Postmenopausal osteoporosis (PMOP) is a significant metabolic bone disease triggered by estrogen deficiency. Macrophages, as pivotal cells in bone metabolism regulation, participate in bone remodeling and inflammatory modulation through differentiation into osteoclasts and polarization phenotype switching. This article systematically reviews the mechanistic roles of macrophages in PMOP, encompassing their interactions with osteoclasts, polarization effects, immune-inflammatory responses, and impacts of oxidative stress. Furthermore, it explores the potential applications of macrophages in molecular diagnosis and pharmacological interventions for PMOP, while proposing future research directions.
