tissue mechanics: fracture and size regulation

2026

1. arXiv

   

   Divergence of detachment forces in the finite Voronoi model

   Wei Wang and Brian A. Camley

   arXiv:2604.15481 [cond-mat.soft] , Apr 2026

   Abs DOI Bib HTML Code

   

   Detachment and fracture are central to many tissue-level processes, but they are challenging to simulate with Voronoi-type models that typically assume a confluent tissue. Here we analyze the finite Voronoi model, a nonconfluent extension of conventional Voronoi models, in which cell boundaries are composed of straight Voronoi edges and circular arcs of fixed radius ℓ. When the line tension on cell-medium interfaces exceeds the tension on cell-cell contacts, we find that the model exhibits a strong time-step dependence in the fracture timescale of initially intact active clusters: decreasing Δt can unphysically suppress cluster rupture events. We trace this behavior to a divergence of detachment forces in the finite Voronoi model and introduce a simple regularization. Finally, we calibrate the near-detachment mechanics against a deformable polygon model and examine how key physical parameters control the tissue fracture timescale under two different calibration strategies. Our results show that, for studies focused on fracture or intercellular adhesion in nonconfluent monolayers, a physically motivated calibration of near-detachment mechanics in the finite Voronoi model is essential.

   @article{wang2026divergence,
     title = {Divergence of detachment forces in the finite Voronoi model},
     author = {Wang, Wei and Camley, Brian A.},
     journal = {arXiv:2604.15481},
     year = {2026},
     month = apr,
     doi = {10.48550/arXiv.2604.15481},
   }

2. Phys. Rev. E

   

   Controlling tissue size by active fracture

   Wei Wang and Brian A. Camley

   Phys. Rev. E, Mar 2026

   Abs DOI Bib HTML Code

   

   Groups of cells, including clusters of cancerous cells, multicellular organisms, and developing organs, may both grow and break apart. What physical factors control these fractures? In these processes, what sets the eventual size of clusters? We first develop a one-dimensional framework for understanding cell clusters that can fragment due to cell motility using an active particle model. We compute analytically how the break rate of cell-cell junctions depends on cell speed, cell persistence, and cell-cell junction properties. Next, we find the cluster size distributions, which differ depending on whether all cells can divide or only the cells on the edge of the cluster divide. Cluster size distributions depend solely on the ratio of the break rate to the growth rate—allowing us to predict how cluster size and variability depend on cell motility and cell-cell mechanics. Our results suggest that organisms can achieve better size control when cell division is restricted to the cluster boundaries or when fracture can be localized to the cluster center. Additionally, we derive a universal survival probability for an intact cluster 𝑆⁡(𝑡)=𝑒−𝑘𝑑⁢𝑡 at steady state if all cells can divide, which is independent of the rupture kinetics and depends solely on the cell division rate 𝑘𝑑. Finally, we further corroborate the one-dimensional analytics with two-dimensional simulations, finding quantitative agreement with some—but not all—elements of the theory across a wide range of cell motility. Our results link the general physics problem of a collective active escape over a barrier to size control, providing a quantitative measure of how motility can regulate organ or organism size.

   @article{dk15-hwzg,
     title = {Controlling tissue size by active fracture},
     author = {Wang, Wei and Camley, Brian A.},
     journal = {Phys. Rev. E},
     volume = {113},
     issue = {3},
     pages = {034405},
     numpages = {20},
     year = {2026},
     month = mar,
     publisher = {American Physical Society},
     doi = {10.1103/dk15-hwzg},
     url = {https://link.aps.org/doi/10.1103/dk15-hwzg},
   }

2025

1. PRX Life

   

   Confinement, Jamming, and Adhesion in Cancer Cells Dissociating from a Collectively Invading Strand

   Wei Wang, Robert A. Law, Emiliano Perez Ipiña, Konstantinos Konstantopoulos, and Brian A. Camley

   PRX Life, Feb 2025

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   When cells in a primary tumor work together to invade into nearby tissue, this can lead to cell dissociations—cancer cells breaking off from the invading front—leading to metastasis. What controls the dissociation of cells and whether they break off singly or in small groups? Can this be determined by cell-cell adhesion or chemotactic cues given to cells? We develop a physical model for this question, based on experiments that mimic aspects of cancer cell invasion using microfluidic devices with microchannels of different widths. Experimentally, most dissociation events (“ruptures”) involve single cells breaking off, but we observe some ruptures of large groups (∼20 cells) in wider channels. The rupture probability is nearly independent of channel width. We recapitulate the experimental results with a phase-field cell motility model by introducing three different cell states (follower, guided, and high-motility “leader” cells) based on their spatial position. These leader cells may explain why single-cell rupture is the universal most probable outcome. Our simulation results show that cell-channel adhesion is necessary for cells in narrow channels to invade, and strong cell-cell adhesion leads to fewer but larger ruptures. Chemotaxis also influences the rupture behavior: Strong chemotaxis strength leads to larger and faster ruptures. Finally, we study the relationship between biological jamming transitions and cell dissociations. Our results suggest unjamming is necessary but not sufficient to create ruptures.

   @article{PRXLife.3.013012,
     title = {Confinement, Jamming, and Adhesion in Cancer Cells Dissociating from a Collectively Invading Strand},
     author = {Wang, Wei and Law, Robert A. and Perez Ipi\~na, Emiliano and Konstantopoulos, Konstantinos and Camley, Brian A.},
     journal = {PRX Life},
     volume = {3},
     issue = {1},
     pages = {013012},
     numpages = {20},
     year = {2025},
     month = feb,
     publisher = {American Physical Society},
     doi = {10.1103/PRXLife.3.013012},
     url = {https://link.aps.org/doi/10.1103/PRXLife.3.013012},
   }