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Regulation of TNF-Induced Osteoclast Differentiation
Open accessAbstract
Increased osteoclast (OC) differentiation and activity is the critical event that results in bone loss and joint destruction in common pathological bone conditions, such as osteoporosis and rheumatoid arthritis (RA). RANKL and its decoy receptor, osteoprotegerin (OPG), control OC differentiation and activity. However, there is a specific concern of a rebound effect of denosumab discontinuation in treating osteoporosis. TNFα can induce OC differentiation that is independent of the RANKL/RANK system. In this review, we discuss the factors that negatively and positively regulate TNFα induction of OC formation, and the mechanisms involved to inform the design of new anti-resorptive agents for the treatment of bone conditions with enhanced OC formation. Similar to, and being independent of, RANKL, TNFα recruits TNF receptor-associated factors (TRAFs) to sequentially activate transcriptional factors NF-κB p50 and p52, followed by c-Fos, and then NFATc1 to induce OC differentiation. However, induction of OC formation by TNFα alone is very limited, since it also induces many inhibitory proteins, such as TRAF3, p100, IRF8, and RBP-j. TNFα induction of OC differentiation is, however, versatile, and Interleukin-1 or TGFβ1 can enhance TNFα-induced OC formation through a mechanism which is independent of RANKL, TRAF6, and/or NF-κB. However, TNFα polarized macrophages also produce anabolic factors, including insulin such as 6 peptide and Jagged1, to slow down bone loss in the pathological conditions. Thus, the development of novel approaches targeting TNFα signaling should focus on its downstream molecules that do not affect its anabolic effect.
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“Different concentrations of TGF-β have different effects on the RANKL/OPG ratio and ultimately on osteoclast differentiation (low concentrations of TGF-β increase the stimulation of osteoclast differentiation, while high concentrations of TGF-β have the opposite effect) [98, 99].”
From Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature (2024) · cites this paper as [99]
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Background
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Systemic complications of rheumatoid arthritis: Focus on pathogenesis and treatment
Wu, D., Luo, Y., Li, T., Zhao, X., Lv, T., Fang, G., Ou, P., Li, H., Luo, X., Huang, A., et al. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1051082 · Cited by 295
“Inflammatory cytokines induce osteoclast maturation and inhibit osteoblast activation to perturb bone homeostasis, thus, anti-TNF therapy can improve bone homeostasis in RA patients (143, 144).”
BackgroundInsights and implications of sexual dimorphism in osteoporosis
Zhang, Y., Xie, N., Sun, X., Nice, E. C., Liou, Y., Huang, C., Zhu, H., & Shen, Z. (2024) · Bone Research · doi:10.1038/s41413-023-00306-4 · Cited by 164
“166,167 Estradiol also reduces in fl ammation by downregulating the nuclear factor-κ B (NF-κ B) pathway, Fig.”
BackgroundImpact of the host response and osteoblast lineage cells on periodontal disease
Zhou, M., & Graves, D. T. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.998244 · Cited by 122
The RANK/RANKL/OPG system and tumor bone metastasis: Potential mechanisms and therapeutic strategies
Zhang, Y., Liang, J., Liu, P., Wang, Q., Liu, L., & Zhao, H. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1063815 · Cited by 111
Obesity and lipid metabolism in the development of osteoporosis (Review)
Wang, X., Zhang, C., Zhao, G.-T., Yang, K., & Tao, L. (2024) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2024.5385 · Cited by 70
“TNF‑ α slows the differen‑ tiation of osteoblasts and enhances the activity of osteoclasts by recruiting TRAF and activating the NF‑ κ B/c‑Fos/nuclear factor of activated T‑cells cytoplasmic 1 (NFATc1) pathway, which is independent of the RANKL/RANK system (53,54).”
Background
Metadata
- Authors
- Yao, Z., Getting, S. J., & Locke, I. C.
- Affiliations
- University of Rochester Medicine (US)
- University of Westminster (GB)
- Corresponding author
- Yao, Zhenqiang
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2021-12-31
- Volume
- 11
- Issue
- 1
- Pages
- 132
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC8750957
- OpenAlex
- W4205952184
- Cited by
- 280
- References
- 201
- Citations by year
- 2026: 45 · 2025: 87 · 2024: 69 · 2023: 54 · 2022: 25
- FWCI
- 3.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- WestminsterResearch (University of Westminster) (acceptedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (AG049994)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Rheumatology › Osteomyelitis and Bone Disorders Research
- Keywords
- TNF-α, osteoclastogenesis, TNF receptor-associated factors, NF-κB signaling, NFATc1, TRAF3, interleukin-1, TGF-β1, osteoporosis, rheumatoid arthritis, bone loss, antiresorptive agents, Jagged1, macrophages
- MeSH terms
- Animals, Arthritis, Rheumatoid, Cell Differentiation, Humans, Osteoclasts, Osteoporosis, Tumor Necrosis Factor-alpha, Signal Transduction
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