Black phosphorus nanomaterials may help coordinate immune regulation and bone repair in senile osteoporosis models.
Evidence
This Perspective synthesizes mechanistic and experimental evidence on BP effects in the aged osteoimmune microenvironment, including about 60% lower pro-inflammatory cytokine expression and bone defect bridging rates up to 93%.
Caveat
Clinical translation remains uncertain because aging-related immune mechanisms are complex, long-term safety data are insufficient, and translational pathways are unclear.
Simplified
The pathogenesis of senile osteoporosis involves immune cell imbalance, , and dysregulation of the RANKL/OPG bone-immune axis, collectively defining the concept of immunoporosis. These interrelated processes mutually reinforce one another, leading to a 2-3-fold prolongation of bone healing time, while conventional single-target therapies fail to achieve coordinated regulation of bone regeneration and the immune microenvironment. Black phosphorus (BP) nanomaterials, as an emerging class of biomaterials, represent a paradigm shift from "passive scaffolds" to "active immuno-bone synergistic regulators." BP exerts multifunctional effects by restoring macrophage M1/M2 polarization balance, scavenging reactive oxygen species (ROS) to disrupt inflammatory feedback loops, and modulating the , thereby promoting a transition from a pro-inflammatory, destructive state to an anti-inflammatory, reparative phenotype. Experimental evidence indicates that BP can reduce pro-inflammatory cytokine expression by approximately 60% and achieve bone defect bridging rates of up to 93%. However, the clinical translation of BP remains challenged by the complexity of aging-related immune mechanisms, insufficient long-term safety data, and unclear translational pathways. This Perspective systematically discusses the regulatory mechanisms of BP in the aged osteoimmune microenvironment, the current limitations, and future research directions.
Key numbers
60%
Reduction in Pro-inflammatory Cytokines
Decrease in TNF-α expression in response to BP treatment.
93%
Bone Defect Bridging Rate
Achieved in experimental models using BP-based therapies.
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