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Tumor necrosis factor --- Cytokines --- Lymphotoxin-alpha --- Tumor Necrosis Factor --- Congresses --- Lymphotoxin-alpha. --- Tumor Necrosis Factor-alpha. --- -Tumor necrosis factor --- -Cachectin --- Lymphotoxin --- TNF (Immunology) --- Glycoproteins --- Growth factors --- Macrophages --- Cellular immunity --- Immune response --- Regulation --- -Congresses --- Tumor Necrosis Factor-alpha --- Cachectin-Tumor Necrosis Factor --- TNF Superfamily, Member 2 --- TNFalpha --- Cachectin --- TNF-alpha --- Tumor Necrosis Factor Ligand Superfamily Member 2 --- Cachectin Tumor Necrosis Factor --- Tumor Necrosis Factor alpha --- Certolizumab Pegol --- Adalimumab --- Infliximab --- Necrosis --- Tumor Lysis Syndrome --- Lymphotoxin-alpha3 --- Soluble Lymphotoxin-alpha --- alpha-Lymphotoxin --- TNF Superfamily, Member 1 --- TNF-beta --- Tumor Necrosis Factor Ligand Superfamily Member 1 --- Tumor Necrosis Factor-beta --- Lymphotoxin alpha --- Lymphotoxin alpha3 --- Lymphotoxin-alpha, Soluble --- Soluble Lymphotoxin alpha --- Tumor Necrosis Factor beta --- alpha Lymphotoxin --- Kankercellen. (Congres) --- Gezwellen (Kwaadaardige). (Congres) --- Cytotoxinen. (Congres) --- Antinéoplastiques. (Congrès) --- Cellules cancéreuses. (Congrès) --- Tumeurs malignes. (Congrès) --- Cytotoxines. (Congrès) --- Antineoplastische middelen. (Congres) --- Tumor necrosis factor - Congresses --- Cytokines - Congresses --- Lymphotoxin-alpha - congresses --- Tumor Necrosis Factor - congresses
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Rheumatoid Arthritis (RA) is a chronic inflammatory disease leading to joint inflammation and destruction. Treatment of RA includes the use of conventional (cs), biologic (b) disease-modifying anti-rheumatic drugs (DMARDs), and oral or intraarticular (IA) glucocorticoids (GCs). All different classes of drugs have shown to halt disease progression in clinical studies. In real life, a physician has more options than just adding or switching to a new ts/bDMARD if any kind of DMARDs has failed. They can modify or optimize the therapy with concomitant csDMARDs, and oral or IA-GC can be added to the treatment regimen. The EULAR states that therapeutic adjustment including the "optimization of csDMARDs dose or route of administration or intra-articular injections of GCs" is recommended. Thus, a new therapeutic agent can be embedded in a whole strategy with parallel optimization of the csDMARD and GC treatment. The idea of treating to target (T2T) for the treatment of RA patients has been around since the late 1990s. Many clinical studies (Ticora, BsSt, Camera) have demonstrated the superiority of a T2T approach. When I talk to physicians, I understand that most of them only rarely inject joints with GC. Therefore, I would like to create an issue on the T2T approach in reality including primary data, reviews, and real-life data demonstrating the general opinion and execution of T2T in treating RA.
Medicine --- rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging --- n/a
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Rheumatoid Arthritis (RA) is a chronic inflammatory disease leading to joint inflammation and destruction. Treatment of RA includes the use of conventional (cs), biologic (b) disease-modifying anti-rheumatic drugs (DMARDs), and oral or intraarticular (IA) glucocorticoids (GCs). All different classes of drugs have shown to halt disease progression in clinical studies. In real life, a physician has more options than just adding or switching to a new ts/bDMARD if any kind of DMARDs has failed. They can modify or optimize the therapy with concomitant csDMARDs, and oral or IA-GC can be added to the treatment regimen. The EULAR states that therapeutic adjustment including the "optimization of csDMARDs dose or route of administration or intra-articular injections of GCs" is recommended. Thus, a new therapeutic agent can be embedded in a whole strategy with parallel optimization of the csDMARD and GC treatment. The idea of treating to target (T2T) for the treatment of RA patients has been around since the late 1990s. Many clinical studies (Ticora, BsSt, Camera) have demonstrated the superiority of a T2T approach. When I talk to physicians, I understand that most of them only rarely inject joints with GC. Therefore, I would like to create an issue on the T2T approach in reality including primary data, reviews, and real-life data demonstrating the general opinion and execution of T2T in treating RA.
rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging --- n/a
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Rheumatoid Arthritis (RA) is a chronic inflammatory disease leading to joint inflammation and destruction. Treatment of RA includes the use of conventional (cs), biologic (b) disease-modifying anti-rheumatic drugs (DMARDs), and oral or intraarticular (IA) glucocorticoids (GCs). All different classes of drugs have shown to halt disease progression in clinical studies. In real life, a physician has more options than just adding or switching to a new ts/bDMARD if any kind of DMARDs has failed. They can modify or optimize the therapy with concomitant csDMARDs, and oral or IA-GC can be added to the treatment regimen. The EULAR states that therapeutic adjustment including the "optimization of csDMARDs dose or route of administration or intra-articular injections of GCs" is recommended. Thus, a new therapeutic agent can be embedded in a whole strategy with parallel optimization of the csDMARD and GC treatment. The idea of treating to target (T2T) for the treatment of RA patients has been around since the late 1990s. Many clinical studies (Ticora, BsSt, Camera) have demonstrated the superiority of a T2T approach. When I talk to physicians, I understand that most of them only rarely inject joints with GC. Therefore, I would like to create an issue on the T2T approach in reality including primary data, reviews, and real-life data demonstrating the general opinion and execution of T2T in treating RA.
Medicine --- rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging --- rheumatoid arthritis --- sleep --- sleep disorders --- pain --- osteoporosis --- fracture --- fracture risk assessment tool --- treat-to-target --- certolizumab pegol --- csDMARDs --- glucocorticoids --- intra-articular injections --- DAS 28 --- ACR response --- HAQ-DI --- TNFα --- golimumab --- efficacy --- tolerability --- immunogenicity --- methotrexate --- posology --- titration --- oral route --- subcutaneous route --- bioavailability --- effectiveness --- periodontitis --- periodontal disease --- anti-citrullinated protein autoantibodies --- rheumatoid factor --- smoking --- medication --- Porphyromonas gingivalis --- Rheumatoid arthritis --- matrix metalloproteinase 3 --- infliximab --- pharmacogenomics --- anti-TNF --- personalized medicine --- baricitinib --- disease-modifying antirheumatic drugs --- pain perception --- outcomes research --- patient perspective --- Rheumatoid Arthritis --- therapy --- DMARD --- MTX --- Tumor Necrosis Factor-Alpha Inhibitors --- ankylosing spondylitis --- biosimilar --- switching --- synovial fibroblasts --- cytokine --- osteoclast --- herbal medicine --- methylation --- next-generation sequencing --- recovery of function --- fatigue --- productivity --- tofacitinib --- oral --- Th1.17 --- IL-17A --- IFN-γ, CD73 --- adenosine --- psoriatic arthritis --- regulation --- pseudoerosions --- hand --- foot --- ultrasonography --- radiography --- computed tomography --- magnetic resonance imaging
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Arthritis has a high prevalence globally and includes over 100 different types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. The exact etiology of arthritis remains unclear and no cure exists. Anti-inflammatory drugs are commonly used in the treatment of arthritis but are associated with significant side effects. Novel modes of therapy and additional prognostic biomarkers are urgently needed for arthritis patients. This book summarizes and discusses the global picture of the current understanding of arthritis.
receptor activator of nuclear factor ?B --- infliximab --- tripterine --- triptolide --- osteoblast --- tumor necrosis factor-alpha --- synovial cell --- anti-arthritis --- biosimilars --- Epstein-Barr virus --- cytokines --- SOX9 --- parathyroid hormone --- nitric oxide --- rat --- etanercept --- angiogenesis --- glycosylation --- mitogen activated protein kinase --- Th9 lymphocytes --- rheumatoid arthritis --- IL-6 --- clodronate --- bone erosion --- mesenchymal stem cells --- collagen-induced arthritis --- biological --- gene expression --- inflammatory arthritis --- osteoarthritis --- fraxinellone --- nuclear factor kappa B --- messenger RNA --- inflammation --- miRNA --- disease-modifying --- adipokines --- WNT --- glycoprotein 42 --- miR-199a-5p --- proliferation --- next-generation sequencing --- collagen --- osteoarthritis (OA) --- experimental arthritis --- bone morphogenetic protein --- TNF-? --- computational modeling --- basic research --- osteoclast --- therapeutics --- certolizumab pegol --- chondrocytes --- progenitor cells --- adjuvant arthritis --- adalimumab --- triterpenoid --- sclareol --- TNF? --- fibroblast growth factor 2 --- antibodies --- osteoblasts --- molecular pathology --- Th17 --- immunology --- obesity --- visfatin --- articular cartilage --- autoimmune --- biomarkers --- celastrol --- MAPK --- disease pathways --- IL1? --- arthritis --- bioinformatics --- anticitrullinated peptide antibodies --- drug delivery system --- antagonists --- shared epitope --- pathology --- SMA- and MAD-related protein --- small-molecule inhibitor --- transforming growth factor ? --- mice --- golimumab --- spinal fusion --- antirheumatic drug --- early osteoarthritis --- stem cell --- rheumatoid factor --- therapeutic antibody --- bisphosphonate --- osteoclastogenesis --- interleukin --- spondyloarthropathies --- clinical translation --- therapy --- Traditional Chinese medicine --- chemokines --- structure --- cell signaling --- microRNA
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