Rational Surface Engineering Reduces Advanced Glycation End‐Product Adsorption and Improves Implant Integration

Advanced glycation end-products (AGEs) accumulate in metabolic diseases such as diabetes and are closely associated with poor outcomes following implantation. However, how these molecules influence events at the biomaterial interface has remained largely unknown. Here, we identify AGEs as critical biointerfacial modifiers that adsorb onto implant surfaces, reprogram immune responses, promote fibrotic encapsulation, impair angiogenesis, and compromise osseointegration. This suggests a potential mechanism by which metabolic disease disrupts biomaterial-tissue integration. By engineering titanium surfaces enriched with amine or carboxyl functionalities, we create AGE-resistant biointerfaces that effectively suppress pro-inflammatory M1 macrophage polarization, promote an anti-inflammatory M2 macrophage phenotype, reduce fibrotic encapsulation, enhance angiogenesis, and improve osseointegration across ex vivo, in vitro, and in vivo diabetic models. These findings establish disease-informed surface chemistry as a design paradigm for next-generation implants intended for metabolically compromised and other high-risk patient populations.

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Publication Details

Journal
Advanced Science
Published
2026-10-27
DOI
https://doi.org/10.1002/advs.78507
Primary Topic
Bone Tissue Engineering Materials
Type
article
Field-Weighted Citation Impact
0.00

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article

Rational Surface Engineering Reduces Advanced Glycation End‐Product Adsorption and Improves Implant Integration

Giles Best, Vi Khanh Truong, Richard Bright, Jitraporn Pimm Vongsvivut et al.
3 links
Advanced Science
Bone Tissue Engineering Materials
article

Rational Surface Engineering Reduces Advanced Glycation End‐Product Adsorption and Improves Implant Integration

Giles Best, Vi Khanh Truong, Richard Bright, Jitraporn Pimm Vongsvivut, Jordan Y Z Li, Thien Ngoc Le, Krasimir A. Vasilev, Tien Thanh Nguyen, Markos Negash Alemie, Tengxiao Huang, Xuan Duy Do, Yunpeng Zhao, Wenhao Chen, Weiwei Li
article en

Abstract

Advanced glycation end-products (AGEs) accumulate in metabolic diseases such as diabetes and are closely associated with poor outcomes following implantation. However, how these molecules influence events at the biomaterial interface has remained largely unknown. Here, we identify AGEs as critical biointerfacial modifiers that adsorb onto implant surfaces, reprogram immune responses, promote fibrotic encapsulation, impair angiogenesis, and compromise osseointegration. This suggests a potential mechanism by which metabolic disease disrupts biomaterial-tissue integration. By engineering titanium surfaces enriched with amine or carboxyl functionalities, we create AGE-resistant biointerfaces that effectively suppress pro-inflammatory M1 macrophage polarization, promote an anti-inflammatory M2 macrophage phenotype, reduce fibrotic encapsulation, enhance angiogenesis, and improve osseointegration across ex vivo, in vitro, and in vivo diabetic models. These findings establish disease-informed surface chemistry as a design paradigm for next-generation implants intended for metabolically compromised and other high-risk patient populations.

Advanced Science
Shandong University (CN), Flinders University (AU), Flinders Medical Centre (AU), Australian Synchrotron (AU), Adelaide Institute for Sleep Health (AU), Qilu Hospital of Shandong University (CN)
Australian Nuclear Science and Technology Organisation, Shandong University, Government of South Australia, Diabetes Australia, Flinders University, National Natural Science Foundation of China, Natural Science Foundation of Shandong Province, Australian Research Council, National Health and Medical Research Council
Good health and well-being
Openalex Percentile: Top 25%
Bone Tissue Engineering Materials
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