Low-intensity extracorporeal shock wave therapy for pediatric respiratory diseases: current evidence and translational barriers

Low-intensity extracorporeal shock wave therapy (Li-ESWT) has demonstrable mechanobiologic activity in nonpulmonary systems, where it has been linked to adenosine triphosphate (ATP) release and downstream signaling, macrophage and fibroblast responses, matrix remodeling, and tissue repair. Whether those effects extend to pediatric respiratory disease is uncertain. Adult clinical studies indicate biologic responsiveness in selected inflammatory or reparative settings, but effect sizes are variable and durability is often undemonstrated. Direct pulmonary evidence comes from bronchial cell cultures, including chronic obstructive pulmonary disease (COPD)-derived fibroblasts, and acute lung injury/acute respiratory distress syndrome models. These show biological responses without establishing a calibrated lung-tissue dose or a pulmonary safety window. The air-filled, acoustically heterogeneous lung presents physical challenges to pressure-wave delivery that nonpulmonary experience cannot resolve: interface reflections, inflation-dependent energy scatter, and uncertain lesion depth collectively mean that energy deposition in lung tissue remains poorly characterized. In children, these physical uncertainties are compounded by ongoing alveolarization, age-dependent chest-wall mechanics, and the absence of pediatric device data. This narrative review integrates cross-organ mechanistic studies, pulmonary cellular and animal data, pediatric respiratory biology, and ethics and device-governance literature to define what lung-directed preclinical work is needed and why pediatric pulmonary trials are not yet justified. Pulmonary dosimetry, injury-threshold characterization, standardized adverse-event monitoring, and adult pulmonary pilot safety data must precede any consideration of pediatric enrollment.