Cited by 280Bone Metabolism and DiseasesRheumatoid Arthritis Research and TherapiesOsteomyelitis and Bone Disorders Research

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Regulation of TNF-Induced Osteoclast Differentiation

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Yao, Zhenqiang, Getting, Stephen J., Locke, Ian C.·2021·Cells

DOI 10.3390/cells11010132PMC PMC8750957

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Abstract

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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Figure 1 Key factors that mediate TNF-induced OC differentiation. (1) Similar to, and independent of, RANKL, TNFα sequentially activates NF-κB p50 and p52, then c-Fos, followed by NFATc1 to induce OC differentiation; (2) TNFα pre-activated OCPs expressing c-Fos attach to bone, and (3) are stimulated by bone matrix proteins, such as dentin sialoprotein (DSP), to produce IL-1β, which mediates the terminal differentiation of pre-activated OCPs into mature OCs to degrade bone.CC BY · PubMed Central

Figure 2 NF-κB signaling pathway. (1) Canonical NF-κB activation. Cytokines, such as RANKL and TNFα, induce canonical signaling by recruiting TRAF6 and TRAF2/5, respectively, to their receptors to activate a complex consisting of IKK-α, IKK-β, and IKK-γ (NEMO), which induces phosphorylation and degradation of IκB-α, and the release of p65/p50 heterodimers, which translocate to the nucleus to activate the target gene expression. (2) Non-canonical NF-κB activation. In unstimulated cells, the TRAF3–TRA2 complex results in constitutive NIK degradation, and thus, p100 binds RelB to be remained trapped in cytoplasm. Cytokines, such as CD40L and RANKL, recruit cIAP to the TRAF2–TRA3 complex, resulting in TRAF3 ubiquitin degradation, and allowing newly synthesized NIK accumulation. NIK then phosphorylates IKK-α, which leads to proteasomal processing of p100 to p52, releasing RelB:p52 heterodimers for translocation to the nucleus. TNFα does not degrade TRAF3, and thus, NIK is degraded, leading to the accumulation of p100 in the cytoplasm of osteoclast precursors to limit their differentiation.CC BY · PubMed Central

Figure 3 Notch signaling regulation of OC differentiation. Notch ligand binding to Notch receptors results in the cleavage and release of Notch NICD. As a result, NICD translocates into the nucleus, where it associates with RBPjκ and NF-κB to regulate the transcription of genes that control OC differentiation. NICD association with RBPjκ inhibits the expression of NFATc1 by attenuating c-Fos, and suppressing Blimp1, and promotes IRF8 expression. Notch also inhibits cFms expression, but associates with NF-κB RelA to promote NFATc1 expression. In addition, Notch inhibits OC differentiation, indirectly downregulating RANKL, while promoting OPG expression by MPCs and osteocytes.CC BY · PubMed Central

