Heat emitting damage in skin: a thermal pathway for mechanical algesia

TL;DR

This study demonstrates that mechanical injuries in skin can generate significant heat, activating thermal pain receptors and revealing a new thermal pathway for mechanical algesia, with implications for pain management and damage detection.

Contribution

The paper provides experimental evidence of heat generation during skin tearing and introduces a novel thermal pathway for mechanical pain in biological tissues.

Findings

Local temperature increases up to 24°C around skin ruptures

Faster tears produce higher temperature elevations

Thermal dissipation accounts for a significant part of skin fracture energy

Abstract

Mechanical pain (or mechanical algesia) can both be a vital mechanism warning us for dangers or an undesired medical symptom important to mitigate. Thus, a comprehensive understanding of the different mechanisms of this type of pain is paramount. In this work, we study the tearing of porcine skin in front of an infrared camera, and show that mechanical injuries in biological tissues can generate enough heat to stimulate the neural network. In particular, we report local temperature elevations of up to 24 degrees Celsius around fast cutaneous ruptures, which shall exceed the threshold of the neural nociceptors usually involved in thermal pain. Slower fractures exhibit lower temperature elevations, and we characterise such dependency to the damaging rate. Overall, we bring experimental evidence of a novel - thermal - pathway for direct mechanical algesia. In addition, the implications of this pathway are discussed for mechanical hyperalgesia as well, in which a role of the cutaneous thermal sensors has long been suspected. We also show that thermal dissipation shall actually account for a significant portion of the total skin's fracture energy, making temperature monitoring an efficient way to detect biological damages.