Exploring the Role of Hormones and Cytokines in Osteoporosis Development
Abstract
:1. Introduction
2. Pathomechanism of Osteoporosis
2.1. Roles of Hormones and Cytokines in Osteoporosis
2.1.1. Hormones
Growth Hormone (GH)
Glucocorticoids
PTH
Estrogen Hormone
Testosterone Hormone
Calcitonin Hormone
2.1.2. Cytokines
Pro-Inflammatory Cytokines
- TNF-alpha (TNF-α)
- IL-1
- IL-6
- IL-17
- IL-8
- IL-18
- IL-23
- IL-33
Anti-Inflammatory Cytokines
- IL-10
- IL-4
- IL-13
- IL-35
Cytokine | Family | Effects on Osteoblast | Effects on Osteoclasts | Effects on Osteocytes | Increase | Decrease | References |
---|---|---|---|---|---|---|---|
TNF- | TNF- | Osteoblasts are stimulated to produce RANKL and M-CSF. At low concentrations, these molecules enhance the differentiation of mesenchymal precursor cells into osteoblasts, whereas at high concentrations, they impede osteoblast function and halt bone formation. Additionally, the suppression of IGF-1 and Runt-related transcription factor 2 (RUNX2) expressions inhibits osteoblast differentiation. | Stimulates osteoclast development and enhances RANK expression in osteoclast precursors. Supports osteoclast formation via RANKL signaling. Increases c-Fos expression in osteoclast precursors. | TNF-α is known to directly increase RANKL expression in osteocytes and induce osteoclast formation both in vitro and in vivo. Additionally, TNF-α has been observed to upregulate sclerostin expression in osteocytes, which subsequently leads to an increase in RANKL expression. | Bone resorption, osteoclast differentiation and activation | It reduces bone formation by inhibiting osteoblast function. | [131,132,236,237] |
IL-1 | IL-1 | - | Promotes osteoclastogenesis. | IL-1α promotes osteoclast formation by increasing RANKL expression in osteocytes. Additionally, IL-1α supports the survival of osteocytes and plays a significant role in osteogenesis. IL-1α interacts with osteocytes through complex pathways such as Ca and NO signaling, affecting the balance of bone formation and resorption. | M-CSF, PGE2, bone loss, osteoclast. | OPG | [11,146,238,239,240,241] |
IL-1 | IL-1 | Induces bone resorption in osteoblasts by activating p38 MAPK. Inhibits human osteoblast migration. | Activates osteoclasts and promotes osteoclast maturation, facilitating multinucleation and viability. | IL-1β influences bone metabolism by increasing sclerostin secretion in osteocytes and inducing osteocyte apoptosis. Furthermore, IL-1β has been reported to enhance osteocyte-mediated osteoclastogenesis, an effect that can be mitigated by mechanical loading. IL-1β promotes the differentiation and mineralization of mesenchymal stem cells into osteoblasts, can increase inflammation in the bone microenvironment, and stimulates the production of FGF23. | RANKL, bone loss, osteoclast. | Bone formation rate. | [149,153,241,242,243,244,245,246] |
IL-4 | Th2 | - | Suppresses osteoclast formation both directly and indirectly, inhibiting the bone resorption activity of mature, differentiated osteoclasts. | IL-4 and IL-10 are key regulators in the interactions between osteocytes and bone health. IL-4, together with IL-10, promotes the osteogenic differentiation of osteoblasts, induces an anti-inflammatory phenotype in macrophages, and inhibits osteoclastogenesis. These cytokines play crucial roles in supporting bone formation and maintaining the balance between bone formation and resorption. | OPG | RANKL, osteoclastogenesis, Th2 cells produced in the presence of IL-4 prevent bone loss. | [179,219,220,221,245] |