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Betulinic Acid Attenuates Osteoarthritis via Limiting NLRP3 Inflammasome Activation to Decrease Interleukin-1β Maturation and Secretion
Liu, B., Wu, Y., Liang, T., Zhou, Y., Chen, G., He, J., Ji, C., Liu, P., Zhang, C., Lin, J., et al. (2023) · Mediators of Inflammation · doi:10.1155/2023/3706421 · Cited by 17
Disulfidptosis-related Protein RPN1 may be a Novel Anti-osteoporosis Target of Kaempferol
Pan, C., Zhang, C., Lin, Z., Liang, Z., Cui, Y., Shang, Z., Wei, Y., & Chen, F. (2024) · Combinatorial Chemistry & High Throughput Screening · doi:10.2174/0113862073273655231213070619 · Cited by 17
Dehydromiltirone inhibits osteoclast differentiation in RAW264.7 and bone marrow macrophages by modulating MAPK and NF-κB activity
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“However, after RANKL stimulation, NF-κB is degraded and released into the cytoplasm, inducing the generation of mature osteoclasts (Lawrence, 2009; Yao et al., 2021).”
Background
Plumbagin is a NF-κB-inducing kinase inhibitor with dual anabolic and antiresorptive effects that prevents menopausal-related osteoporosis in mice
Shen, G., Liu, X., Lei, W., Duan, R., & Yao, Z. (2022) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2022.101767 · Cited by 19
“This is an open access article under the CC NF-κB family of transcriptional factors plays a central role in OC differentiation by sequentially activating c-Fos followed by NFATc1 (19, 20), the two other transcriptional factors critical for OC differentiation; (2) NIK, the key kinase that activates noncanonical NF-κB s…”
BackgroundSelf-citation
Babam2 negatively regulates osteoclastogenesis by interacting with Hey1 to inhibit Nfatc1 transcription
Jin, F., Zhu, Y., Liu, M., Wang, R., Cui, Y., Wu, Y., Liu, G., Wang, Y., Wang, X., & Ren, Z. (2022) · International Journal of Biological Sciences · doi:10.7150/ijbs.72487 · Cited by 16
“As TNF family mediated signaling is implicated in regulating bone resorption [31, 32], it promotes us to explore the role of Babam2 modulation in osteoclast formation.”
Background
Tumor necrosis factor α and its role in pathologies
Терещенко, И. В., & Каюшев, П. Е. (2022) · Russian Medical Inquiry · doi:10.32364/2587-6821-2022-6-9-523-527 · Cited by 16
Research Advances on Stem Cell-Derived Extracellular Vesicles Promoting the Reconstruction of Alveolar Bone through RANKL/RANK/OPG Pathway
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Isolation and characterization of a novel homopolysaccharide (SFP-1) from Sargassum fusiforme: Promising anti-osteoporosis activity by modulating adipo-osteogenic differentiation
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The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis
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“48, 81 According to reports in the literature, OPG inhibits OCs differentiation and bone resorption by enhancing autophagy in vitro, and the mechanism is that OPG activates AMPK protein, which regulates OCs autophagy through the AMPK/ mTOR/p70S6K pathway.”
Background
Developmental Toxicity of PEDOT:PSS in Zebrafish: Effects on Morphology, Cardiac Function, and Intestinal Health
Yang, G., Gou, D., Bu, L.-K., Wei, X., Hu, H., Huo, W., Sultan, M., & Pei, D. (2024) · Toxics · doi:10.3390/toxics12020150 · Cited by 15
Bone Health Impairment in Patients with Hemoglobinopathies: From Biological Bases to New Possible Therapeutic Strategies
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“OCs are terminally differentiated multinucleated cells localized on the trabecular surface [53,54].”
Background
Synergistic roles of tristetraprolin family members in myeloid cells in the control of inflammation
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“…of the severe M-triple KO syndrome, and their involvement in in-ﬂ ammatory diseases and disease models has been documented in many previous studies (Deshmane et al, 2009; Lee et al, 2017; Karin & Razon, 2018; Steinkamp et al, 2018; Tokunaga et al, 2018; House et al, 2020; Yao et al, 2021).”
Background
Advancements in bone organoids: perspectives on construction methodologies and application strategies
Huang, S., Wu, Y., Zhao, H., Song, K., Liu, Y., Mao, J., & Li, Q. (2025) · Journal of Advanced Research · doi:10.1016/j.jare.2025.06.011 · Cited by 18
“Several factors inﬂuence the differentiation of OCs, and macrophage colony-stimulating factor (M − CSF) secreted by OBs and MSCs, and receptor activator of nuclear factor-j B ligand (RANKL) secreted by OBs and OCs, are the two key cytokines that regulate their differentiation [32].”
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Uncovering the mechanisms of Zhubi decoction against rheumatoid arthritis through an integrated study of network pharmacology, metabolomics, and intestinal flora
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Self‐Replenishable Metabolically Augmented Synbiotic Microspheres Remodel Gut‐Bone Homeostasis
