The Experts below are selected from a list of 327 Experts worldwide ranked by ideXlab platform
Anne Grete Semb - One of the best experts on this subject based on the ideXlab platform.
-
effects of long term statin treatment on coronary atherosclerosis in patients with inflammatory Joint Diseases
PLOS ONE, 2019Co-Authors: Mona Svanteson, E Ikdahl, Silvia Rollefstad, Jonny Hisdal, Nilseinar Klow, Joseph O Sexton, Ylva Haig, Anne Grete SembAbstract:Background The effect of statins over time on coronary atherosclerosis in patients with inflammatory Joint Diseases (IJD) is unknown. Our aim was to evaluate the change in coronary plaque morphology and volume in long-term statin-treated patients with IJD. Methods Sixty-eight patients with IJD and carotid artery plaque(s) underwent coronary computed tomography angiography before and after a mean of 4.7 (range 4.0–6.0) years of statin treatment. The treatment target for low density lipoprotein cholesterol (LDL-c) was ≤1.8 mmol/L. Changes in plaque volume (calcified, mixed/soft and total) and coronary artery calcification (CAC) from baseline to follow-up were assessed using the 17-segment American Heart Association-model. Results Median (IQR) increase in CAC after statin treatment was 38 (5–236) Agatston units (p 1.8mmol/L (21 [2–143] vs. 69 [16–423], p = 0.006 and 0.65 [-1.0–13.9] vs. 13.0 [0.0–60.8] mm3, p = 0.019, respectively). Conclusions A progression of total atherosclerotic plaque volume in statin-treated patients with IJD was observed. However, soft/mixed plaque volume was reduced, suggesting an alteration in plaque composition. Patients with recommended LDL-c levels at follow-up had reduced atherosclerotic progression compared to patients with LDL-c levels above the treatment target, suggesting a beneficial effect of treatment to guideline-recommended lipid targets in IJD patients.
-
sustained improvement of arterial stiffness and blood pressure after long term rosuvastatin treatment in patients with inflammatory Joint Diseases results from the rora as study
PLOS ONE, 2016Co-Authors: E Ikdahl, Silvia Rollefstad, Tore K Kvien, I C Olsen, Jonny Hisdal, Terje R Pedersen, Anne Grete SembAbstract:Objective Patients with inflammatory Joint Diseases (IJD) have a high prevalence of hypertension and increased arterial stiffness. The aim of the present study was to evaluate the effect of long-term rosuvastatin treatment on arterial stiffness, measured by augmentation index (AIx) and aortic pulse wave velocity (aPWV), and blood pressure (BP) in IJD patients with established atherosclerosis. Methods Eighty-nine statin naive IJD patients with carotid atherosclerotic plaque(s) (rheumatoid arthritis n = 55, ankylosing spondylitis n = 23, psoriatic arthritis n = 11) received rosuvastatin for 18 months to achieve low-density lipoprotein cholesterol goal ≤1.8 mmol/L. Change in AIx (ΔAIx), aPWV (ΔaPWV), systolic BP (ΔsBP) and diastolic BP (ΔdBP) from baseline to study end was assessed by paired samples t-tests. Linear regression was applied to evaluate associations between cardiovascular disease (CVD) risk factors, rheumatic disease specific variables and medication, and ΔAIx, ΔaPWV, ΔsBP and ΔdBP. Results AIx, aPWV, sBP and dBP were significantly reduced from baseline to study end. The mean (95%CI) changes were: ΔAIx: -0.34 (-0.03, -0.65)% (p = 0.03), ΔaPWV: -1.69 (-0.21, -3.17)m/s2 (p = 0.03), ΔsBP: -5.27 (-1.61, -8.93)mmHg (p = 0.004) and ΔdBP -2.93 (-0.86, -5.00)mmHg (p = 0.01). In linear regression models, ∆aPWV was significantly correlated with ΔsBP and ΔdBP (for all: p<0.001). Conclusions There is an unmet need of studies evaluating CVD prevention in IJD patients. We have shown for the first time that long-term intensive lipid lowering with rosuvastatin improved arterial stiffness and induced a clinically significant BP reduction in patients with IJD. These improvements were linearly correlated and may represent novel insight into the pleiotropic effects by statins. Trial Registration ClinicalTrials.gov NCT01389388
-
association of chest pain and risk of cardiovascular disease with coronary atherosclerosis in patients with inflammatory Joint Diseases
