Thermo-elastic model and surface evaporation model to Reveal the damage mechanism of melanocytes induced by laser ablation

This study aims to investigate the interaction between laser irradiation and melanosome particles in Ota’s nevus, as well as to elucidate the thermomechanical damage mechanism of melanin particles. Thermo-elastic and surface evaporation models were employed to simulate the effects of laser ablation on melanin. These models were utilized to analyze the pressure gradient at the melanosome-tissue interface and the formation of vaporization nuclei on melanosome surfaces. Experimental observations were conducted on a tattooed dorsal skin model to examine tissue cavitation and skin whitening. Transient laser heating induced a significant pressure gradient at the melanosome-tissue interface, contributing to mechanical damage. Pulse width exhibited minimal impact on surface evaporation when smaller than the thermal relaxation time of melanosome, while energy density determined the formation of vaporization nuclei. After laser irradiation with an energy density of 4–5 J/cm², the tissue undergoes vaporization caused by cavitation. Bubble formation resulting from surface vaporization of melanosome explained tissue cavitation and skin whitening. Melanosome particle clusters with smaller spacing exhibited higher peak temperatures and more intense phase transitions, leading to structural damage through rapid bubble expansion. Conversely, larger spacing between melanosome particles resulted in thermal diffusion within cells and overall cell thermal injury. When the particle spacing increased to 0.15 μm, it was observed that the region of microbubble formation in the melanocytes continued to expand, even in the absence of vaporization nuclei formation. Short pulsed laser irradiation effectively treats Ota’s nevus by inducing thermomechanical damage to melanosome particles.