ArticleInternational journal of molecular sciences2020
Impact of Janus Kinase Inhibition with Tofacitinib on Fundamental Processes of Bone Healing.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Dual Inhibition of GSK3 and JAK by BIO Suppresses Osteoblast Differentiation and Mineralization of Human Mesenchymal Cells.Current issues in molecular biology · 2026Article
- Immunometabolic mechanisms of osteosarcopenic obesity: chronic inflammation, trained immunity, and systemic immune dysregulation.Frontiers in immunology · 2026Review
- Review
- Targeted and biologic therapies and risk of total knee or hip replacement in axial spondyloarthritis and psoriatic arthritis.Clinical rheumatology · 2025Article
- ["Paradoxical fractures": pathological fractures under anti-osteoporotic and antirheumatic treatment].Zeitschrift fur Rheumatologie · 2025Review
- Osteoimmunology: The Crosstalk between T Cells, B Cells, and Osteoclasts in Rheumatoid Arthritis.International journal of molecular sciences · 2024Review
- JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases.International journal of molecular sciences · 2023Review
- Molecular Basic of Pharmacotherapy of Cytokine Imbalance as a Component of Intervertebral Disc Degeneration Treatment.International journal of molecular sciences · 2023Review
- The effect of disease-modifying antirheumatic drugs (DMARDs) on bone homeostasis in rheumatoid arthritis (RA) patients.Inflammopharmacology · 2023Review
- Mechanisms of Systemic Osteoporosis in Rheumatoid Arthritis.International journal of molecular sciences · 2022Review
- Combination of Dexamethasone and Tofacitinib Reduces Xenogeneic MSC-Induced Immune Responses in a Mouse Model of Alzheimer's Disease.Biomedicines · 2022Article
- Effects of targeted therapies on bone in rheumatic and musculoskeletal diseases.Nature reviews. Rheumatology · 2022Review
- Effects of Biological/Targeted Therapies on Bone Mineral Density in Inflammatory Arthritis.International journal of molecular sciences · 2022Review
- Inflammation and Bone Metabolism in Rheumatoid Arthritis: Molecular Mechanisms of Joint Destruction and Pharmacological Treatments.International journal of molecular sciences · 2022Review
- Fracture in clinical studies of tofacitinib in rheumatoid arthritis.Therapeutic advances in musculoskeletal disease · 2022Article
- Stimulatory Effect of Tofacitinib on Bone Marrow Adipocytes Differentiation.Frontiers in endocrinology · 2022Article
- Effects of one-year tofacitinib therapy on bone metabolism in rheumatoid arthritis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2021Article
- Extra-Articular Manifestations and Comorbidities in Psoriatic Disease: A Journey Into the Immunologic Crosstalk.Frontiers in medicine · 2021Review
- A Human Osteochondral Tissue Model Mimicking Cytokine-Induced Key Features of Arthritis In Vitro.International journal of molecular sciences · 2020Article
- JAK/STAT Activation: A General Mechanism for Bone Development, Homeostasis, and Regeneration.International journal of molecular sciences · 2020Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Both inflammatory diseases like rheumatoid arthritis (RA) and anti-inflammatory treatment of RA with glucocorticoids (GCs) or non-steroidal anti-inflammatory drugs (NSAIDs) negatively influence bone metabolism and fracture healing. Janus kinase (JAK) inhibition with tofacitinib has been demonstrated to act as a potent anti-inflammatory therapeutic agent in the treatment of RA, but its impact on the fundamental processes of bone regeneration is currently controversially discussed and at least in part elusive. Therefore, in this study, we aimed to examine the effects of tofacitinib on processes of bone healing focusing on recruitment of human mesenchymal stromal cells (hMSCs) into the inflammatory microenvironment of the fracture gap, chondrogenesis, osteogenesis and osteoclastogenesis. We performed our analyses under conditions of reduced oxygen availability in order to mimic the in vivo situation of the fracture gap most optimal. We demonstrate that tofacitinib dose-dependently promotes the recruitment of hMSCs under hypoxia but inhibits recruitment of hMSCs under normoxia. With regard to the chondrogenic differentiation of hMSCs, we demonstrate that tofacitinib does not inhibit survival at therapeutically relevant doses of 10-100 nM. Moreover, tofacitinib dose-dependently enhances osteogenic differentiation of hMSCs and reduces osteoclast differentiation and activity. We conclude from our data that tofacitinib may influence bone healing by promotion of hMSC recruitment into the hypoxic microenvironment of the fracture gap but does not interfere with the cartilaginous phase of the soft callus phase of fracture healing process. We assume that tofacitinib may promote bone formation and reduce bone resorption, which could in part explain the positive impact of tofacitinib on bone erosions in RA. Thus, we hypothesize that it will be unnecessary to stop this medication in case of fracture and suggest that positive effects on osteoporosis are likely.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.