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Mechanical pain (or mechanical algesia) can both be a vital mechanism warningus for dangers or an undesired medical symptom important to mitigate. Thus, acomprehensive understanding of the different mechanisms of this type of pain isparamount. In this work, we study the tearing of porcine skin in front of aninfrared camera, and show that mechanical injuries in biological tissues cangenerate enough heat to stimulate the neural network. In particular, we reportlocal temperature elevations of up to 24 degrees Celsius around fast cutaneousruptures, which shall exceed the threshold of the neural nociceptors usuallyinvolved in thermal pain. Slower fractures exhibit lower temperatureelevations, and we characterise such dependency to the damaging rate. Overall,we bring experimental evidence of a novel - thermal - pathway for directmechanical algesia. In addition, the implications of this pathway are discussedfor mechanical hyperalgesia as well, in which a role of the cutaneous thermalsensors has long been suspected. We also show that thermal dissipation shallactually account for a significant portion of the total skin's fracture energy,making temperature monitoring an efficient way to detect biological damages.

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