For example if you have a sore throat it’s because an infection is being fought by your natural killer cells and they are destroying infected cells causing necrosis and inflammation. Is this correct? If so is there a particular threshold of cells to be killed before the feeling of pain arises? How is this communicated exactly? Is it a gradual scale that on lower levels we cannot perceive until enough cell death has occurred and caused necrosis and inflammation to trigger the nerves? How does the process exactly work on this initial level? Is the cell death in this case the main catalyst for the pain or is it something else? Is this different than the pain felt from cell death by radiation for example?
In: Biology
Nerves do not detect *cell death*. They directly detect certain types of damage… or sources of likely damage. For example pain from touching a hot coffee mug or something doesn’t mean cells are *already* dying, though if it was a little hotter it could really injure you. Also, pain from stretching or overexerting muscle doesn’t mean cells are *already* dying and these sorts of exercise can be good for you, but if you push much harder it could hurt you.
The purpose of pain is to let you know you’re doing or touching something which *could* cause injury so you can stop it, and avoid that injury.
And these things are detected in a variety of ways with nerve cells that detect heat, physical pressure, chemical changes, etc, but not directly because cells died. As you suspect, this happens all the time and is not always due to something bad going on.
Pain is usually caused by specific pain receptor nerves noticing a certain ph that’s made by damaged skin. That’s why putting an acid like lemon juice on a cut stings so bad.
The aching pain is something different that I don’t know but the basic ouch/sting/cut type of pain is that.
For a sore throat, although infected cells are dying, it isn’t really a lot of cells. As the other post says, nerves sense a lot of things. Some can detect chemical signals of damaged cells, and convey that as pain, but that isn’t really the source of pain signals in something like a sore throat. That pain is from the overall inflammation. If a large area of cells dies, then there will actually be no pain, since the nerves in the area will be dead too. So, for example, in a bad burn, no pain is a sign of worse injury than some pain. In a heart attack, the area of the heart that is dead isn’t causing chest pain, it is the area around that, which is about to die that is causing pain.
To add on to what other people are saying, most cell death that occurs in the body is programmed. This is called apoptosis. Apoptosis does not cause inflammation, so our body does not generally react to it. Instead, it just cleanly eats up the debris and moves on. In the context of an illness or another cell injury, the injury induces a soup of inflammatory cytokines that are basically signals telling your body that there is a problem, and it needs to react to it. Once a threshold of signals in the inflammatory soup has been achieved, pain receptors can be triggered. Other pain receptors have different triggers like heat or cold or chemical damage, etc.
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