We think Hitomi’s hypothesis is correct. Here is why (this is paraphrased from our blog post on subungal hematomas and our revolutionary thinking on why they occur and it seems to fit well with pincer nail formation as well).
… when the skin is pulled at a differential rate over the distal phalange (from gripping of the toes rather than downward pressing through the toe pad) there will be a net lifting response of the nail from its bed as the skin is drawn forward of the backward drawn phalange (there is a NET movement of skin forward thus lifting the nail from its bedding). For an at-home example of this, put your hand AND fingers flat on a table top. Now activate JUST your distal long finger flexors so that only the tip of the fingers are in contact with the table top (there will be a small lifting of the fingers). There should be minimal flexion of the distal fingers at this point. Note the spreading and flattening of the nail. Now, without letting the finger tip-skin contact point move at all from the table, go ahead and increase your long flexor tone/pull fairly aggressively. You are in essence trying to pull the finger backward into flexion while leaving the skin pad in the same place on the table. Feel the pressure building under the distal tip of the finger nail as the skin is RELATIVELY drawn forward.] This is fat pad and skin being drawn forward (relative to the phalange bone being drawn backward) into the apex of the nail. Could this be magnifying the curvature of the nail and not offsetting the “automatic curving and shrinkage” function of the nail ? We think it is quite possible.
We have more to say on this topic, the above is just an excerpt of our blog post. More here, in the link below