Glucose transport as a design constraint in white-zone meniscus tissue engineering: a reaction-diffusion framework
- 1Orthopaedic Research Laboratory, Rutgers - Robert Wood Johnson Medical School , , ,
Abstract
The adult knee meniscus has a strong vascular gradient: the peripheral red zone is vascularized, whereas the inner white zone is largely avascular and has limited intrinsic healing potential after injury. Although biologic augmentation and scaffold-based strategies are being explored to improve meniscal repair, it remains unclear whether modifying local glucose transport can improve glucose availability at deep white-zone tears. This study uses a one-dimensional reaction-diffusion framework to model normalized glucose concentration from a vascularized red-zone boundary toward a simulated 2.5 mm white-zone tear. Glucose diffusivity values were selected from reported meniscus glucose-diffusion measurements under different compressive strain conditions, and the model compares native diffusivity cases with an augmented sustained-source case representing a hypothetical scaffold- or microchannel-assisted transport scenario. The framework reports threshold-free glucose profiles, mathematical fractional-restoration comparison levels (C/C0 = 0.20, 0.30, 0.40, and 0.50), source-release kinetics, tear-depth sensitivity, initial-condition sensitivity, extended simulation windows, and model-derived diffusivity enhancement estimates. The comparison levels are not validated healing thresholds or clinical targets. Native glucose diffusivity cases remained below C/C0 = 0.30 at a tear located 2.5 mm from the red-zone boundary, even when selected simulations were extended to 24 h. In contrast, an augmented sustained-source example reached C/C0 = 0.20, 0.30, and 0.40 within the 4-h transport window. Initial condition sensitivity showed that the main interpretation remained unchanged when the model was initialized with a reference steady glucose profile rather than a depleted domain. These results do not demonstrate biological healing, but they provide a hypothesis-generating framework for defining glucose transport experiments and planning future ex vivo validation studies.
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BibTeX
@article{patel2026glucose,
title = {{Glucose transport as a design constraint in white-zone meniscus tissue engineering: a reaction-diffusion framework}},
author = {Tiya Patel},
journal = {Frontiers in bioengineering and biotechnology},
year = {2026},
month = oct,
doi = {10.3389/fbioe.2026.1880978},
url = {https://europepmc.org/article/PMC/PMC13716718},
note = {CC BY},
}
RIS
TY - JOUR
TI - Glucose transport as a design constraint in white-zone meniscus tissue engineering: a reaction-diffusion framework
AU - Tiya Patel
PY - 2026
DA - 2026/10/15
JO - Frontiers in bioengineering and biotechnology
DO - 10.3389/fbioe.2026.1880978
UR - https://europepmc.org/article/PMC/PMC13716718
AB - The adult knee meniscus has a strong vascular gradient: the peripheral red zone is vascularized, whereas the inner white zone is largely avascular and has limited intrinsic healing potential after injury. Although biologic augmentation and scaffold-based strategies are being explored to improve meniscal repair, it remains unclear whether modifying local glucose transport can improve glucose availability at deep white-zone tears. This study uses a one-dimensional reaction-diffusion framework to model normalized glucose concentration from a vascularized red-zone boundary toward a simulated 2.5 mm white-zone tear. Glucose diffusivity values were selected from reported meniscus glucose-diffusion measurements under different compressive strain conditions, and the model compares native diffusivity cases with an augmented sustained-source case representing a hypothetical scaffold- or microchannel-assisted transport scenario. The framework reports threshold-free glucose profiles, mathematical fractional-restoration comparison levels (C/C0 = 0.20, 0.30, 0.40, and 0.50), source-release kinetics, tear-depth sensitivity, initial-condition sensitivity, extended simulation windows, and model-derived diffusivity enhancement estimates. The comparison levels are not validated healing thresholds or clinical targets. Native glucose diffusivity cases remained below C/C0 = 0.30 at a tear located 2.5 mm from the red-zone boundary, even when selected simulations were extended to 24 h. In contrast, an augmented sustained-source example reached C/C0 = 0.20, 0.30, and 0.40 within the 4-h transport window. Initial condition sensitivity showed that the main interpretation remained unchanged when the model was initialized with a reference steady glucose profile rather than a depleted domain. These results do not demonstrate biological healing, but they provide a hypothesis-generating framework for defining glucose transport experiments and planning future ex vivo validation studies.
SN - 2296-4185
ER -