Melatonin attenuates titanium particle-induced osteolysis via activation of Wnt/β-catenin signaling pathway

Different effects of Wnt/β‐catenin activation and parathyroid hormone on diaphyseal and metaphyseal in the early phase of femur bone healing of mice

“…When taking only the diaphysis for analysis, it was found that β‐catenin activation was more powerful than PTH in accelerating diaphyseal fracture healing, which consistent with the findings of Agholme and Sandberg et al . And they promoted diaphysis fracture healing better than wild group, and promoted the expression levels of OCN, RUNX2, LEF‐1 in the defect, as others report . In rat, a low dose of PTH enhanced metaphyseal repair, whereas the Scl‐ab had mainly cortical bone effects with less influence on metaphyseal healing.…”

Melatonin up‐regulates bone marrow mesenchymal stem cells osteogenic action but suppresses their mediated osteoclastogenesis via MT2‐inactivated NF‐κB pathway

“…Except for anabolic effects on bone, melatonin is able to suppress bone loss by regulating immune disorder and reversing the abnormal cytokine framework back to normal status. Many studies have suggested that an excessive dose (1–100 μM) of melatonin could alleviate foreigner antigen‐induced negative nonspecific responses and inflammatory cytokines, including TNF‐α and IL‐1β, which helped to inhibit the acceleration of bone loss (Lian et al, ; Liu et al, ; Ping et al, ). However, Zhang et al found that a lower concentration of melatonin played a more beneficial role (50 mg·kg −1 was better than 100 mg·kg −1 ) in improving bone microstructure in type 2 diabetic osteoporosis rats by regulating bone immunity (Zhang et al, ).…”

Wnt4 signaling mediates protective effects of melatonin on new bone formation in an inflammatory environment

“…Melatonin has gained growing attention as an attractive therapeutic candidate for bone-loss diseases based on its following roles in bone homeostasis: 1) melatonin induces differentiation and mineralization of osteogenic precursor cells in vitro via multiple acknowledged signaling pathways, including MAPKs, BMP-Smad, and Wnt-b-catenin (23)(24)(25)(26); 2) melatonin suppresses osteoclastogenesis through down-regulation of the NF-kB pathway and modulation of the balance between receptor activator NF-kB ligand and osteoprotegerin expression (27,28); 3) melatonin administration significantly increases bone mineral density (BMD) in animal models of osteoporosis through its dual effect of enhancing bone formation by osteogenic precursor cells and suppressing bone resorption by OCs (29,30); 4) melatonin administration has shown encouraging outcomes of increased femoral neck and vertebral BMD and changes in the bone resorptionbone formation ratio in clinical trials for the treatment of postmenopausal osteoporosis (31-33); 5) melatonin is an over-the-counter inexpensive supplement commonly used to improve sleep quality and psychologic well-being for elderly and menopausal populations, which has great overlap with the osteoporosis community (34). These results strongly indicate that melatonin has great potential for the treatment of osteoporosis.…”