Biomechanical analysis of pneumothorax: tissue failure, computational simulation, and clinical translation

From a biomechanical perspective, the development and persistence of pneumothorax are closely associated with damage to or functional failure of tissue structures responsible for maintaining pleural-cavity airtightness and pressure coupling. This review aims to summarize advances in the understanding of the mechanical mechanisms and computational modeling of pneumothorax development, lung collapse, and re-expansion, and to evaluate their potential for clinical translation. Three conceptual modes of tissue failure are outlined: stress-driven, material-driven, and overload-driven failure. The review also discusses the applications of hyperelastic, viscoelastic, and poroelastic constitutive models, as well as computational methods, including cohesive zone models (CZMs), the extended finite element method (XFEM), finite element analysis (FEA), and fluid–structure interaction (FSI) modeling. Current research remains constrained by insufficient characterization of material properties, limited representation of tissue heterogeneity, and inadequate experimental and clinical validation. These limitations reduce the comparability of model predictions and hinder their application to individualized clinical management. At present, these models are primarily used to elucidate biomechanical mechanisms and compare tissue responses under different conditions. Their practical utility in risk assessment, surgical planning, and optimization of drainage strategies requires further validation. Future research should prioritize the measurement of material properties, patient-specific model development, and rigorous experimental and clinical validation to provide a more reliable quantitative basis for mechanistic investigations and clinical decision-making in pneumothorax.