Aspirin prevents estrogen deficiency-induced bone loss by inhibiting osteoclastogenesis and promoting osteogenesis

Abstract

Background Aspirin is a commonly used antipyretic, analgesic, and anti-inflammatory drug. Numerous researches have demonstrated that aspirin exerts multiple biological effects on bone metabolism. However, its spatiotemporal roles remain controversial according to the specific therapeutic doses used for different clinical conditions, and the detailed mechanisms have not been fully elucidated. Hence, in the present study, we aimed to identify the dual effects of different aspirin dosages on osteoclastic activity and osteoblastic bone formation in vitro and in vivo. Methods The effects of varying doses of aspirin on osteoclast and osteoblast differentiation were evaluated in vitro. The underlying molecular mechanisms were detected using quantitative real-time polymerase chain reaction, western blotting, and immunofluorescence techniques. An ovariectomized rat osteoporosis model was used to assess the bone-protective effects of aspirin in vivo. Results Aspirin dose-dependently suppressed RANKL-induced osteoclasts differentiation and bone resorption in vitro and reduced the expression of osteoclastic marker genes, including TRAP, cathepsin K, and CTR. Further molecular analysis revealed that aspirin impaired the RANKL-induced NF-κB and MAPK signaling pathways and prevented the nuclear translocation of the NF-κB p65 subunit. Low-dose aspirin promoted osteogenic differentiation, whereas these effects were attenuated when high-dose aspirin was administered. Both low and high doses of aspirin prevented bone loss in an ovariectomized rat osteoporosis model in vivo. Conclusion Aspirin inhibits RANKL-induced osteoclastogenesis and promotes osteogenesis in a dual regulatory manner, thus preventing bone loss in vivo. These data indicate that aspirin has potential applications in the prevention and treatment of osteopenia.

Multifaceted Materials for Enhanced Osteogenesis and Antimicrobial Properties on Bioplastic Polyetheretherketone Surfaces: A Review

“…175 The anti-inflammatory mechanism of aspirin is that it inactivates cyclooxygenase (COX), thereby inhibiting the conversion of free arachidonic acid oil into prostaglandins. 176 In the field of oral medicine, aspirin is used to treat periodontitis. 177 Therefore, the aspirin modification of PEEK surfaces can effectively inhibit the inflammatory response around bone implants.…”

“…NSAIDs have anti-inflammatory, antirheumatic, analgesic, and antipyretic effects. , Aspirin is widely used in the treatment of osteomyelitis, osteoarthritis, and various painful conditions . The anti-inflammatory mechanism of aspirin is that it inactivates cyclooxygenase (COX), thereby inhibiting the conversion of free arachidonic acid oil into prostaglandins . In the field of oral medicine, aspirin is used to treat periodontitis .…”

Molecular mechanism of an aspirin compound for alleviation of osteoporosis using nerwork pharmacology and molecular docking

“…Molecular docking studies provide a more intuitive explanation of the interaction between AC and its predicted protein targets in relation to OP [16]. Docking analysis demonstrated that all eight major proteins are targets of AC in osteoporosis.…”