Frontiers of Medicine in China, 2015Co-Authors: Silvia Rollefstad, E Ikdahl, Tore K Kvien, Jonny Hisdal, Terje R Pedersen, Anne Grete SembAbstract:Objectives: The relation between chest pain and coronary atherosclerosis (CA) in patients with inflammatory Joint Diseases (IJD) has not been explored previously. Our aim was to evaluate the associations of the presence of chest pain and the predicted 10-year risk of cardiovascular disease (CVD) by use of several CVD risk algorithms, with multi-detector computer tomography (MDCT) coronary angiography verified CA. Methods: Detailed information concerning chest pain and CVD risk factors was obtained in 335 patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). In addition, 119 of these patients underwent MDCT coronary angiography. Results: Thirty-one percent of the patients (104/335) reported chest pain. Only 6 patients (1.8%) had atypical angina pectoris (pricking pain at rest). In 69 patients without chest pain, two thirds had CA, while in those who reported chest pain (n=50), CA was present in 48.0%. In a logistic regression analysis, chest pain was not associated with CA (dependent variable) (p=0.43). About 30% (Nagelkerke R2) of CA was explained by any of the CVD risk calculators: SCORE, Framingham Risk Score or Reynolds Risk Score. Conclusion: The presence of chest pain was surprisingly infrequently reported in patients with IJD who were referred for a CVD risk evaluation. However, when present, chest pain was weakly associated with CA, in contrast to the predicted CVD risk by several risk calculators which was highly associated with the presence of CA. These findings suggest that clinicians treating patients with IJD should be alert of coronary atherosclerotic disease also in absence of chest pain symptoms.
-
rosuvastatin improves endothelial function in patients with inflammatory Joint Diseases longitudinal associations with atherosclerosis and arteriosclerosis results from the rora as statin intervention study
Arthritis Research & Therapy, 2015Co-Authors: E Ikdahl, Silvia Rollefstad, Tore K Kvien, I C Olsen, Jonny Hisdal, Terje R Pedersen, Anne Grete SembAbstract:Introduction Endothelial dysfunction is an early step in the atherosclerotic process and can be quantified by flow-mediated vasodilation (FMD). Our aim was to investigate the effect of long-term rosuvastatin therapy on endothelial function in patients with inflammatory Joint Diseases (IJD) with established atherosclerosis. Furthermore, to evaluate correlations between change in FMD (ΔFMD) and change in carotid plaque (CP) height, arterial stiffness [aortic pulse wave velocity (aPWV) and augmentation index (AIx)], lipids, disease activity and inflammation.
-
systemic inflammation in patients with inflammatory Joint Diseases does not influence statin dose needed to obtain ldl cholesterol goal in cardiovascular prevention
Annals of the Rheumatic Diseases, 2015Co-Authors: Silvia Rollefstad, E Ikdahl, Tore K Kvien, Jonny Hisdal, Terje R Pedersen, Ingar Holme, Anne Grete SembAbstract:Objectives There is a lipid paradox in rheumatoid arthritis describing that despite low lipids related to systemic inflammation, there is an increased cardiovascular (CV) risk. Our aim was to evaluate if baseline lipid levels or baseline systemic inflammation were associated with the statin dose sufficient to achieve lipid targets in patients with inflammatory Joint Diseases. Methods In this longitudinal, short-term follow-up observational report, we evaluated 197 patients who did and 36 patients who did not reach the recommended low density lipoprotein cholesterol (LDL-c) target. The patients were, after CV risk evaluation, classified to either primary or secondary CV prevention with lipid lowering treatment (LLT). LLT was initiated with statins and adjusted until at least two lipid targets were achieved. Intensive LLT was defined as rosuvastatin ≥20 mg, atorvastatin and simvastatin at the highest dose (80 mg), and conventional LLT were defined as all lower doses. Results In an independent sample t test, systemic inflammation or lipid levels at baseline were not associated with the statin dose (intensive or conventional) needed to achieve recommended LDL-c target (C reactive protein/erythrocyte sedimentation rate: p=0.10 and p=0.11, and LDL-c/total cholesterol: p=0.17 and p=0.34, respectively). The baseline inflammatory status and lipid levels in patients who did and did not obtain LDL-c goal were comparable (C reactive protein/erythrocyte sedimentation rate: p=0.32 and p=0.64, and LDL-c/total cholesterol: p=0.20 and p=0.83, respectively). Conclusions Systemic inflammation or lipid levels did not influence the intensity of statin treatment needed to obtain guideline recommended lipid targets in CV prevention. Whether the background inflammation in patients with inflammatory Joint Diseases over time influences the CV risk reduction related to statins is yet unknown.
