Molecular Mechanisms and Therapeutic Targets for Pain Following Osteoporotic Vertebral Fractures

Osteoporotic vertebral fractures (OVF) are among the most common fractures in older adults. They are strongly linked to severe pain, disability, and a reduced quality of life. Pain from OVFs often becomes chronic and differs from pain caused by fractures in normal bone. This review systematically summarizes the molecular mechanisms of OVF-related pain. It focuses on how changes in bone metabolism, inflammation, non-coding RNA regulation, and neural pathways affect each other. Major factors that drive the onset and persistence of OVF pain include increased osteoclast activity, abnormal Wnt/β-catenin signaling, inflammatory mediators, and neuropeptides. Recent studies also report new molecular targets that are closely related to OVF pain, such as TRPA1, WWP1, STK11, and specific microRNAs. Targeted treatments may improve pain control and function in patients with OVF. These include anti-neurosensitization drugs, anti-osteoporosis therapies, anti-inflammatory treatments, and neural modulators. More research is still needed to clarify these mechanisms and to develop safer, more effective, and more personalized treatments that improve outcomes and quality of life.