Hydrogen Gas Helps Heal Broken Bones Faster in Older Adults

Authors
Journal
Nature Communications
Year
DOI
10.1038/s41467-023-43618-z
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Bone Fractures
Body System
Musculoskeletal

TL;DR

Scientists have developed a special scaffold that releases hydrogen gas to reduce inflammation and reverse aging effects in bones, improving bone repair in elderly mice.

Key Finding

Local hydrogen gas release reduced inflammation and improved bone repair in aged mice by repolarizing immune cells and restoring the tissue's natural regenerative environment.

Summary

This study tested whether hydrogen gas could help repair bone injuries in aged mice by reducing inflammation and restoring the body's natural healing abilities. Researchers created a special scaffold (a support structure) that slowly releases hydrogen gas directly at the injury site. They found that the hydrogen gas reduced inflammation, changed immune cells to promote healing, and significantly improved bone repair in older mice with large bone defects.

Practical Takeaway

This early research in aged mice suggests hydrogen gas delivery to injury sites may help restore age-related declines in bone healing, but this is a preclinical animal study and human applications remain unknown. The scaffold design used here is not yet available as a consumer product, and much more research—including human trials—would be needed before any therapeutic claims could be made.

Abstract

The senescence microenvironment, which causes persistent inflammation and loss of intrinsic regenerative abilities, is a main obstacle to effective tissue repair in elderly individuals. In this work, we find that local H2 supply can remodel the senescence microenvironment by anti-inflammation and anti-senescence effects in various senescent cells from skeletally mature bone. We construct a H2-releasing scaffold which can release high-dosage H2 (911 mL/g, up to 1 week) by electrospraying polyhydroxyalkanoate-encapsulated CaSi2 nanoparticles onto mesoporous bioactive glass. We demonstrate efficient remodeling of the microenvironment and enhanced repair of critical-size bone defects in an aged mouse model. Mechanistically, we reveal that local H2 release alters the microenvironment from pro-inflammation to anti-inflammation by senescent macrophages repolarization and secretome change. We also show that H2 alleviates the progression of aging/injury-superposed senescence, facilitates the recruitment of endogenous cells and the preservation of their regeneration capability, thereby creating a pro-regenerative microenvironment able to support bone defect regeneration.