Hand hygiene.pdf

4. PHYSIOLOGY OF NORMAL SKIN
The primary function of the skin is to reduce water loss, provide protection against abrasive
action and microorganisms, and generally act as a permeability barrier to the environment.
Its basic structure is: the superficial region, termed the stratum corneum or horny layer, is
between 10 and 20 μm thick; underlying this region are the viable epidermis (50–100 μm),
dermis (1–2 mm) and hypodermis (1–2 mm). The barrier to percutaneous absorption lies
within the stratum corneum, the thinnest and smallest compartment. The stratum corneum
contains the corneocytes or horny cells, which are flat polyhedral-shaped non-nucleated
cells, remnants of the terminally differentiated keratinocytes found in the viable epidermis.
Corneocytes are composed primarily of insoluble bundled keratins surrounded by a cell
envelope stabilized by cross-linked proteins and covalently bound lipids. Interconnecting
the corneocytes of the stratum corneum are polar structures such as corneodesmosomes,
which contribute to stratum corneum cohesion.
The intercellular region of the stratum corneum is composed of lipids primarily generated
from the exocytosis of lamellar bodies during the terminal differentiation of the keratinocytes.
The intercellular lipid is required for a competent skin barrier and forms the acontinuous
tissue. Directly under the stratum corneum is a stratified epidermis, composed primarily
of 10–20 layers of keratinizing epithelial cells, which are responsible for the synthesis of
the stratum corneum. This layer also contains melanocytes involved in skin pigmentation;
Langerhans cells, which are important for antigen presentation and immune responses; and
Merkel cells whose precise role in sensory reception has yet to be fully delineated. As
keratinocytes undergo terminal differentiation, they begin to flatten out and assume the
dimensions characteristic of the corneocytes, i.e. their diameter changes from 10–12 μm
to 20–30 μm and their volume increases 10-fold to 20-fold. The viable epidermis does not
contain a vascular network, and the keratinocytes obtain their nutrients from below by passive
diffusion through the interstitial fluid.
The skin is a dynamic structure. Barrier function does not simply arise from the dying,
degeneration and compaction of the underlying epidermis. Rather, the processes of cornification
and desquamation are intimately linked; synthesis of the stratum corneum occurs
at the same rate as loss. There is now substantial evidence that the formation of the skin
barrier is under homeostatic control. This is illustrated by the epidermal response to barrier
perturbation by skin stripping or solvent extraction. There is circumstantial evidence that
the rate of keratinocyte proliferation directly influences the integrity of the skin barrier. A
general increase in the rate of proliferation will result in a decrease in the time available for
(i) uptake of nutrients, such as essential fatty acids; (ii) synthesis of protein and lipid; and (iii)
processing of the precursor molecules required for skin barrier function. It remains unclear if
chronic but quantitatively smaller increases in the rate of epidermal proliferation also lead to
changes in skin barrier function. Thus, equally unclear is the extent to which the decreased
barrier function caused by irritants is due to an increased epidermal proliferation.
The current understanding of the formation of the stratum corneum has come from studies
of the epidermal responses to perturbation of the skin barrier. Experimental manipulations
that disrupt the skin barrier include: (i) extraction of skin lipids with apolar solvents; (ii)
physical stripping of the stratum corneum using adhesive tape; and (iii) chemically induced
irritation. All such experimental manipulations lead to a decreased skin barrier as determined
by transepidermal water loss. Perhaps the most studied experimental system is the
treatment of mouse skin with acetone. This leads to a marked and immediate increase
in transepidermal water loss, indicating a decrease in skin barrier function. Since acetone