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pH-responsive cinnamaldehyde-TiO2 nanotube coating: fabrication and functions in a simulated diabetes condition
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“TNF-α and NF-κβ are considered as key factor for activation of osteoclastic differentiation [52].”
Background
Lobetyolin Suppressed Osteoclastogenesis and Alleviated Bone Loss in Ovariectomy-Induced Osteoporosis via Hindering p50/p65 Nuclear Translocation and Downstream NFATc1/c-Fos Expression
Xiu, C., Luo, H., Huang, W., Fan, S., Yuan, C., Chen, J., Xu, C., Yao, C., Hong, D., & Zhang, L. (2025) · Drug Design Development and Therapy · doi:10.2147/dddt.s515930 · Cited by 13
Bavachinin selectively modulates PPAR γ and maintains bone homeostasis in Type 2 Diabetes
Liu, J., Li, X., Wang, H., Ren, Y., Li, Y., & Guo, F. (2023) · Phytotherapy Research · doi:10.1002/ptr.7912 · Cited by 13
“RANKL signaling would recruit and form RANKL and TNF receptor-associated factor 6 (TRAF6) interaction, further activating the mitogen-activated protein kinase signaling pathway (Armstrong et al., 2002; Yao et al., 2021).”
Background
Effect of pilose antler polypeptide on the mechanism of bone homeostasis in osteoporosis
Wang, G., Meng, Y., Ouyang, W., Zhao, C., & Zhao, W. (2023) · Frontiers in Medicine · doi:10.3389/fmed.2023.1289843 · Cited by 13
“Not only does negatively impacts bone formation by osteoblasts but can also independently induce osteoclast differentiation with the involvement of p50, p52, and NF-κ B (72, 73).”
Background
TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination
Ma, Q., Yu, J., Liu, L., Ma, X., Zhang, J., Zhang, J., Wang, X., Deng, G., & Wu, X. (2023) · Cell Death Discovery · doi:10.1038/s41420-023-01731-4 · Cited by 13
“Meanwhile, it was found that TRAF6 is involved in the regulation of diverse cellular processes such as development and differentiation, cell cycle progression, and most notably autophagy [24, 25].”
Background
Bub1 suppresses inflammatory arthritis–associated bone loss in mice through inhibition of TNFα–mediated osteoclastogenesis
Yoshida, S., Ikedo, A., Yanagihara, Y., Sakaue, T., Saeki, N., & Imai, Y. (2024) · Journal of Bone and Mineral Research · doi:10.1093/jbmr/zjae015 · Cited by 13
“17-19 Meanwhile, endogenous negative regulators for osteoclastogenesis such as IRF8, 20 BCL6, and BLIMP1 21 have been identified and are important to further understand the inhibitory mechanisms of osteoclastogenesis especially during inflammatory conditions for the treatment of RA– mediated bone…”
Regulation of osteoclast-mediated bone resorption by lipids
Luo, F., Chen, T., Chen, S., Bai, D., & Li, X. (2025) · Bone · doi:10.1016/j.bone.2025.117423 · Cited by 13
Narirutin mitigates inflammatory arthritis and osteoporosis through modulating macrophage phenotype and osteoclastogenesis
Wang, Q., Peng, X., Xu, H., Zhao, Y., Lu, X., Lu, C., Wang, Q., Lü, W., Sheng, Q., Lu, X., et al. (2025) · Journal of Orthopaedic Translation · doi:10.1016/j.jot.2025.07.008 · Cited by 12
“While the RANKL-mediated classical signaling pathway in osteoclastogenesis has been extensively studied, elevated inflammatory cytokine levels can exacerbate osteoclast hyperactivation via non-classical pathways [17, 18], contributing to systemic osteoporosis.”
Gingival crevicular fluid periodontal ligament‐associated protein‐1, sclerostin, and tumor necrosis factor‐alpha levels in periodontitis
Gür, B., Afacan, B., Çevik, Ö. D., Köse, T., & Emingil, G. (2023) · Journal of Periodontology · doi:10.1002/jper.22-0750 · Cited by 12
Effects of a calcium/vitamin D/Zinc combination on anti-osteoporosis in ovariectomized rats
Wang, S., Luo, Z., Luo, H.-J., Li, Z., Yuan, Z., Tang, J., Lin, L., Du, Z., & Zhou, J. (2023) · Journal of Trace Elements in Medicine and Biology · doi:10.1016/j.jtemb.2023.127138 · Cited by 11
The multiple regulatory effects of white adipose tissue on bone homeostasis
Liu, X., Du, Y., Zhao, Z., Zou, J., Zhang, X., & Zhang, L. (2023) · Journal of Cellular Physiology · doi:10.1002/jcp.31025 · Cited by 12
“osteoporosis by regulating osteoblasts and osteoclasts (Yao et al., 2021).”
Identification of neutrophil extracellular traps and crosstalk genes linking inflammatory bowel disease and osteoporosis by integrated bioinformatics analysis and machine learning
Xu, G., Zhang, W., Yang, J., Sun, N., & Qu, X. (2023) · Scientific Reports · doi:10.1038/s41598-023-50488-4 · Cited by 11
Research on the role and mechanism of IL-17 in intervertebral disc degeneration
Peng, B., Qian, L., Chen, J., & Wang, Z. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.111992 · Cited by 13
A review of bacterial and osteoclast differentiation in bone infection
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The potential link between the development of Alzheimer’s disease and osteoporosis
Nasme, F., Behera, J., Tyagi, P., Debnath, N., Falcone, J. C., & Tyagi, N. (2025) · Biogerontology · doi:10.1007/s10522-024-10181-z · Cited by 12
