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Resumen diario |
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Mi-S3.4-SE:Bmat: Sesión Especial: Biomateriales y terapias avanzadas Lugar: Aula 1.05 Presidente de la sesión: Ángel Raya | |
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17:15 - 17:30
Modeling Diabetic and Pro-inflammatory Bone Microenvironments Using a Bone-on-a-Chip Platform 1: M2BE: Multiscale in Mechanical and Biological Engineering, Instituto de Investigación en Ingeniería de Aragón (I3A), Universidad de Zaragoza, Zaragoza, España.; 2: Departamento de Diagnóstico en Patología y Medicina Oral, Facultad de Odontología, Universidad de la República, Montevideo, Uruguay.; 3: Division of Biomaterials and Tissue Engineering, UCL Eastman Dental Institute, University College London, London, UK. In the field of regenerative medicine, bone regeneration under pathological conditions remains a major challenge. Diabetes mellitus (DM) is a group of systemic diseases with high global prevalence that compromise physiological bone regeneration, affecting angiogenesis and osteoblastic activity. These impairments are partly due to the establishment of a pro-inflammatory microenvironment and redox imbalance. Such alterations hinder the success of conventional regenerative treatments and justify the need for new therapeutic strategies. Current in vitro assays do not fully reproduce pathological conditions, highlighting the importance of advanced models to investigate bone cell responses in disease-relevant environments. The aim of this work was to adapt and validate a bone-on-a-chip platform capable of simulating diabetic and pro-inflammatory microenvironments, using primary osteoblast cultures exposed to high glucose (HG), IL-1β, and their combination (HG+IL-1β). Cell morphology and differentiation were analyzed by confocal microscopy, morphometric parameters (area, perimeter, solidity, and form factor), and expression of osteogenic markers (Runx2, ALP, and osteocalcin). Under control conditions, osteoblasts progressively increased in size, developed cellular extensions, and formed interconnected networks by day 21, accompanied by a dynamic nuclear-to-cytoplasmic translocation of Runx2. In contrast, HG and IL-1β limited cellular expansion, promoted compact morphologies, and reduced differentiation marker expression, with HG+IL-1β showing the strongest effects. In conclusion, this study demonstrates that hyperglycemia and pro-inflammatory signals synergistically impair osteoblast function, and validates the bone-on-a-chip as a robust tool to model diabetic bone pathophysiology and for future applications in biomaterial testing or therapeutic strategies.
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