfeFNational Arthritis Data WorkgroupEstimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part IIArthritis Rheum.200858263532666641816349710.1002/art.23176 ZhangWMoskowitzRWNukiGAbramsonSAltmanRDArdenNBierma-ZeinstraSBrandtKDCroftPDohertyMDougadosMHochbergMHunterDJKwohKLohmanderLSTugwellPOARSI recommendations for the management of hip and knee osteoarthritis. Part II: OARSI evidence-based, expert consensus guidelinesOsteoarthritis Cartilage.2008161371621:STN:280:DC%2BD1c7it12itg%3D%3D1827976610.1016/j.joca.2007.12.013 LeeDHSonnCHHanSBOhYLeeKMLeeSHSynovial fluid CD34− CD44+ CD90+ mesenchymal stem cell levels are associated with the severity of primary knee osteoarthritisOsteoarthritis Cartilage.2012201061091:CAS:528:DC%2BC38XhsVCisw%3D%3D2215573110.1016/j.joca.2011.11.010 KotlarzHGunnarssonCLFangHRizzoJAOsteoarthritis and absenteeism costs: evidence from US National Survey DataJ Occup Environ Med.2010522632682019065610.1097/JOM.0b013e3181cf00aa RobionFCDoizeBBoureLMarcouxMIonescuMReinerAPooleARLavertySUse of synovial fluid markers of cartilage synthesis and turnover to study effects of repeated intra-articular administration of methylprednisolone acetate on articular cartilage in vivoJ Orthop Res.2001192502581:CAS:528:DC%2BD3MXjvFalt74%3D1134769810.1016/S0736-0266(00)90008-1 SeshadriVCoyleCHChuCRLidocaine potentiates the chondrotoxicity of methylprednisoloneArthroscopy.2009253373471934191910.1016/j.arthro.2009.01.003 JonesEAEnglishAHenshawKKinseySEMarkhamAFEmeryPMcGonagleDEnumeration and phenotypic characterization of synovial fluid multipotential mesenchymal progenitor cells in inflammatory and degenerative arthritisArthritis Rheum.2004508178271502232410.1002/art.20203 SekiyaIOjimaMSuzukiSYamagaMHorieMKogaHTsujiKMiyaguchiKOgishimaSTanakaHMunetaTHuman mesenchymal stem cells in synovial fluid increase in the knee with degenerated cartilage and osteoarthritisJ Orthop Res.2012309439492214763410.1002/jor.22029 18163497 - Arthritis Rheum. 2008 Jan;58(1):26-35 22147634 - J Orthop Res. 2012 Jun;30(6):943-9 22155731 - Osteoarthritis Cartilage. 2012 Feb;20(2):106-9 15885481 - J Orthop Res. 2005 May;23(3):602-10 22186921 - Knee Surg Sports Traumatol Arthrosc. 2012 Sep;20(9):1809-14 18390894 - Rheumatology (Oxford). 2008 Aug;47(8):1137-43 17617900 - BMC Musculoskelet Disord. 2007;8:63 17587446 - BMC Musculoskelet Disord. 2007;8:51 12508768 - Clin Exp Rheumatol. 2002 Nov-Dec;20(6):773-81 21384211 - Clin Orthop Relat Res. 2011 Oct;469(10):2941-7 20190656 - J Occup Environ Med. 2010 Mar;52(3):263-8 23993145 - Arthroscopy. 2013 Oct;29(10):1676-84 9385288 - Acta Orthop Scand Suppl. 1997 Oct;275:132-4 18279766 - Osteoarthritis Cartilage. 2008 Feb;16(2):137-62 15022324 - Arthritis Rheum. 2004 Mar;50(3):817-27 12571845 - Arthritis Rheum. 2003 Feb;48(2):370-7 16625636 - Cochrane Database Syst Rev. 2006;(2):CD005328 19341919 - Arthroscopy. 2009 Apr;25(4):337-47 22632687 - PM R. 2012 May;4(5 Suppl):S10-9 20048105 - J Bone Joint Surg Am. 2010 Jan;92(1):129-37 23324960 - J Bone Joint Surg Am. 2013 Jan 16;95(2):132-7 5921793 - J Bone Joint Surg Am. 1966 Oct;48(7):1383-8 11347698 - J Orthop Res. 2001 Mar;19(2):250-8 16682240 - Eur J Pain. 2007 Feb;11(2):125-38 21092406 - Cell Transplant. 2011;20(6):797-811 Nakazawa (R15-57-20210317) 2002; 20 Mankin (R13-57-20210317) 1966; 48 Papacrhistou G sic, A Anagnostou (R16-57-20210317) 1997; 275 |
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Snippet | Background
Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have... Corticosteroids are a common, short-term, local antiinflammatory and analgesic for treating patients with musculoskeletal disorders. Studies have shown the... |
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SubjectTerms | Adrenal Cortex Hormones - administration & dosage Adrenal Cortex Hormones - toxicity Adult Anti-Inflammatory Agents - administration & dosage Anti-Inflammatory Agents - toxicity Basic Research Cell Survival - drug effects Chondrocytes - drug effects Conservative Orthopedics Dose-Response Relationship, Drug Female Humans Male Medicine Medicine & Public Health Mesenchymal Stromal Cells - drug effects Middle Aged Orthopedics Sports Medicine Surgery Surgical Orthopedics |
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Title | Differential Cytotoxicity of Corticosteroids on Human Mesenchymal Stem Cells |
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