Cytokines and Bone: Osteoimmunology

Lorenzo, Joseph

doi:10.1007/164_2019_346

Cited by 22 publications

(12 citation statements)

References 489 publications

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“…On the other hand, infliximab directly promotes the differentiation of osteoclast precursor cells in PBMC and lacunar resorption induced by RANKL. Addition of infliximab has been shown to markedly increase the number of TRAP-positive multinucleated cells (TRAP+ MNCs) and the extent of lacunar resorption in comparison with control cultures [128,129].…”

Section: Bdmards and Bone Metabolismmentioning

confidence: 99%

Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis

Kondo

Kuroda

Kobayashi

2021

IJMS

253

112

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Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic systemic inflammation causing progressive joint damage that can lead to lifelong disability. The pathogenesis of RA involves a complex network of various cytokines and cells that trigger synovial cell proliferation and cause damage to both cartilage and bone. Involvement of the cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 is central to the pathogenesis of RA, but recent research has revealed that other cytokines such as IL-7, IL-17, IL-21, IL-23, granulocyte macrophage colony-stimulating factor (GM-CSF), IL-1β, IL-18, IL-33, and IL-2 also play a role. Clarification of RA pathology has led to the development of therapeutic agents such as biological disease-modifying anti-rheumatic drugs (DMARDs) and Janus kinase (JAK) inhibitors, and further details of the immunological background to RA are emerging. This review covers existing knowledge regarding the roles of cytokines, related immune cells and the immune system in RA, manipulation of which may offer the potential for even safer and more effective treatments in the future.

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Section: Bdmards and Bone Metabolismmentioning

confidence: 99%

Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis

Kondo

Kuroda

Kobayashi

2021

IJMS

253

112

View full text Add to dashboard Cite

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“…Those that are most frequently associated with skeletal fragility include leukemia and other cancers, systemic inflammatory and autoimmune disorders (such as, but not limited to, inflammatory bowel disease, and rheumatic conditions including systemic lupus erythematosus, systemic-onset juvenile arthritis, juvenile dermatomyositis, systemic vasculitis, and overlap syndromes), renal diseases (e.g., nephrotic syndrome), neuromuscular conditions (e.g., DMD), and organ transplantation. Importantly, many of the underlying diseases themselves carry risk of skeletal fragility, particularly the neuromuscular disorders due to lack of weight-bearing, and the systemic inflammatory and hematological disorders because of the adverse effect of disease-related cytokines on skeletal metabolism (e.g., interleukin [IL] 6 and 1, tumor-necrosis factor-alpha [TNF-α]) (2).…”

Section: The Effects Of Glucocorticoids On the Pediatric Skeleton Anmentioning

confidence: 99%

Glucocorticoid-Induced Osteoporosis: Why Kids Are Different

Ward

2020

Front. Endocrinol.

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Glucocorticoids (GC) are an important risk factor for bone fragility in children with serious illnesses, largely due to their direct adverse effects on skeletal metabolism. To better appreciate the natural history of fractures in this setting, over a decade ago the Canadian STeroid-associated Osteoporosis in the Pediatric Population (“STOPP”) Consortium launched a 6 year, multi-center observational cohort study in GC-treated children. This study unveiled numerous key clinical-biological principles about GC-induced osteoporosis (GIO), many of which are unique to the growing skeleton. This was important, because most GIO recommendations to date have been guided by adult studies, and therefore do not acknowledge the pediatric-specific principles that inform monitoring, diagnosis and treatment strategies in the young. Some of the most informative observations from the STOPP study were that vertebral fractures are the hallmark of pediatric GIO, they occur early in the GC treatment course, and they are frequently asymptomatic (thereby undetected in the absence of routine monitoring). At the same time, some children have the unique, growth-mediated ability to restore normal vertebral body dimensions following vertebral fractures. This is an important index of recovery, since spontaneous vertebral body reshaping may preclude the need for osteoporosis therapy. Furthermore, we now better understand that children with poor growth, older children with less residual growth potential, and children with ongoing bone health threats have less potential for vertebral body reshaping following spine fractures, which can result in permanent vertebral deformity if treatment is not initiated in a timely fashion. Therefore, pediatric GIO management is now predicated upon early identification of vertebral fractures in those at risk, and timely intervention when there is limited potential for spontaneous recovery. A single, low-trauma long bone fracture can also signal an osteoporotic event, and a need for treatment. Intravenous bisphosphonates are currently the recommended therapy for pediatric GC-induced bone fragility, typically prescribed to children with limited potential for medication-unassisted recovery. It is recognized, however, that even early identification of bone fragility, combined with timely introduction of intravenous bisphosphonate therapy, may not completely rescue the osteoporosis in those with the most aggressive forms, opening the door to novel strategies.

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“…Considering that inﬂammatory factors can hamper osteogenesis, studies have aimed to investigate the association between m6A, inﬂammation and osteoporosis. Several cytokines have been identified that participate in the development of osteoporosis, including RANKL, colony-stimulating factor (CSF)-1, interleukin-34( 157 ) and granulocyte-macrophage-CSF ( 158 ). A study revealed that osteoblast differentiation and Smad-dependent signalling is inhibited after disrupting METTL3 by stabilising Smad7 and Smurf1 mRNA transcripts, which is mediated by YTHDF2( 159 ).…”

Section: M6a and Osteoporosismentioning

confidence: 99%

Role of m6A in osteoporosis, arthritis and osteosarcoma (Review)

Zhao

2021

Exp Ther Med

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RNA modification is a type of post-transcriptional modification that regulates important cellular pathways, such as the processing and metabolism of RNA. The most abundant form of methylation modification is RNA N6-methyladenine (m6A), which plays various post-transcriptional regulatory roles in cellular biological functions, including cell differentiation, embryonic development and disease occurrence. Bones play a pivotal role in the skeletal system as they support and protect muscles and other organs, facilitate movement and ensure haematopoiesis. The development and remodelling of bones require a delicate and accurate regulation of gene expression by epigenetic mechanisms that involve modifications of histone, DNA and RNA. The present review discusses the enzymes and proteins involved in mRNA m6A methylation modification and summarises current research progress and the mechanisms of mRNA m6A methylation in common orthopaedic diseases, including osteoporosis, arthritis and osteosarcoma.

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Cytokines and Bone: Osteoimmunology

Cited by 22 publications

References 489 publications

Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis

Cytokine Networks in the Pathogenesis of Rheumatoid Arthritis

Glucocorticoid-Induced Osteoporosis: Why Kids Are Different

Role of m6A in osteoporosis, arthritis and osteosarcoma (Review)

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