I'm guessing the answer to this question is rather large. Skin cells die all the time, it seems, and that never registers as painful. But suppose you rupture or otherwise destroy a group of cells, say in the dermis or something, which enough precision to be able to specify the exact count. How many would you have to destroy before it would be perceptible? What if you add a delay between the destruction of each cell in the group? If it was staggered in time, would that make it imperceptible again?


2 Answers 2


Although any number estimation would be inaccurate, I can think on two factors that can influence the count.

  1. Cells location: Pain is trigger when specialize cells (Nociceptors) fires action potentials. The density of those nociceptors is greater in the tip of your finger than in your back. So the number of cell damage that trigger the pain would be different in those areas too.
  2. Cell death rate: The delay that you mention is a key factor. Slow death like the normal on skin is done by a regulated mechanism (Apoptosis), in this process the cellular components are recycled. In fast cell death, the cellular components are released causing inflammation, which increases the nociceptors sensitivity.
  • $\begingroup$ Would it still be true that "any number estimation would be inaccurate" if we hold the cell location constant? Surely this could be studied empirically? Not that it would necessarily be a good idea to do that. $\endgroup$
    – lanf
    Commented Feb 23, 2021 at 22:43
  • $\begingroup$ Have in mind that pain is felt when nociceptors are activated. If you have a method clean enough to kill cells without activate nociceptors directly, then the debris of the death cells can cause nociceptors activation because of the inflammatory process. $\endgroup$
    – heracho
    Commented Feb 24, 2021 at 21:21
  • $\begingroup$ @bxw the location matters a mot, for instance you could destroy most of the brain without pain, since it has few pain receptors. $\endgroup$
    – John
    Commented Sep 22, 2021 at 22:59

There is no specific number of dead cells to be honest that serves as the threshold for pain, it is the molecules that are responsible for decreasing or increasing the threshold of pain either peripherally (at the site of nociceptors) or centrally (endogenous opioids). Here is a diagram that kind of summarizes pain pathophysiology at nociceptor level.

enter image description here

For example, sunburn produces temporary sensitization of the affected area. As a result normally innocuous stimuli, such as light touch or warmth, are perceived as painful (a phenomenon referred to as allodynia), or normally painful stimuli elicit pain of greater intensity (referred to as hyperalgesia)

As correctly stated in the previous answer, Apoptosis would never initiate pain since it doesn't involve any inflammation.

Reference- Basbaum AI, Bautista DM, Scherrer G, Julius D. Cellular and molecular mechanisms of pain. Cell. 2009;139(2):267-284. doi:10.1016/j.cell.2009.09.028



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