The Nail Bed: Theories of Its Functioning and Therapeutic Mechanisms of Dermabrasion

The nail bed is a specialized epithelium attached to the ventral portion of the nail plate. Its appearance is a sequence of ridges and grooves that perfectly correspond to the nail plate (1) (Figure 1). It is not yet clear whether the migration of the nail bed is due to the movement of the cells that compose it or to the growth of the nail plate that slides longitudinally over it, "stretching" it (2). What is clear, in functional terms, is that if the nail bed changes, the shape of the nail also changes and that a large part of the nail dystrophies corresponds to an underlying alteration of the nail bed. Thus: (1) if the nail bed presents a shortening, keratinization, or what is known as "disappearing nail bed" (3), the nail is necessarily forced to thicken since the mitotic activity of the matrix is the same, but the space to deposit its product is less in length (Figure 2); (2) if the nail bed is thin or depressed, the nail increases its thickness and fills the space. If the nail bed is thick, the nail in this portion will be thin (Figure 3).

This behavior allows us to conclude that if we have a flat nail bed with normal morphology and extension, the shape and adhesion of the nail will also be adequate. To illustrate this theory, we use the example of two patients seen in our nail unit service.

We describe through clinical observations the functioning of the nail bed and its response to mechanical dermabrasion.

Historically for the repair of nail bed defects, particularly large ones, surgical methods such as suturing the nail bed, the use of acrylate-based glues (4), or even skin grafts (5) have been the first-line treatments, especially in acute events. The cases described in this article allow us to broaden our perspective and consider other therapeutic options in the approach to nail dystrophies.

Taking into account the premises proposed during the introduction, these results allow a deeper understanding of the functioning of the nail unit, which is, without a doubt, a dynamic structure that responds to forces applied to it. We further hypothesize that mechanical dermabrasion is useful not only for its effect on nail bed hyperkeratosis, but that there must also be an additional effect of the heat and vibration produced during the procedure, which can stimulate the regeneration of the underlying onychocytes. More research is required to understand further the complex response of the nail bed to this therapy, and it would be interesting to carry out a subsequent controlled study to evaluate the efficacy of dermabrasion for the management of this difficult-to-treat entity.

With the previous findings, we present a less invasive technique for recovering the lost nail bed based on its dynamic response to external stimuli and forces.