scholarly journals AB0788 MARKER OF CARTILAGE TISSUE LESION IMMUNOPATHOGENESIS OF RHEUMATOID ARTHRITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1419.2-1419
Author(s):  
O. Rusanova ◽  
A. Trofimenko ◽  
N. Emelyanov ◽  
O. Emelyanova
Keyword(s):  
Rheumatoid Arthritis ◽  
Articular Cartilage ◽  
Disease Activity ◽  
Collagen Type ◽  
Cartilage Lesion ◽  
Elisa Test ◽  
Cartilage Tissue ◽  
Magnetic Sorbents ◽  
Stage 1

Background:Collagen type 2 is the basic protein of cartilaginous tissue composing over 80% of its mass. Finding excessive antibodies to collagen type 2 and immune complexes is a diagnostic and prognostic criterion of immune lesion of articular cartilage.Objectives:To study production of antibodies to collagen type 2 in patients with rheumatoid arthritis using immobilized magnetically controlled forms.Methods:The antigen was represented by commercial formulation of collagen type 2 produced by Serva (Sweden). Antibodies to collagen type 2 were determined in the patients’ blood serum by way of a technique of immunoenzyme assay (ELISA test) using immobilized magnetic sorbents. Magnetic sorbents were polyacrylamide granules from 10 to 100 micron in size containing magnetic material and collagen type 2. We studied 30 apparently healthy donor individuals and 92 patients with a confirmed diagnosis of rheumatoid arthritis.Results:A study of sera from rheumatoid arthritis patients revealed antibodies to collagen type 2 in 63 patients (68.48%). The correlation coefficient between anti-collagen type 2 antibodies, and IgA / IgM amounted to 0.28 and 0.36, correspondingly. At stage 1 and 2 of disease activity the level of antibodies was higher than in donors (р<0.001). The highest level of antibodies to collagen type 2 was seen in patients with stage 3 of disease activity (0.55±0.02). The amount of antibodies to collagen type 2 in patients with visceral manifestations of rheumatoid arthritis was no different from that in patients without any additional organ involvement, which is hardly surprising since collagen type 2 is mostly localized in articular cartilage and is practically absent from the connective tissue of other organs and systems.Conclusion:Thus the presence of antibodies to collagen type 2 correlates with the disease activity and is an important marker of articular cartilage lesion in patients with rheumatoid arthritis.Disclosure of Interests:None declared

scholarly journals Chondroplasty Efficacy of Bone Matrix

2019 ◽  
Vol 2 (1) ◽  
pp. 8-13
Author(s):  
Iryanov Yu.M ◽  
Kiryanov N.A
Keyword(s):  
Articular Cartilage ◽  
Bone Matrix ◽  
Cartilage Lesion ◽  
Cartilage Tissue ◽  
Rejection Reaction ◽  
X Ray ◽  
Osteoclastic Resorption ◽  
Male Wistar Rats ◽  
Experimental Group ◽  
Joint Material

Aim To study the chondroplasty efficacy of the bone matrix obtained using an original technology in restoring cartilage defect of the knee joint. Material and Methods Marginal defects were modeled on the surface of the distal end of the femur in 40 adult male Wistar rats. The bone matrix obtained using an original technology was implanted in the damaged area in animals of the experimental group. Material was investigated by means of light microscopy, transmission and scanning electron microscopy, and electron probe X-ray microanalysis. Results It was found that the bone matrix implanted did not cause an immune rejection reaction, activated reparative chondrogenesis for a prolonged period. In the area of articular cartilage lesion, the regenerate acquiring cellular and histochemical characteristics of the hyaline cartilage tissue was formed. The chondroinductive properties for the bone matrix were ensured by localized growth factors and morphogenetic proteins released during osteoclastic resorption. Conclusion The application of the bone matrix as a stimulator of chondrogenesis is theoretically reasonable and has a good perspective in treatment of damages and diseases of the articular cartilage.

scholarly journals M1-like macrophage contributes to chondrogenesis in vitro

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoshiyuki Miyamoto ◽  
Keigo Kubota ◽  
Yukiyo Asawa ◽  
Kazuto Hoshi ◽  
Atsuhiko Hikita
Keyword(s):  
Regenerative Medicine ◽  
Tissue Regeneration ◽  
Tissue Damage ◽  
Collagen Type ◽  
Experimental System ◽  
Cartilage Tissue ◽  
Oral And Maxillofacial Regions

