Table 1.
Mechanistic studies of inflammation and oxidative stress in osteoporotic bone remodeling.
| Study | Model type | Target pathways or molecules | Main findings | Reference |
|---|---|---|---|---|
| Effect of H2O2 on osteoblasts | In vitro (HEK293 cells) | mTORC1, AMPK | Low-dose H2O2 promotes proliferation via mTORC1; high-dose inhibits proliferation and suppresses Wnt/β-catenin signaling | (10) |
| High-fat culture environment | In vitro (primary murine osteoblasts) | ROS, Wnt/β-catenin | Elevated ROS inhibits Wnt/β-catenin signaling and osteoblast differentiation; promotes adipogenic gene expression | (11) |
| OVX mouse model | In vivo (ovariectomized mice) | IL-1β, TNF-α, NLRP3 inflammasome | Pro-inflammatory cytokines are upregulated; NLRP3 knockout reduces inflammatory marker expression | (12) |
| RANKL-induced osteoclastogenesis | In vitro (mouse/human osteoclast precursors) | TRAF6, NF-κB, MAPK, NFATc1 | ROS enhance osteoclastogenesis through activation of NF-κB and MAPKs | (13, 14) |
| Ethanol-induced ROS production | In vitro (human osteoblasts) | RANKL/OPG | Ethanol upregulates RANKL via ROS; inhibited by NAC or 17β-estradiol | (15) |
| IL-6-mediated osteoclastogenesis | In vitro (mouse osteoclast precursors) | JAK/STAT, S1PR2 | IL-6 enhances osteoclast migration and activity; upregulates S1PR2 | (16) |
| IL-11 and bone loss | Knockout/transgenic mice | JAK1/STAT3, RANKL/OPG | IL-11 promotes bone resorption; IL-11R knockout improves bone volume and osteoblast activity | (17, 18) |
| IL-17-driven bone loss | In vivo (OVX mice) | CXCR3/CCL20, RANKL | IL-17 increases RANK sensitivity; blockade reverses OVX-induced bone loss | (19, 20) |
| Antioxidant NAC intervention | In vitro + in vivo | ROS, GSH/Nrf2 | NAC alleviates bone erosion and oxidative stress | (21) |
| Drynaria fortunei extract | In vitro + in vivo | SIRT1/Notch1, NLRP3 inflammasome | Downregulates IL-1β, TNF-α; suppresses osteoclastogenesis | (22) |
| Resveratrol and osteogenesis | In vitro (human BMSCs)/animal | Wnt/β-catenin, Runx2, GSK3β | Enhances osteogenesis via β-catenin stabilization; prevents bone loss | (23) |
| Ebselen antioxidant therapy | In vivo (OA rats), in vitro (BMSCs, osteoclasts) | PI3K/Akt, RANKL/OPG | Inhibits osteoclastogenesis and oxidative injury; promotes osteoblast function | (24, 25) |
Representative experimental studies elucidating the molecular mechanisms by which inflammation and oxidative stress contribute to osteoporosis. The table summarizes model systems, key molecular targets, primary findings, and corresponding references.