Paula Hoff - One of the best experts on this subject based on the ideXlab platform.
-
Osteoarthritis synovial fluid activates pro-inflammatory cytokines in primary human chondrocytes
International Orthopaedics, 2013Co-Authors: Paula Hoff, Manuela Jakstadt, Kristin Andreas, Georg Matziolis, Timo Gaber, Frank Buttgereit, Gerd-rüdiger Burmester, Carsten Perka, Eric RöhnerAbstract:PURPOSE: Two of the most common Joint Diseases are rheumatoid arthritis (RA) and osteoarthritis (OA). Cartilage degradation and erosions are important pathogenetic mechanisms in both Joint Diseases and have presently gained increasing interest. The aim of the present study was to investigate the effects of the synovial fluid environment of OA patients in comparison with synovial fluids of RA patients on human chondrocytes in vitro.\n\nMETHODS: Primary human chondrocytes were incubated in synovial fluids gained from patients with OA or RA. The detection of vital cell numbers was determined by histology and by using the Casy Cell Counter System. Cytokine and chemokine secretion was determined by a multiplex suspension array.\n\nRESULTS: Microscopic analysis showed altered cell morphology and cell shrinkage following incubation with synovial fluid of RA patients. Detection of vital cells showed a highly significant decrease of vital chondrocyte when treated with RA synovial fluids in comparison with OA synovial fluids. An active secretion of cytokines such as vascular endothelial growth factor (VEGF) of chondrocytes treated with OA synovial fluids was observed.\n\nCONCLUSIONS: Significantly increased levels of various cytokines in synovial fluids of RA, and surprisingly of OA, patients were shown. Activation of pro-inflammatory cytokines of human chondrocytes by synovial fluids of OA patient supports a pro-inflammatory process in the pathogenesis of OA.
-
Inflammatory synovial fluid microenvironment drives primary human chondrocytes to actively take part in inflammatory Joint Diseases
Immunologic Research, 2012Co-Authors: Eric Röhner, Georg Matziolis, Bernd Füchtmeier, Timo Gaber, Frank Buttgereit, Gerd-rüdiger Burmester, Carsten Perka, Paula HoffAbstract:The role of human chondrocytes in the pathogenesis of cartilage degradation in rheumatic Joint Diseases has presently gained increasing interest. An active chondrocyte participation in local inflammation may play a role in the initiation and progression of inflammatory Joint Diseases and in a disruption of cartilage repair mechanisms resulting in cartilage degradation. In the present study, we hypothesized that inflammatory synovial fluid triggers human chondrocytes to actively take part in inflammatory processes in rheumatic Joint Diseases. Primary human chondrocytes were incubated in synovial fluids gained from patients with rheumatoid arthritis, psoriasis arthritis and reactive arthritis. The detection of vital cell numbers was determined by using Casy Cell Counter System. Apoptosis was measured by Annexin-V and 7AAD staining. Cytokine and chemokine secretion was determined by a multiplex suspension array. Detection of vital cells showed a highly significant decrease in chondrocyte numbers. Flow cytometry demonstrated a significant increase in apoptotic chondrocytes after the incubation. An active secretion of cytokines such as MCP-1 and MIF by chondrocytes was observed. The inflammatory synovial fluid microenvironment mediates apoptosis and cell death of chondrocytes. Moreover, in terms of cytokine secretion, it also induces an active participation of chondrocytes in ongoing inflammation.
Eric Röhner - One of the best experts on this subject based on the ideXlab platform.
