ReviewFrontiers in immunology2019
Osteoimmunology of Bone Loss in Inflammatory Rheumatic Diseases.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- [Osteoporosis in rheumatology-Diagnostics, risk assessment and modern treatment strategies].Zeitschrift fur Rheumatologie · 2026Article
- Pyroptotic cell-derived factors promote osteoclast differentiation.bioRxiv : the preprint server for biology · 2026Article
- Macrophage-driven pathological ossification of the posterior longitudinal ligament: mechanistic insights and therapeutic opportunities.Bone research · 2026Review
- Predicting the risk of bone erosion in rheumatoid arthritis using a SHAP-based interpretable machine learning model.Clinical rheumatology · 2026Article
- Emerging pathogenetic mechanisms in adolescent idiopathic scoliosis: the role of inflammation and gut microbiota.Journal of orthopaedic surgery and research · 2026Review
- Low-Dose Methotrexate and Bone Health: Pathophysiological and Clinical Perspectives.Journal of clinical medicine · 2026Review
- Crebanine protects against ovariectomy-induced bone loss by targeting Sirt1 to interfere with NF-κB acetylation and ROS activity.Journal of pharmaceutical analysis · 2026Article
- Creatinine, leucine, and tetrahydrocorticosterone emerge as potential biomarkers for the diagnosis of sarcopenic osteoarthritis in middle-aged and elderly individuals: a cross-sectional exploratory study.Frontiers in molecular biosciences · 2026Article
- Mesothelin as a biomarker and potential therapeutic target in rheumatoid arthritis bone destruction.Cell reports. Medicine · 2025Article
- Inflammasome targeting for periodontitis prevention is sex dependent.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- From Development, Disease, and Decline: A Review of What Defines an Osteoclast Progenitor.International journal of molecular sciences · 2025Review
- Unraveling the mechanisms of bone diseases: targeting dendritic cells in osteoimmunology for internal homeostasis balance.Bone research · 2025Review
- Article
- Article
- Prediction model for bone erosion in rheumatoid arthritis based on musculoskeletal ultrasound and clinical risk factors.Clinical rheumatology · 2025Article
- Review
- Levels of osteocalcin andReumatologia · 2025Article
- Combined application of mesenchymal stem cells and different glucocorticoid dosing alleviates osteoporosis in SLE murine models.Immunity, inflammation and disease · 2024Article
- Association between systemic lupus erythematosus and osteoporosis: a mendelian randomization analysis.BMC rheumatology · 2024Article
- Involvement of interlukin-17A (IL-17A) gene polymorphism and interlukin-23 (IL-23) level in the development of peri-implantitis.BDJ open · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past two decades, the field of osteoimmunology has emerged in response to a range of evidence demonstrating the reciprocal relationship between the immune system and bone. In particular, localized bone loss, in the form of joint erosions and periarticular osteopenia, as well as systemic osteoporosis, caused by inflammatory rheumatic diseases including rheumatoid arthritis, the prototype of inflammatory arthritis has highlighted the importance of this interplay. Osteoclast-mediated resorption at the interface between synovium and bone is responsible for the joint erosion seen in patients suffering from inflammatory arthritis. Clinical studies have helped to validate the impact of several pathways on osteoclast formation and activity. Essentially, the expression of pro-inflammatory cytokines as well as Receptor Activator of Nuclear factor κB Ligand (RANKL) is, both directly and indirectly, increased by T cells, stimulating osteoclastogenesis and resorption through a crucial regulator of immunity, the Nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1). Furthermore, in rheumatoid arthritis, autoantibodies, which are accurate predictors both of the disease and associated structural damage, have been shown to stimulate the differentiation of osteoclasts, resulting in localized bone resorption. It is now also evident that osteoblast-mediated bone formation is impaired by inflammation both in joints and the skeleton in rheumatoid arthritis. This review summarizes the substantial progress that has been made in understanding the pathophysiology of bone loss in inflammatory rheumatic disease and highlights therapeutic targets potentially important for the cure or at least an alleviation of this destructive process.
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