AbstractCartilage tissues have poor self-repairing abilities. Regenerative medicine can be applied to recover cartilage tissue damage in the oral and maxillofacial regions. However, hitherto it has not been possible to predict the maturity of the tissue construction after transplantation or to prepare mature cartilage tissues before transplantation that can meet clinical needs. Macrophages play an important role in cartilage tissue regeneration, although the exact mechanisms remain unknown. In this study, we established and verified an in vitro experimental system for the direct co-culture of cell pellets prepared from mouse auricular chondrocytes and macrophages polarized into four phenotypes (M1-like, M1, M2-like, and M2). We demonstrate that cartilage pellets co-cultured with M1-like promoted collagen type 2 and aggrecan production and induced the most significant increase in chondrogenesis. Furthermore, M1-like shifted to M2 on day 7 of co-culture, suggesting that the cartilage pellet supplied factors that changed the polarization of M1-like. Our findings suggest that cartilage regenerative medicine will be most effective if the maturation of cartilage tissues is induced in vitro by co-culture with M1-like before transplantation.

scholarly journals Characterization of Collagen Type I and II Blended Hydrogels for Articular Cartilage Tissue Engineering

2016 ◽  
Vol 17 (10) ◽  
pp. 3145-3152 ◽  
Author(s):  
Nelda Vázquez-Portalatı́n ◽  
Claire E. Kilmer ◽  
Alyssa Panitch ◽  
Julie C. Liu
Keyword(s):  
Tissue Engineering ◽  
Articular Cartilage ◽  
Collagen Type ◽  
Cartilage Tissue Engineering ◽  
Collagen Type I ◽  
Cartilage Tissue ◽  
Type I

scholarly journals Adipose-Derived Mesenchymal Stem Cell Chondrospheroids Cultured in Hypoxia and a 3D Porous Chitosan/Chitin Nanocrystal Scaffold as a Platform for Cartilage Tissue Engineering

2020 ◽  
Vol 21 (3) ◽  
pp. 1004 ◽  
Author(s):  
Veronica Zubillaga ◽  
Ana Alonso-Varona ◽  
Susana C. M. Fernandes ◽  
Asier M. Salaberria ◽  
Teodoro Palomares
Keyword(s):  
Tissue Engineering ◽  
Articular Cartilage ◽  
Collagen Type ◽  
Porous Scaffold ◽  
Cartilage Tissue Engineering ◽  
Cartilage Regeneration ◽  
Cartilage Tissue ◽  
Type I ◽  
Low Oxygen ◽  
Porous Chitosan

Articular cartilage degeneration is one of the most common causes of pain and disability in middle-aged and older people. Tissue engineering (TE) has shown great therapeutic promise for this condition. The design of cartilage regeneration constructs must take into account the specific characteristics of the cartilaginous matrix, as well as the avascular nature of cartilage and its cells’ peculiar arrangement in isogenic groups. Keeping these factors in mind, we have designed a 3D porous scaffold based on genipin-crosslinked chitosan/chitin nanocrystals for spheroid chondral differentiation of human adipose tissue-derived mesenchymal stem cells (hASCs) induced in hypoxic conditions. First, we demonstrated that, under low oxygen conditions, the chondrospheroids obtained express cartilage-specific markers including collagen type II (COL2A1) and aggrecan, lacking expression of osteogenic differentiation marker collagen type I (COL1A2). These results were associated with an increased expression of hypoxia-inducible factor 1α, which positively directs COL2A1 and aggrecan expression. Finally, we determined the most suitable chondrogenic differentiation pattern when hASC spheroids were seeded in the 3D porous scaffold under hypoxia and obtained a chondral extracellular matrix with a high sulphated glycosaminoglycan content, which is characteristic of articular cartilage. These findings highlight the potential use of such templates in cartilage tissue engineering.

T2 Mapping as a New Method for Quantitative Assessment of Cartilage Damage in Rheumatoid Arthritis

2019 ◽  
Vol 47 (6) ◽  
pp. 820-825 ◽  
Author(s):  
Nina Renner ◽  
Arnd Kleyer ◽  
Gerhard Krönke ◽  
David Simon ◽  
Stefan Söllner ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Articular Cartilage ◽  
Disease Activity ◽  
Disease Duration ◽  
T2 Mapping ◽  
Cartilage Damage ◽  
Relaxation Times ◽  
T2 Relaxation ◽  
Hand Joints ◽  
Magnetic Resonance Imaging Mri