-
Osteoarthritis synovial fluid activates pro-inflammatory cytokines in primary human chondrocytes
International Orthopaedics, 2013Co-Authors: Paula Hoff, Manuela Jakstadt, Kristin Andreas, Georg Matziolis, Timo Gaber, Frank Buttgereit, Gerd-rüdiger Burmester, Carsten Perka, Eric RöhnerAbstract:PURPOSE: Two of the most common Joint Diseases are rheumatoid arthritis (RA) and osteoarthritis (OA). Cartilage degradation and erosions are important pathogenetic mechanisms in both Joint Diseases and have presently gained increasing interest. The aim of the present study was to investigate the effects of the synovial fluid environment of OA patients in comparison with synovial fluids of RA patients on human chondrocytes in vitro.\n\nMETHODS: Primary human chondrocytes were incubated in synovial fluids gained from patients with OA or RA. The detection of vital cell numbers was determined by histology and by using the Casy Cell Counter System. Cytokine and chemokine secretion was determined by a multiplex suspension array.\n\nRESULTS: Microscopic analysis showed altered cell morphology and cell shrinkage following incubation with synovial fluid of RA patients. Detection of vital cells showed a highly significant decrease of vital chondrocyte when treated with RA synovial fluids in comparison with OA synovial fluids. An active secretion of cytokines such as vascular endothelial growth factor (VEGF) of chondrocytes treated with OA synovial fluids was observed.\n\nCONCLUSIONS: Significantly increased levels of various cytokines in synovial fluids of RA, and surprisingly of OA, patients were shown. Activation of pro-inflammatory cytokines of human chondrocytes by synovial fluids of OA patient supports a pro-inflammatory process in the pathogenesis of OA.
-
Inflammatory synovial fluid microenvironment drives primary human chondrocytes to actively take part in inflammatory Joint Diseases
Immunologic Research, 2012Co-Authors: Eric Röhner, Georg Matziolis, Bernd Füchtmeier, Timo Gaber, Frank Buttgereit, Gerd-rüdiger Burmester, Carsten Perka, Paula HoffAbstract:The role of human chondrocytes in the pathogenesis of cartilage degradation in rheumatic Joint Diseases has presently gained increasing interest. An active chondrocyte participation in local inflammation may play a role in the initiation and progression of inflammatory Joint Diseases and in a disruption of cartilage repair mechanisms resulting in cartilage degradation. In the present study, we hypothesized that inflammatory synovial fluid triggers human chondrocytes to actively take part in inflammatory processes in rheumatic Joint Diseases. Primary human chondrocytes were incubated in synovial fluids gained from patients with rheumatoid arthritis, psoriasis arthritis and reactive arthritis. The detection of vital cell numbers was determined by using Casy Cell Counter System. Apoptosis was measured by Annexin-V and 7AAD staining. Cytokine and chemokine secretion was determined by a multiplex suspension array. Detection of vital cells showed a highly significant decrease in chondrocyte numbers. Flow cytometry demonstrated a significant increase in apoptotic chondrocytes after the incubation. An active secretion of cytokines such as MCP-1 and MIF by chondrocytes was observed. The inflammatory synovial fluid microenvironment mediates apoptosis and cell death of chondrocytes. Moreover, in terms of cytokine secretion, it also induces an active participation of chondrocytes in ongoing inflammation.
Silvia Rollefstad - One of the best experts on this subject based on the ideXlab platform.
