Ageing research reviewsSep 5, 2026

Using Biomaterials to Help Older Bones Heal and Stop the Cycle of Aging

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 6, 2026

Abstract

Age-related bone loss involves a multilevel pathological process driven by various interconnected factors.

Bone aging is influenced by a combination of intracellular damage, cellular aging signals, and deteriorating microenvironments.
Intracellular damage and homeostatic imbalance lead to cellular aging, which is characterized by the spread of aging signals.
The spread of aging signals affects metabolism, structure of the supporting tissue, and communication between cells.
The worsening microenvironment further intensifies intracellular damage and homeostatic disruption, creating a self-reinforcing cycle.
Strategies targeting these interconnected mechanisms could improve biomaterial design for bone regeneration in aging populations.

Simplified

With accelerating population aging, age-related bone loss, osteoporosis, and delayed bone defect repair have become major challenges in regenerative medicine. Bone aging is not caused by the decline of a single cell type, but is a multilevel pathological process driven by the continuous coupling and mutual reinforcement of intracellular damage accumulation, senescence signal propagation, and microenvironmental deterioration. Based on established aging theories, this review integrates regenerative impairment in aged bone into three interconnected pathological cycles from the perspectives of dynamic feedback and regenerative intervention. Intracellular damage and homeostatic imbalance promote cellular senescence; senescent cells spread senescence signals through SASP and immune dysregulation, inducing abnormalities in metabolism, extracellular matrix (ECM) structure, and intercellular communication; the deteriorated microenvironment then further aggravates intracellular damage and homeostatic disruption, forming a self-reinforcing pathological loop. Within this framework, we summarize biomaterial strategies targeting intracellular damage, senescent cells and SASP-mediated propagation, and the aged microenvironment, and discuss multifunctional and responsive materials for staged or multi-level intervention. This framework organizes dispersed aging mechanisms into a dynamic network of feedback relationships and actionable nodes, providing guidance for mechanism-oriented biomaterial design and strategy selection in aged bone regeneration.

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Using Biomaterials to Help Older Bones Heal and Stop the Cycle of Aging

Abstract

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