Objective.Rheumatoid arthritis (RA) is associated with damage of the articular cartilage and the periarticular bone. While imaging of bone damage has substantially improved in recent years, direct imaging of the articular cartilage of the hand joints in patients with RA is still challenging. The study used T2 mapping of the finger joints to assess cartilage damage in RA.Methods.Magnetic resonance imaging (MRI) at 3 Tesla was done in 30 patients with RA, and T2 relaxation times visualizing alteration in the collagen network and hydration of articular cartilage were mapped in 6 cartilage regions of the metacarpophalangeal (MCP) joints 2 and 3. Values were related to autoantibody status [anticitrullinated protein antibodies (ACPA), rheumatoid factor (RF)], disease duration, and disease activity as well as sex and age of the patients.Results.T2 relaxation times could be reliably measured in the 6 regions of the MCP joints. Significantly higher relaxation times indicating more advanced cartilage alterations were observed in the metacarpal heads of ACPA-positive (p = 0.001–0.010) and RF-positive patients (p = 0.013–0.025) as well as those with longer disease duration (> 3 yrs; p = 0.028–0.043). Current disease activity, sex, and age did not influence T2 relaxation times.Conclusion.These data show that cartilage damage can be localized and quantified in the hand joints of patients with RA by T2 mapping. Further, ACPA and RF positivity as well as disease duration appear to be the crucial factors influencing cartilage damage.

Suppression of discoidin domain receptor 1 expression enhances the chondrogenesis of adipose-derived stem cells

2015 ◽  
Vol 308 (9) ◽  
pp. C685-C696 ◽  
Author(s):  
Shun-Cheng Wu ◽  
Hsu-Feng Hsiao ◽  
Mei-Ling Ho ◽  
Yung-Li Hung ◽  
Je-Ken Chang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Articular Cartilage ◽  
Collagen Type ◽  
Cartilage Tissue Engineering ◽  
Cartilage Tissue ◽  
Adipose Derived Stem Cells ◽  
Type Ii ◽  
Collagen Type Ii ◽  
Matrix Deposition ◽  
Discoidin Domain Receptor 1

Effectively directing the chondrogenesis of adipose-derived stem cells (ADSCs) to engineer articular cartilage represents an important challenge in ADSC-based articular cartilage tissue engineering. The discoidin domain receptor 1 (DDR1) has been shown to affect cartilage homeostasis; however, little is known about the roles of DDR1 in ADSC chondrogenesis. In this study, we used the three-dimensional culture pellet culture model system with chondrogenic induction to investigate the roles of DDR1 in the chondrogenic differentiation of human ADSCs (hADSCs). Real-time polymerase chain reaction and Western blot were used to detect the expression of DDRs and chondrogenic genes. Sulfated glycosaminoglycan (sGAG) was detected by Alcian blue and dimethylmethylene blue (DMMB) assays. Terminal deoxy-nucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was used to assess cell death. During the chondrogenesis of hADSCs, the expression of DDR1 but not DDR2 was significantly elevated. The depletion of DDR1 expression in hADSCs using short hairpin RNA increased the expression of chondrogenic genes (SOX-9, collagen type II, and aggrecan) and cartilaginous matrix deposition (collagen type II and sGAG) and only slightly increased cell death (2–8%). DDR1 overexpression in hADSCs decreased the expression of chondrogenic genes (SOX-9, collagen type II, and aggrecan) and sGAG and enhanced hADSC survival. Moreover, DDR1-depleted hADSCs showed decreased expression of the terminal differentiation genes runt-related transcription factor 2 (Runx2) and matrix metalloproteinase 13 (MMP-13). These results suggest that DDR1 suppression may enhance ADSC chondrogenesis by enhancing the expression of chondrogenic genes and cartilaginous matrix deposition. We proposed that the suppression of DDR1 in ADSCs may be a candidate strategy of genetic modification to optimize ADSC-based articular cartilage tissue engineering.

scholarly journals AB0083 STUDY OF THE ROLE OF ANGIOPOIETIN-LIKE PROTEIN TYPE 4 IN METABOLIC DISORDERS CAUSED BY INFLAMMATION IN RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1341.2-1341
Author(s):  
A. Aleksandrov ◽  
V. Aleksandrov ◽  
L. Shilova
Keyword(s):  
Rheumatoid Arthritis ◽  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Metabolic Syndrome ◽  
Blood Serum ◽  
Disease Activity ◽  
Metabolic Disorders ◽  
Healthy Individuals