IL-6 | IL-12 | Inhibits osteoblast differentiation. | Directly and indirectly supports osteoclast development while restricting the differentiation of osteoclast progenitors into osteoclasts. | IL-6 plays a critical role in the interaction between osteocytes and bone metabolism. IL-6, secreted by osteocytes in response to mechanical stress, regulates bone remodeling, osteoclastogenesis, and osteoblast activity. It has been shown that IL-6 enhances osteocyte-mediated osteoclastic differentiation via the JAK2/STAT3 pathway and is important in the modulation of bone mass. | Osteogenic capacity, bone resorption, osteoclast differentiation and activation, osteoclastogenesis, rheumatoid arthritis, cancer metastasis, atherosclerosis, and type 2 diabetes. | Osteoblast differentiation, bone trabecular volume. | [129,154,243,247,248,249] |
IL-8 | IL-8 | - | Promotes RANKL-induced osteoclastogenesis. | Osteocytes, embedded within the bone matrix, play a crucial role in bone remodeling and are sensitive to various signaling molecules, particularly inflammatory cytokines like IL-8. These cells communicate with neighboring osteoblasts and osteoclasts through canaliculi, thereby regulating bone homeostasis. It is possible that IL-8 may affect osteocyte function and potentially contribute to bone remodeling processes. | Bone resorption, neutrophil RANKL expression. | Bone density | [11,129,184,250,251] |
IL-10 | IL-10 | Suppresses osteogenic activity in the bone marrow. | Inhibits the differentiation of osteoclast progenitors into osteoclast precursors and suppresses RANK-induced osteoclast formation. | IL-10 plays a significant role in bone metabolism and regulates osteoclastogenesis. IL-10 inhibits bone resorption by upregulating the expression of OPG while downregulating the expression of RANKL and colony-stimulating factor-1 (CSF-1). Additionally, IL-10, in conjunction with IL-4, promotes the osteogenic differentiation of osteoblasts and induces an anti-inflammatory phenotype in macrophages. This indicates that IL-10 both inhibits bone resorption and supports bone formation. | Bone formation, bone fragility. | Inhibits osteoclast differentiation, reduces bone resorption, bone loss, reduced osteoclast production, decreased bone mass. It suppresses osteogenic differentiation by inhibiting bone mineralization and synthesis of bone proteins. | [211,245,252,253] |
IL-13 | Th2 | - | Inhibits osteoclast formation and bone resorption. | Osteocytes play a crucial role in bone remodeling and are sensitive to cytokines. IL-13, known for its anti-inflammatory properties, may affect osteocyte function and bone metabolism. Although the specific effects of IL-13 on osteocytes are not well-detailed, it is possible that IL-13, like IL-10 and IL-4, modulates osteocyte activity and bone homeostasis. | Bone formation, bone resorption control, and bone mass preservation, bone tissue strength. | Bone loss | [217,224,225] |
IL-17 | IL-17 | Enhances the expression of cytokines such as TNF-α, IL-6, and RANKL that promote osteoclasts in osteoblasts. Supports osteoblast differentiation while preventing osteoblast calcification. | Initiates osteoclast formation. At low concentrations, it enhances autophagy and osteoclast formation in osteoclast precursors, while at high concentrations, it inhibits the differentiation of osteoclast precursors into osteoclasts. | IL-17, a proinflammatory cytokine, has significant effects on osteocytes. IL-17 promotes bone resorption by regulating RANKL production in osteocytes. Additionally, IL-17 receptor signaling mediates PTH-induced bone loss and increases osteocytic RANKL production. IL-17 also promotes bone resorption and fluid shear stress regulation through osteocyte-specific signaling pathways. | Bone loss, RANKL, pro-osteoclastogenic cytokine. | Bone resorption | [11,147,174,177,178,179,180,254,255,256] |
