  Maintenance of epidermal thickness is critical to the barrier function of the
skin. Decreased tissue thickness, specifically in the stratum corneum (the
outermost layer of the tissue), causes discomfort and inflammation, and is
related to several severe diseases of the tissue. In order to maintain both
stratum corneum thickness and overall tissue thickness it is necessary for the
system to balance cell proliferation and cell loss. Cell proliferation in the
epidermis occurs in the basal layer and causes constant upwards movement in the
tissue. Cell loss occurs when dead cells at the top of the tissue are lost to
the environment through a process called desquamation. Desquamation is thought
to occur through a gradual reduction in adhesion between cells, due to the
cleaving of adhesion proteins by enzymes, in the stratum corneum.
  In this paper we will investigate combining a (mass action) subcellular model
of desquamation with a three dimensional (cell centre based) multicellular
model of the interfollicular epidermis to better understand maintenance of
epidermal thickness. These investigations show that hypothesised biological
models for the degradation of cell-cell adhesion from the literature are able
to provide a consistent rate of cell loss in the multicellular model. This loss
balances proliferation, and hence maintains a homeostatic tissue thickness.
Moreover, we find that multiple proliferative cell populations in the basal
layer can be represented by a single proliferative cell population, simplifying
investigations with this model.
  The model is used to investigate a disorder (Netherton Syndrome) which
disrupts desquamation. The model shows how biochemical changes can cause
disruptions to the tissue, resulting in a reduced tissue thickness and
consequently diminishing the protective role of the tissue. A hypothetical
treatment result is also investigated. [ABR]