-
effects of long term statin treatment on coronary atherosclerosis in patients with inflammatory Joint Diseases
PLOS ONE, 2019Co-Authors: Mona Svanteson, E Ikdahl, Silvia Rollefstad, Jonny Hisdal, Nilseinar Klow, Joseph O Sexton, Ylva Haig, Anne Grete SembAbstract:Background The effect of statins over time on coronary atherosclerosis in patients with inflammatory Joint Diseases (IJD) is unknown. Our aim was to evaluate the change in coronary plaque morphology and volume in long-term statin-treated patients with IJD. Methods Sixty-eight patients with IJD and carotid artery plaque(s) underwent coronary computed tomography angiography before and after a mean of 4.7 (range 4.0–6.0) years of statin treatment. The treatment target for low density lipoprotein cholesterol (LDL-c) was ≤1.8 mmol/L. Changes in plaque volume (calcified, mixed/soft and total) and coronary artery calcification (CAC) from baseline to follow-up were assessed using the 17-segment American Heart Association-model. Results Median (IQR) increase in CAC after statin treatment was 38 (5–236) Agatston units (p 1.8mmol/L (21 [2–143] vs. 69 [16–423], p = 0.006 and 0.65 [-1.0–13.9] vs. 13.0 [0.0–60.8] mm3, p = 0.019, respectively). Conclusions A progression of total atherosclerotic plaque volume in statin-treated patients with IJD was observed. However, soft/mixed plaque volume was reduced, suggesting an alteration in plaque composition. Patients with recommended LDL-c levels at follow-up had reduced atherosclerotic progression compared to patients with LDL-c levels above the treatment target, suggesting a beneficial effect of treatment to guideline-recommended lipid targets in IJD patients.
-
guideline recommended treatment to targets of cardiovascular risk is inadequate in patients with inflammatory Joint Diseases
International Journal of Cardiology, 2019Co-Authors: E Ikdahl, Grunde Wibetoe, Silvia Rollefstad, Anne Salberg, Kjetil Bergsmark, Tore K Kvien, I C Olsen, D M Soldal, Gunnstein Bakland, Ase Stavland LexbergAbstract:Abstract Objectives Patients with inflammatory Joint Diseases (IJD) have an increased risk of cardiovascular disease (CVD). Our goal was to examine indications for, and use of, lipid-lowering therapy (LLT) and antihypertensive treatment (AntiHT) in patients with IJD. Furthermore, to investigate the frequency of low-density lipoprotein cholesterol (LDL-c) and blood pressure (BP) goal attainment among IJD patients. Methods The cohort was derived from the NOrwegian Collaboration on Atherosclerosis in patients with Rheumatic Joint Diseases (NOCAR). Indications for AntiHT were: systolic/diastolic BP ≥ 140/90 mm Hg, self-reported hypertension or AntiHT. CVD risk was estimated by the systematic coronary risk evaluation (SCORE) algorithm. LDL-c goals were 8 mmol/L or a SCORE estimate ≥ 5%, and Results In total, 2277 patients (rheumatoid arthritis: 1376, axial spondyloarthritis: 474, psoriatic arthritis: 427) were included. LLT and AntiHT were indicated in 36.1% and 52.6% of the patients, of whom 37.6% and 47.0% were untreated, respectively. LDL-c and BP targets were obtained in 26.2% and 26.3%, respectively. Guideline recommended treatment and/or corresponding treatment targets were not initiated or obtained in approximately 50%. Rheumatoid arthritis patients were particularly likely to be undertreated with LLT, whereas hypertension undertreatment was most common in psoriatic arthritis. Conclusions Inadequate CVD prevention encompasses all the three major IJD entities. The unmet need for CVD preventive measures is not only prevalent in RA, but exists across all the major IJD entities.