Background:Objectives:To assess the potential role of angiopoietin-like protein type 4 (ANGPTL4) in metabolic disorders caused by inflammation in rheumatoid arthritis (RA).Methods:The study included 88 patients with significant RA, 64 patients with other rheumatic diseases (RD) (36 patients with osteoarthritis (OA); 28 patients with psoriatic arthritis (PsA); 17 patients with ankylosing spondylitis (AS)) and 32 healthy individuals. Estimation of ANGPTL4 was carried out by enzyme immunoassay using the commercial test system “RayBio Human ANGPTL4 ELISA Kit” (RayBiotech, USA) in blood serum. Levels of ESR, CRP, RF, antibodies to cyclic citrullinated peptide (anti-CCP) and modified vimentin (anti-MCV) in the ELISA test were determined for all patients with RA.Results:The level of ANGPTL4 in the blood serum of patients with RA was significantly higher than in healthy people (p <0.001) and patients with other RD (p = 0.012 compared with OA; p = 0.046 with PsA; p = 0.008 with AS). ANGPTL4 indices in patients with RA correlated with the age of onset of RA (r = -0.658, p <0.001), disease activity according to DAS-28 (r = 0.449, p = 0.001), level of education (r = 0.235, p = 0.029), dose of glucocorticoid hormones (r = 0.321, p = 0.009) and methotrexate (r = -0.496, p = 0.05), the presence of osteopenia (r = 0.44), signs of kidney damage - proteinuria (r = 0.309, p = 0.037) and hypoalbuminemia (r = 0.386, p = 0.022), as well as with CRP levels (r = 0.488, p = 0.003), ESR (r = 0.458, p = 0.002), serum vitamin D (r = -0.417) and urinary calcium when recalculated to creatinine (r = 0.797, p = 0.032).Patients with RA showed a high frequency of insulin resistance (according to the HOMA-IR index) (1.27 [0.84–1.62] in patients with RA; 0.76 [0.44–1.02] in healthy individuals; p <0.001) and the presence of coronary heart disease, as well as a positive correlation between disease activity (according to DAS-28) and insulin resistance (according to the HOMA-IR index) (p = 0.033).Higher values of C-reactive protein (p = 0.04) and serum ANGPTL4 levels (p = 0.042, compared with patients with RA without type 2 diabetes; p = 0.026, compared with healthy individuals) were determined in the group of patients with RA with the presence of type 2 diabetes. ANGPTL4 acts as an inhibitor of lipoprotein lipase. His contribution to the development of dyslipidemia in RA can be demonstrated by the results we obtained when comparing groups of patients with / without signs of metabolic syndrome (MS). A positive correlation between ANGPTL4 and triglyceride levels (r = 0.42, p = 0.018) was found. An increase in the level of ANGPTL4 in blood serum of patients with RA with MS (p = 0.027 compared with RA without MS) can predict the development of cardiac pathology in this group of patients.Conclusion:ANGPTL4 is directly involved in the regulation of glucose homeostasis, lipid metabolism, and insulin sensitivity. Cardiovascular diseases associated with atherosclerosis, insulin resistance and metabolic syndrome are known as the most common extraarticular manifestations of RA; the study of the role of ANGPTL4 in metabolic disorders caused by inflammation can show a new direction in the development of laboratory and therapeutic technologies in RA.Disclosure of Interests:None declared

scholarly journals Increased expression of blood mononuclear cell nitric oxide synthase type 2 in rheumatoid arthritis patients.

1996 ◽  
Vol 184 (3) ◽  
pp. 1173-1178 ◽  
Author(s):  
E W St Clair ◽  
W E Wilkinson ◽  
T Lang ◽  
L Sanders ◽  
M A Misukonis ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Nitric Oxide ◽  
Disease Activity ◽  
Mononuclear Cells ◽  
Normal Subjects ◽  
Blood Mononuclear Cells ◽  
Nitrite Nitrate ◽  
Nos2 Expression