“…signalling pathway also contributes in the differentiation of osteoclasts by inducing TNF-α to stimulate osteoblasts to produce granulocyte macrophage colony-stimulating factor (GM-CSF) and IL-6 (Kitaura et al. 2020; Zhou et al. 2022; Ruef et al. 2017; Kitaura et al. 2013; Yao et al. 2022).”
The Function of Myostatin in Ameliorating Bone Metabolism Abnormalities in Individuals with Type 2 Diabetes Mellitus by Exercise
Zhong, C., Zeng, X., Yi, X., Yang, Y., Hu, J., Yin, R., & Chen, X. (2025) · Current Issues in Molecular Biology · doi:10.3390/cimb47030158 · Cited by 11
JAK inhibition and axial spondyloarthritis: new steps on the path to understanding pathophysiology
Ciccia, F., McGonagle, D., Thomas, R., Marzo-Ortega, H., Martin, D. A., Yndestad, A., & Volkov, M. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1488357 · Cited by 11
“The erosive stage of the disease can largely be attributed to the capacity of TNF to stimulate osteoclastogenesis (40, 41).”
Epimedin B attenuates ovariectomy-induced bone loss by suppressing osteoclastogenesis through decreasing ROS production and targeting ESR1
Lai, Y., Li, H., Zhou, T., Chen, H., Yang, J., Mo, G., Li, Y., Li, Q., Deng, X., Fan, S., et al. (2025) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2025.08.033 · Cited by 11
Tailoring Biomaterials Ameliorate Inflammatory Bone Loss
Cheng, S., Wang, K., Zhou, L., Sun, Z., & Zhang, L. (2024) · Advanced Healthcare Materials · doi:10.1002/adhm.202304021 · Cited by 11
Interaction between immuno-stem dual lineages in jaw bone formation and injury repair
Liu, Z., Luo, X., & Xu, R. (2024) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2024.1359295 · Cited by 11
“The damaged macrophages produced numerous pro-in ﬂ ammatory factors, including IL-1 β , TNF-α , and IL-6, which act on MSCs through paracrine, resulting in the inhibition of osteogenic differentiation of MSCs (MUCCI and ROZENFELD, 2015; YAO et al., 2021).”
Background
OsteoMac: A new player on the bone biology scene
Iglesias‐Velázquez, Ó., Tresguerres, F. G. F., Tresguerres, I. F., Berrocal, M. I. L., López‐Pintor, R. M., Baca, L., & Torres, J. (2024) · Annals of Anatomy - Anatomischer Anzeiger · doi:10.1016/j.aanat.2024.152244 · Cited by 13
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SIRT1 and exercise-induced bone metabolism: a regulatory nexus
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“However, under conditions of estrogen deficiency or aging, the failure of M1 to M2 polarization leads to the activation of RANKL and NF-κB-mediated osteoclast differentiation and bone resorption (Yao et al., 2021).”
Association of lipid-lowering drugs with osteoarthritis outcomes from a drug-target Mendelian randomization study
Ma, W., Chen, H., Zhang, Z., & Xiong, Y. H. (2024) · PLoS ONE · doi:10.1371/journal.pone.0293960 · Cited by 9
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Background
Analysis of inflammation and bone remodeling of atmospheric plasma therapy in experimental periodontitis
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Hecogenin alleviates LPS-induced osteolysis via regulating pyroptosis and ROS involved Nrf2 activation
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Epiregulin ameliorates ovariectomy-induced bone loss through orchestrating the differentiation of osteoblasts and osteoclasts
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“…and IL-6 affects the expression of NGF and its receptor on osteoclasts, as well as signalling, and TNF-α upregulates the expression of the NGF receptor on osteoclast precursor cells, which enhances the promotion of osteoclast differentiation, thereby exacerbating bone resorption (Yao et al., 2022).”
Bisabolangelone targets CSF1R to impede osteoclastogenesis and attenuate estrogen-deficiency bone loss
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Association between gut microbiota and bone metabolism: Insights from bibliometric analysis
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“TNF-α also suppresses the release of osteoprotegerin, which alleviates the inhibition of osteoclast activity (Yao et al., 2021).”
Background
Overexpression of SENP3 promotes PPAR-γ transcription through the increase of HIF-1α stability via SUMO2/3 and participates in molecular mechanisms of osteoporosis
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Authors: Yao, Z., Getting, S. J., & Locke, I. C.
Affiliations: University of Rochester Medicine (US)
University of Westminster (GB)
Corresponding author: Yao, Zhenqiang
ORCID: Yao, Zhenqiang
Getting, Stephen J.
Locke, Ian C.
Venue: Cells
Publisher: MDPI AG
Published: 2021-12-31
Volume: 11
Issue: 1
Pages: 132
ISSN: 2073-4409 (ISSN-L)
DOI: 10.3390/cells11010132
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: cc-by
creativecommons.org/licenses/by/4.0/ (vor)
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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Regulation of TNF-Induced Osteoclast Differentiation

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