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Abstract
The core mechanism of skeletal aging involves comprehensive disruption of microenvironmental homeostasis.
- Osteoporosis and osteoarthritis may share a common immune-aging mechanism, driven by immune cell dysfunction in the bone marrow.
- Dysfunctional immune cells could trigger a cycle of inflammation and bone remodeling, known as inflammaging.
- The senescence-associated secretory phenotype (SASP) is linked to the imbalance in bone formation and resorption.
- Emerging mechanisms such as mitochondrial dysfunction and exosomal communication are associated with the immune microenvironment's role in bone aging.
- This review establishes a theoretical framework for potential targeted therapies against skeletal aging.
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