Diabetic peri‐implantitis (DPI) is characterized by persistent and dysregulated inflammation in a hostile microenvironment, where conventional therapies fail to achieve long‐term control. Increasing evidence indicates that the key pathological feature lies not only in excessive inflammatory activation, but in the failure of inflammation resolution. Here, we propose an all‐stage inflammatory regulation strategy targeting the full progression of DPI, including initiation, propagation, and resolution. An adaptive composite gel (CGCI) was developed by integrating predominantly amorphous copper‐doped bioactive glass with a boron‐modified poly(vinyl alcohol) hydrogel. The system forms a shear‐thinning and self‐healing network, enabling injectability and effective biological sealing. The amorphous bioactive glass mediates rapid Cu ion release for early antibacterial intervention, while the hydrogel provides sustained interleukin‐10 delivery to promote macrophage‐mediated efferocytosis and vascular/lymphatic remodeling. To enable programmable delivery, structural entropy was operationalized within a model to quantitatively describe degradable hydrogel network evolution and establish a predictive framework linking structure to release kinetics. Guided by this model, CGCI achieves stage‐specific therapeutic delivery aligned with inflammation dynamics. Single‐cell transcriptomics reveals coordinated macrophage–endothelial interactions, and in DPI beagle model, CGCI enables effective all‐stage inflammatory regulation and tissue regeneration.
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Li et al. (2026) studied this question.
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