IL-18 | IL-1 | - | Inhibits TNF-α-induced osteoclastogenesis through apoptosis via Fas/FasL and NO in myeloid cells. Indirectly inhibits osteoclast formation through IFN-γ and GM-CSF. | Since osteocytes are sensitive to various signaling molecules, it is possible that IL-18 could affect osteocyte function and bone metabolism. Further research is needed to understand the specific effects of IL-18 on osteocytes. | In the presence of TNF-α, IL-12 and IL-18 synergistically increase NO production. An increase in IL-18 level causes a decrease in IL-18BP level. TNF-α, IL-1β, and IL-6 increase osteoclast differentiation and activation. | Osteoclast differentiation and activation. | [186,187,188,189,190,191] |
IL-23 | IL-12 | - | Participates in T-cell-mediated osteoclast formation, regulates osteoclast differentiation, and indirectly inhibits osteoclast formation. | It is possible that IL-23 could affect osteocyte function and bone metabolism. Given its role in inflammation and immune responses, IL-23 may regulate bone remodeling and cell communication. Further research is needed to understand the specific effects of IL-23 on osteocytes. | It transforms CD4(+) cells into Th17 cells, thus increasing the production of IL-17 by Th17 cells. Osteoclast differentiation and activation. | Osteoblast apoptosis. | [177,178,199,200,201,202] |
IL-33 | IL-1 | Stimulates osteoblast function, promotes matrix mineral deposition, and reduces sclerostin mRNA. | Terminates the osteoclast formation initiated by RANKL and suppresses the gene expression associated with osteoblasts. It induces apoptosis in osteoclasts while preventing osteoclast formation and bone resorption induced by TNF. | IL-33 has been shown to induce IL-6 expression and regulate osteocyte function by interacting with ST2L receptors on the plasma membrane and activating specific signaling pathways. These findings suggest that IL-33 may play a significant role in regulating osteocyte function and bone metabolism, highlighting a potential connection between IL-33 and osteocytes. | IL-33 increases during inflammation, increasing osteoblast activity. | Inhibiting osteoclast formation. | [11,13,205,206,207,208,257] |
IL-35 | IL-12 | Promote the differentiation of mesenchymal stem cells into osteoblasts. | Prevent TNF-induced osteoclast formation and promote apoptosis, support the formation of functional osteoclasts, and increase the expression of osteoclast differentiation factors. | The connection between IL-35 and osteocytes has not been directly addressed in the literature. However, based on the effects of cytokines on bone cells, it can be hypothesized that IL-35 may influence osteocyte function and bone metabolism. Further research into the role of IL-35 in bone remodeling, osteoclastogenesis, and osteoblast activity could provide insights into this connection. | JAK1/STAT1, β-catenin and Axin2, bone formation and resorption. | Osteoclast formation, TNF-induced osteoclastogenesis and bone resorption, NF-κB, MAPK, NFATc1, c-Fos, and TRAP, apoptosis and adipogenic differentiation, adipogenesis. | [11,228,230,231,232,233,258] |
2.2. GFs
2.2.1. IGFs
2.2.2. TGFs
2.2.3. FGFs
FGF-2
FGF-19
FGF-21
FGF-23
2.2.4. EGF
2.2.5. HGF
2.2.6. VEGF
2.2.7. PDGF
2.2.8. NGF
3. Conclusions and Future Perspective
Author Contributions
Funding
Conflicts of Interest
References
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Umur, E.; Bulut, S.B.; Yiğit, P.; Bayrak, E.; Arkan, Y.; Arslan, F.; Baysoy, E.; Kaleli-Can, G.; Ayan, B. Exploring the Role of Hormones and Cytokines in Osteoporosis Development. Biomedicines 2024, 12, 1830. https://doi.org/10.3390/biomedicines12081830
Umur E, Bulut SB, Yiğit P, Bayrak E, Arkan Y, Arslan F, Baysoy E, Kaleli-Can G, Ayan B. Exploring the Role of Hormones and Cytokines in Osteoporosis Development. Biomedicines. 2024; 12(8):1830. https://doi.org/10.3390/biomedicines12081830
Chicago/Turabian StyleUmur, Egemen, Safiye Betül Bulut, Pelin Yiğit, Emirhan Bayrak, Yaren Arkan, Fahriye Arslan, Engin Baysoy, Gizem Kaleli-Can, and Bugra Ayan. 2024. "Exploring the Role of Hormones and Cytokines in Osteoporosis Development" Biomedicines 12, no. 8: 1830. https://doi.org/10.3390/biomedicines12081830