Tumor necrosis factor-inhibiting therapy preferentially targets bone destruction but not synovial inflammation in a tumor necrosis factor-driven model of rheumatoid arthritis

2013 ◽  
Vol 65 (3) ◽  
pp. 608-617 ◽  
Author(s):  
Nikolaus B. Binder ◽  
Antonia Puchner ◽  
Birgit Niederreiter ◽  
Silvia Hayer ◽  
Harald Leiss ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Bone Destruction ◽  
Synovial Inflammation ◽  
Necrosis Factor

scholarly journals Biologic therapies for the treatment of rheumatoid arthritis

2021 ◽  
Vol 64 (2) ◽  
pp. 95-104
Author(s):  
Sung-Jae Choi
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Bone Destruction ◽  
Patient Characteristics ◽  
Necrosis Factor Alpha ◽  
Biological Products ◽  
Combined Use ◽  
Factor Alpha ◽  
Necrosis Factor

Rheumatoid arthritis (RA) is a chronic autoimmune disease that primarily affects the synovial joints. If left untreated, persistent synovial inflammation can lead to cartilage and bone destruction, ultimately causing significant longterm disability and mortality. However, since the late 1990s, the combined use of methotrexate, a synthetic diseasemodifying antirheumatic drug (DMARD), and a biological DMARD has revolutionized the treatment of RA. As of 2021, the Korea Food and Drug Administration has approved seven biological DMARDs for RA treatment: four tumor necrosis factor-alpha inhibitors (infliximab, etanercept, adalimumab, and golimumab) and three non-tumor necrosis factor biological products (abatacept, rituximab, and tocilizumab). Although the use of biological products has allowed significant advances in the treatment of RA, there are certain drawbacks, such as high cost, increased infection risk, and the necessity for parenteral route product administration. Therefore, discontinuation of biological DMARD use without a resulting disease flare is the next treatment goal and a desirable result from the standpoint of risk reduction and cost-effectiveness, especially for patients with clinical remission. It is still unclear which biological product is the best. Clinicians must, therefore, personalize the sequence and strategy of treatment by considering patient characteristics, disease activity, comorbidity, and economic condition

Metformin one in a Million Efficient Medicines for Rheumatoid Arthritis Complications: Inflammation, Osteoblastogenesis, Cardiovascular Disease, Malignancies

2019 ◽  
Vol 15 (2) ◽  
pp. 116-122 ◽  
Author(s):  
Elham Rajaei ◽  
Habib Haybar ◽  
Karim Mowla ◽  
Zeinab D. Zayeri
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Disease ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Bone Destruction ◽  
Janus Kinase ◽  
Laboratory Animals ◽  
Factor Α ◽  
Necrosis Factor

Background: Rheumatoid arthritis is a widespread autoimmune disease and inflammation and bone destruction are two main issues in rheumatoid arthritis. Objective: To discussing metformin effects on rheumatoid arthritis complications. Methods: : We conducted a narrative literature search including clinical trials, experimental studies on laboratory animals and cell lines. Our search covered Medline, PubMed and Google Scholar databases from 1999 until 2018. We used the terms” Metformin; Rheumatoid arthritis; Cardiovascular disease; Cancer; Osteoblastogenesis. Discussion: Inflammatory pro-cytokines such as Interlukin-6 play important roles in T. helper 17 cell lineage differentiation. Interlukin-6 and Tumor Necrosis Factor-α activate Janus kinase receptors signal through signaling transducer and activator of transcription signaling pathway which plays important role in inflammation, bone destruction and cancer in rheumatoid arthritis patients. Interlukin-6 and Tumor Necrosis Factor-α synergistically activate signaling transducer and activator of transcription and Nuclear Factor-kβ pathways and both cytokines increase the chance of cancer development in rheumatoid arthritis patients. Metformin is AMPK activators that can suppress mTOR, STAT3 and HIF-1 so AMPK activation plays important role in suppressing inflammation and osteoclastogenesis and decreasing cancer. Conclusion: Metformin effect on AMPK and mTOR pathways gives the capability to change Treg/Th17 balance and decrease Th17 differentiation and inflammation, osteoclastogenesis and cancers in RA patients. Metformin can be useful in protecting bones especially in first stages of RA and it can decrease inflammation, CVD and cancer in RA patients so Metformin beside DAMARs can be useful in increasing RA patients’ life quality with less harm and cost.</P>

scholarly journals Critical Roles for Interleukin 1 and Tumor Necrosis Factor α in Antibody-induced Arthritis

2002 ◽  
Vol 196 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Hong Ji ◽  
Allison Pettit ◽  
Koichiro Ohmura ◽  
Adriana Ortiz-Lopez ◽  
Veronique Duchatelle ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Inflammatory Cytokines ◽  
Inflammatory Arthritis ◽  
Tumor Necrosis ◽  
Environmental Changes ◽  
Bone Erosion ◽  
Bone Destruction ◽  
Tnf Α ◽  
Necrosis Factor

In spontaneous inflammatory arthritis of K/BxN T cell receptor transgenic mice, the effector phase of the disease is provoked by binding of immunoglobulins (Igs) to joint surfaces. Inflammatory cytokines are known to be involved in human inflammatory arthritis, in particular rheumatoid arthritis, although, overall, the pathogenetic mechanisms of the human affliction remain unclear. To explore the analogy between the K/BxN model and human patients, we assessed the role and relative importance of inflammatory cytokines in K/BxN joint inflammation by transferring arthritogenic serum into a panel of genetically deficient recipients. Interleukin (IL)-1 proved absolutely necessary. Tumor necrosis factor (TNF)–α was also required, although seemingly less critically than IL-1, because a proportion of TNF-α–deficient mice developed robust disease. There was no evidence for an important role for IL-6. Bone destruction and reconstruction were also examined. We found that all mice with strong inflammation exhibited the bone erosion and reconstruction phenomena typical of K/BxN arthritis, with no evidence of any particular requirement for TNFα for bone destruction. The variability in the requirement for TNF-α, reminiscent of that observed in treated rheumatoid arthritis patients, did not appear genetically programmed but related instead to subtle environmental changes.

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