-
sustained improvement of arterial stiffness and blood pressure after long term rosuvastatin treatment in patients with inflammatory Joint Diseases results from the rora as study
PLOS ONE, 2016Co-Authors: E Ikdahl, Silvia Rollefstad, Tore K Kvien, I C Olsen, Jonny Hisdal, Terje R Pedersen, Anne Grete SembAbstract:Objective Patients with inflammatory Joint Diseases (IJD) have a high prevalence of hypertension and increased arterial stiffness. The aim of the present study was to evaluate the effect of long-term rosuvastatin treatment on arterial stiffness, measured by augmentation index (AIx) and aortic pulse wave velocity (aPWV), and blood pressure (BP) in IJD patients with established atherosclerosis. Methods Eighty-nine statin naive IJD patients with carotid atherosclerotic plaque(s) (rheumatoid arthritis n = 55, ankylosing spondylitis n = 23, psoriatic arthritis n = 11) received rosuvastatin for 18 months to achieve low-density lipoprotein cholesterol goal ≤1.8 mmol/L. Change in AIx (ΔAIx), aPWV (ΔaPWV), systolic BP (ΔsBP) and diastolic BP (ΔdBP) from baseline to study end was assessed by paired samples t-tests. Linear regression was applied to evaluate associations between cardiovascular disease (CVD) risk factors, rheumatic disease specific variables and medication, and ΔAIx, ΔaPWV, ΔsBP and ΔdBP. Results AIx, aPWV, sBP and dBP were significantly reduced from baseline to study end. The mean (95%CI) changes were: ΔAIx: -0.34 (-0.03, -0.65)% (p = 0.03), ΔaPWV: -1.69 (-0.21, -3.17)m/s2 (p = 0.03), ΔsBP: -5.27 (-1.61, -8.93)mmHg (p = 0.004) and ΔdBP -2.93 (-0.86, -5.00)mmHg (p = 0.01). In linear regression models, ∆aPWV was significantly correlated with ΔsBP and ΔdBP (for all: p<0.001). Conclusions There is an unmet need of studies evaluating CVD prevention in IJD patients. We have shown for the first time that long-term intensive lipid lowering with rosuvastatin improved arterial stiffness and induced a clinically significant BP reduction in patients with IJD. These improvements were linearly correlated and may represent novel insight into the pleiotropic effects by statins. Trial Registration ClinicalTrials.gov NCT01389388
-
association of chest pain and risk of cardiovascular disease with coronary atherosclerosis in patients with inflammatory Joint Diseases
Frontiers of Medicine in China, 2015Co-Authors: Silvia Rollefstad, E Ikdahl, Tore K Kvien, Jonny Hisdal, Terje R Pedersen, Anne Grete SembAbstract:Objectives: The relation between chest pain and coronary atherosclerosis (CA) in patients with inflammatory Joint Diseases (IJD) has not been explored previously. Our aim was to evaluate the associations of the presence of chest pain and the predicted 10-year risk of cardiovascular disease (CVD) by use of several CVD risk algorithms, with multi-detector computer tomography (MDCT) coronary angiography verified CA. Methods: Detailed information concerning chest pain and CVD risk factors was obtained in 335 patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). In addition, 119 of these patients underwent MDCT coronary angiography. Results: Thirty-one percent of the patients (104/335) reported chest pain. Only 6 patients (1.8%) had atypical angina pectoris (pricking pain at rest). In 69 patients without chest pain, two thirds had CA, while in those who reported chest pain (n=50), CA was present in 48.0%. In a logistic regression analysis, chest pain was not associated with CA (dependent variable) (p=0.43). About 30% (Nagelkerke R2) of CA was explained by any of the CVD risk calculators: SCORE, Framingham Risk Score or Reynolds Risk Score. Conclusion: The presence of chest pain was surprisingly infrequently reported in patients with IJD who were referred for a CVD risk evaluation. However, when present, chest pain was weakly associated with CA, in contrast to the predicted CVD risk by several risk calculators which was highly associated with the presence of CA. These findings suggest that clinicians treating patients with IJD should be alert of coronary atherosclerotic disease also in absence of chest pain symptoms.
-
rosuvastatin improves endothelial function in patients with inflammatory Joint Diseases longitudinal associations with atherosclerosis and arteriosclerosis results from the rora as statin intervention study
Arthritis Research & Therapy, 2015Co-Authors: E Ikdahl, Silvia Rollefstad, Tore K Kvien, I C Olsen, Jonny Hisdal, Terje R Pedersen, Anne Grete SembAbstract:Introduction Endothelial dysfunction is an early step in the atherosclerotic process and can be quantified by flow-mediated vasodilation (FMD). Our aim was to investigate the effect of long-term rosuvastatin therapy on endothelial function in patients with inflammatory Joint Diseases (IJD) with established atherosclerosis. Furthermore, to evaluate correlations between change in FMD (ΔFMD) and change in carotid plaque (CP) height, arterial stiffness [aortic pulse wave velocity (aPWV) and augmentation index (AIx)], lipids, disease activity and inflammation.
Gerd-rüdiger Burmester - One of the best experts on this subject based on the ideXlab platform.
