Glucose transport as a design constraint in white-zone meniscus tissue engineering: a reaction-diffusion framework
In brief
A modeled glucose source reaches 0.40 at deep meniscus tears within 4 hours
In a one-dimensional model of a tear 2.5 mm into the meniscus, native glucose transport stayed below 0.30 of the reference concentration, while a hypothetical sustained source reached 0.40 within 4 hours. These normalized levels are not validated healing targets, and the model does not show that tissue heals; it points to transport experiments for future testing.
- Journal
- Frontiers in bioengineering and biotechnology (Q1)
- Published
- 15 October 2026
- Study design
- Unclassified
- Evidence level
- Level 5, Expert Opinion (CEBM 5)
- Authors
- Tiya Patel
- PMID
- 42959109
- DOI
- 10.3389/fbioe.2026.1880978
Why clinicians should know about it
- Picked for Histology (top studies of the week, 1 November 2026): Meniscal vascular gradient links tissue structure with glucose transport
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.
Abstract as published, via PubMed.
For healthcare professionals. The summary is generated by AI from the published abstract, and the evidence level is assigned automatically from the study design on the Oxford CEBM hierarchy. Neither is medical advice. Read the full paper before changing practice.