Injectable Matrix Metalloproteinase-Responsive Nanoparticle Hydrogel Scaffold for Sustained Local Drug Delivery in Fibrous Dysplasia

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ID: 315174
2026
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Ranked #114 of 119 articles by views in journal of bone and mineral research : the official journal of the american society for bone and mineral research

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Abstract
Receptor activator of nuclear factor kappa-B ligand (RANKL) inhibition has shown significant therapeutic benefit in fibrous dysplasia. However, sustained RANKL inhibition is required to maintain its therapeutic effect. Moreover, disease rebound following discontinuation of denosumab, a human monoclonal RANKL antibody, poses a major clinical challenge to fibrous dysplasia treatment, thereby highlighting the need for strategies that preserve lesion-level efficacy while limiting systemic exposure. Matrix metalloproteinases (MMPs), which are essential for osteoclast function and bone remodeling, have emerged as a key pathogenic pathway in fibrous dysplasia. Lesion profiling revealed elevated expression of MMP-9, -13, and -14 in osteoclast-rich fibrous dysplasia lesions, with dynamic regulation in response to pharmacologic RANKL inhibition and withdrawal. We hypothesized that matrix metalloproteinases may serve as lesion-associated biological cues for localized drug delivery in fibrous dysplasia. We developed an injectable, sustained, and matrix metalloproteinase-responsive local drug delivery system by integrating triglycerol monostearate nanoparticles within a dynamically crosslinked hyaluronic acid-based hydrogel scaffold (HPD/TGMS). To validate this strategy, the small-molecule RANKL inhibitor AS2676293 was loaded into triglycerol monostearate to generate HPD/TGMS@A. Matrix metalloproteinase-mediated cleavage of the ester linkage in triglycerol monostearate enabled protease-responsive drug release, further regulated by hydrogel-constrained perilesional retention. HPD/TGMS@A demonstrated favorable injectability, self-healing behavior, cytocompatibility, and matrix metalloproteinase-dependent anti-osteoclastic activity in vitro. HPD/TGMS@A significantly attenuated fibrous dysplasia lesion progression and improved bone microarchitecture in a GNASR201C knock-in fibrous dysplasia mouse model through perilesional injection. Altogether, these findings establish HPD/TGMS as a localized, lesion-responsive drug delivery strategy in fibrous dysplasia.
Reference Key
openalex_W7162693661 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Lu Xing, Zhongyu Liu, Kaichao Wang, Xiaoqi Zhang, Jie Shen, Jing Shuai, Jiang Liu, Hongyun Zhao, Xianglong Han, Ding Bai, Qianming Chen, Xuefeng Zhao
Journal journal of bone and mineral research : the official journal of the american society for bone and mineral research
Year 2026
DOI
10.1093/jbmr/zjag091
URL
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