-
Osteoarthritis synovial fluid activates pro-inflammatory cytokines in primary human chondrocytes
International Orthopaedics, 2013Co-Authors: Paula Hoff, Manuela Jakstadt, Kristin Andreas, Georg Matziolis, Timo Gaber, Frank Buttgereit, Gerd-rüdiger Burmester, Carsten Perka, Eric RöhnerAbstract:PURPOSE: Two of the most common Joint Diseases are rheumatoid arthritis (RA) and osteoarthritis (OA). Cartilage degradation and erosions are important pathogenetic mechanisms in both Joint Diseases and have presently gained increasing interest. The aim of the present study was to investigate the effects of the synovial fluid environment of OA patients in comparison with synovial fluids of RA patients on human chondrocytes in vitro.\n\nMETHODS: Primary human chondrocytes were incubated in synovial fluids gained from patients with OA or RA. The detection of vital cell numbers was determined by histology and by using the Casy Cell Counter System. Cytokine and chemokine secretion was determined by a multiplex suspension array.\n\nRESULTS: Microscopic analysis showed altered cell morphology and cell shrinkage following incubation with synovial fluid of RA patients. Detection of vital cells showed a highly significant decrease of vital chondrocyte when treated with RA synovial fluids in comparison with OA synovial fluids. An active secretion of cytokines such as vascular endothelial growth factor (VEGF) of chondrocytes treated with OA synovial fluids was observed.\n\nCONCLUSIONS: Significantly increased levels of various cytokines in synovial fluids of RA, and surprisingly of OA, patients were shown. Activation of pro-inflammatory cytokines of human chondrocytes by synovial fluids of OA patient supports a pro-inflammatory process in the pathogenesis of OA.
-
Inflammatory synovial fluid microenvironment drives primary human chondrocytes to actively take part in inflammatory Joint Diseases
Immunologic Research, 2012Co-Authors: Eric Röhner, Georg Matziolis, Bernd Füchtmeier, Timo Gaber, Frank Buttgereit, Gerd-rüdiger Burmester, Carsten Perka, Paula HoffAbstract:The role of human chondrocytes in the pathogenesis of cartilage degradation in rheumatic Joint Diseases has presently gained increasing interest. An active chondrocyte participation in local inflammation may play a role in the initiation and progression of inflammatory Joint Diseases and in a disruption of cartilage repair mechanisms resulting in cartilage degradation. In the present study, we hypothesized that inflammatory synovial fluid triggers human chondrocytes to actively take part in inflammatory processes in rheumatic Joint Diseases. Primary human chondrocytes were incubated in synovial fluids gained from patients with rheumatoid arthritis, psoriasis arthritis and reactive arthritis. The detection of vital cell numbers was determined by using Casy Cell Counter System. Apoptosis was measured by Annexin-V and 7AAD staining. Cytokine and chemokine secretion was determined by a multiplex suspension array. Detection of vital cells showed a highly significant decrease in chondrocyte numbers. Flow cytometry demonstrated a significant increase in apoptotic chondrocytes after the incubation. An active secretion of cytokines such as MCP-1 and MIF by chondrocytes was observed. The inflammatory synovial fluid microenvironment mediates apoptosis and cell death of chondrocytes. Moreover, in terms of cytokine secretion, it also induces an active participation of chondrocytes in ongoing inflammation.
-
[Tissue engineering: chances and challenges for application in rheumatic Diseases]
Z Rheumatol, 2003Co-Authors: Thomas Häupl, Jochen Ringe, Christoph Erggelet, Christian Kaps, Gerd-rüdiger BurmesterAbstract:Current technologies of tissue engineering offer new strategies for the treatment of cartilage and bone defects. Beyond implantation of cell suspensions, second generation products of biomaterial enforced with in vitro preformed tissues are clinically applied. Ongoing research and development focus on differentiation factors and tissue protection. In search for sources of autologous cells which are easier to collect and which may serve for more complex tissues like osteochondral implants, mesenchymal stem cells are investigated. The design of in vitro experiments, which are required for these investigations, has produced tissue engineering technologies, which may serve for pathophysiology research in inflammatory Joint Diseases and for exploration of treatment strategies. These together with the advances in biological therapies of rheumatic Diseases are the basis of new concepts, which promise application of tissue engineering also in inflammatory Joint Diseases
