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Cavitation has long been recognized as a crucial predictor, or precursor, to the ultimate failure of various materials, ranging from ductile metals to soft and biological materials. Traditionally, cavitation in solids is defined as an unstable expansion of a void or a defect within a material. The critical applied load needed to trigger this instability -- the critical pressure -- is a lengthscale independent material property and has been predicted by numerous theoretical studies for a breadth of constitutive models. While these studies usually assume that cavitation initiates from defects in the bulk of an otherwise homogeneous medium, an alternative and potentially more ubiquitous scenario can occur if the defects are found at interfaces between two distinct media within the body. Such interfaces are becoming increasingly common in modern materials with the use of multimaterial composites and layer-by-layer additive manufacturing methods. However, a criterion to determine the threshold for interfacial failure, in analogy to the bulk cavitation limit, has yet to be reported. In this work, we fill this gap. Our theoretical model captures a lengthscale independent limit for interfacial cavitation, and is shown to agree with our observations at two distinct lengthscales, via two different experimental systems. To further understand the competition between the two cavitation modes (bulk versus interface), we expand our investigation beyond the elastic response to understand the ensuing unstable propagation of delamination at the interface. A phase diagram summarizes these results, showing regimes in which interfacial failure becomes the dominant mechanism.

Biofilms are aggregates of bacterial cells surrounded by an extracellular matrix. Much progress has been made in studying biofilm growth on solid substrates; however, little is known about the biophysical mechanisms underlying biofilm development in three-dimensional confined environments in which the biofilm-dwelling cells must push against and even damage the surrounding environment to proliferate. Here, combining single-cell imaging, mutagenesis, and rheological measurement, we reveal the key morphogenesis steps ofVibrio choleraebiofilms embedded in hydrogels as they grow by four orders of magnitude from their initial size. We show that the morphodynamics and cell ordering in embedded biofilms are fundamentally different from those of biofilms on flat surfaces. Treating embedded biofilms as inclusions growing in an elastic medium, we quantitatively show that the stiffness contrast between the biofilm and its environment determines biofilm morphology and internal architecture, selecting between spherical biofilms with no cell ordering and oblate ellipsoidal biofilms with high cell ordering. When embedded in stiff gels, cells self-organize into a bipolar structure that resembles the molecular ordering in nematic liquid crystal droplets. In vitro biomechanical analysis shows that cell ordering arises from stress transmission across the biofilm–environment interface, mediated by specific matrix components. Our imaging technique and theoretical approach are generalizable to other biofilm-forming species and potentially to biofilms embedded in mucus or host tissues as during infection. Our results open an avenue to understand how confined cell communities grow by means of a compromise between their inherent developmental program and the mechanical constraints imposed by the environment.