Relationship of Aging, Inflammation, and Skeletal Stem Cells and Their Effects on Fracture Repair
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Updated: Aug 28, 2025

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
Published on: May 23, 2014
L Henry Goodnough1, Stuart B Goodman2,3,4,5,6,7,8,9
1Department of Orthopaedic Surgery, Stanford University School of Medicine, 450 Broadway Avenue, M/C 6342, Redwood City, CA, 94063, USA. henryg@stanford.edu.
Purpose Of Review:
This review summarizes recent investigations into the cellular and molecular effects of skeletal aging on the inflammatory response and stem cell function after fracture.
Recent Findings:
Proper regulation of the inflammatory phase of fracture healing is essential. Aging is associated with chronic inflammation, which inhibits bone formation and promotes bone resorption. Osteogenic differentiation and anti-senescence pathways in skeletal stem cells are impaired in geriatric fractures. As the population ages, fragility fractures will continue to represent a significant clinical problem, which will require innovative clinical solutions. Skeletal stem cells in geriatric individuals demonstrate defects in anti-senescence pathways that lead to impaired osteogenic differentiation in vitro in humans. Small molecule-based therapies can partially reverse the aging phenotype. In the future, molecular- or cell-based therapies modulating either inflammatory cells or skeletal stem cells represent potential therapeutic targets to augment contemporary fracture healing interventions in osteoporotic or aging individuals.
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