Nitric oxide (NO) is an important inflammatory mediator in nonhuman animal models of rheumatoid arthritis (RA). The purpose of the present study was to determine whether blood mononuclear cells from patients with active RA (as compared to control subjects) have higher levels of NO synthase type 2 (NOS2) and produce more NO in vitro. Leukocytes from 25 RA patients and 20 normal subjects were examined. Arthritis activity was assessed by tender and swollen joint counts, duration of morning stiffness, patient assessment of pain, physician and patient global assessment of disease activity, the modified Stanford Health Assessment Questionnaire, and by blood levels of acute phase reactants. Blood mononuclear cell NOS enzyme activity/antigen content and nitrite/nitrate formation in vitro were measured. Blood mononuclear cells from RA patients had increased NOS activity and increased NOS2 antigen content as compared to those from normal subjects, and responded to interferon-gamma with increased NOS expression and nitrite/nitrate production in vitro. NOS activity of freshly isolated blood mononuclear cells correlated significantly with disease activity, as assessed by render and swollen joint counts. Our results demonstrate that patients with RA have systemic activation for NOS2 expression, and that the degree of activation correlates with disease activity. Increased NOS2 expression and NO generation may be important in the pathogenesis of RA.

scholarly journals Autogenous Osteochondral Graft Associated with IGF-1 in Induced Articular Cartilage Lesion in Rabbits

2018 ◽  
Vol 46 (1) ◽  
pp. 10
Author(s):  
Fernando Yoiti Kitamura Kawamoto ◽  
Leonardo Augusto Lopes Muzzi ◽  
Antônio Carlos Cunha Lacreta Junior ◽  
Djeison Lutier Raymundo ◽  
Rodrigo Gabellini Leonel Alves ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Tissue Repair ◽  
Collagen Type ◽  
Physiological Solution ◽  
Trochlear Groove ◽  
Osteochondral Graft ◽  
Osteochondral Grafts ◽  
Significant Difference ◽  
Osteochondral Grafting

Background: Articular cartilage has a limited capacity for regeneration and of the various treatments proposed, none have reached appropriate therapeutic effectiveness. This study aimed to evaluate autogenous osteochondral grafts in intact or macerated format, in association with or without insulin-like growth factor type-1 (IGF-1) in the repair of osteochondral defects induced in the femoral trochlear groove of rabbits.Materials, Methods & Results: Seventeen healthy White New Zealand rabbits were selected for this study. The rabbits were female, six months old, and had an average body weight of 4.5 kg. All 34 stifle joints were subjected to autogenous osteochondral grafting in the femoral trochlear groove. The joints were divided into four groups designated as intact osteochondral graft with IGF-1 (INT + IGF), intact osteochondral graft with physiological solution (INT + FIS), macerated osteochondral graft with IGF-1 (MAC + IGF), and macerated osteochondral graft with physiological solution (MAC + FIS). Serial evaluations were performed by orthopedic and radiographic examination. After 6 and 12 weeks postoperatively, the grafted area was subjected to macroscopic, histological, and immunohistochemical analyses. Although no statistically significant differences were found between the groups in relation to clinical, macroscopic, histological, and immunohistochemical aspects, a tendency of IGF-1 to promote tissue repair was evident. In the radiographic evaluation, the articular surface and the recipient site in both groups with IGF-1 showed significantly more effective filling (P ≤ 0.05). Regardless of the group, collagen type 2 production, as assessed by immunohistochemistry, was found to be appropriate on the grafted articular surface.Discussion: In extensive cartilage lesions, the use of intact osteochondral grafts may be infeasible due to donor site morbidity. An alternative is the use of macerated osteochondral grafts, which cover a larger area and act as a support and cellular source in the repair process. Growth factors have been evaluated in association with grafted tissues to aid tissue repair, and IGF-1 is currently prominent. In the radiographic analysis of the present study, when comparing sites subjected to osteochondral grafting, presence of the whole graft evidenced adequate local filling in all groups. However, graft integration was apparently rapid and effective in the INT + IGF and MAC + IGF groups from the sixth and ninth weeks of the procedure, respectively. In the macroscopic evaluation at the twelfth week, graft integration with the original cartilaginous tissue was more evident, especially in both groups treated with IGF-1. It is likely that the property of IGF-1 to increase chondrogenesis in the cartilage repair of articular lesions in vivo may have contributed to these results in radiographic and macroscopic examinations. Histological examination showed no significant difference between groups in the same period of time; however, it was observed that addition of IGF-1 promoted a more evident tissue reaction and cellular activation, potentiating the process of reabsorption and repair in the grafted tissue. Immunohistochemical analysis showed similar immunoreactivity for collagen type 2 in all groups as early as the sixth week. However, a small portion of these tissues cannot be considered true hyaline cartilage due to the absence of some typical features. In summary, addition of IGF-1 to the autogenous osteochondral graft seemed to stimulate reabsorption and replacement processes in the grafted tissue. The grafts showed adequate ability to repair articular cartilage, displaying formation of collagen type 2 similar to that in the original tissue.

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