The SC is the outer most layer of the skin and is the principal barrier tissue preventing water loss and the final cellular chapter of epidermal differentiation. This mechanism involves a progression of several biochemical processes and the ultimate result is a tissue that prevents TEWL (Trans Epidermal Water Loss) by the formation of a continuous matrix of highly organized lipid lamellae into which is embedded an extensive network of ‘dead’ cells called corneocytes. 
In this perpetual process of cellular activity, keratinocytes divide in the deepest epidermal layers and their proliferation compensates, under normal conditions, for the loss of cornified cells at the skin surface. It is just before they desquamate that keratinocytes form a highly resistant, compact, and non-nucleated horny layer.
Corneocyte morphology is crucial to the role of the SC as a perfunctorily defiant barrier tissue. In the surface area of the skin, layers of corneocytes are tightly and stably bound to each other to form the SC, the sheer but tough barrier at the outermost area of the skin directly facing free radical attack of the external environment. 
The cells themselves are plate-like, stacked in layers, the number of which varies throughout the body’s skin and the corneocytes retain structural characteristics of the parent cell. Each corneocyte originates from a keratinocyte, which is actively proliferating in the epidermis under the SC. These cells are packed with keratin intermediate filaments that provide the structural integrity and also elasticity to resist stretching and compression forces. Concurrently, corneocytes serially detach and smoothly drop off the skin surface for replacement to maintain the integrity and thickness of the SC, keeping it healthy.
As all the varying components of the SC must be synthesized in viable cell layers, the entire chain of the delicate revisions occurring within the horny layer leads to the shedding of most superficial cells and is found to be a pre-programmed action. This shedding process of the corneocyte from the SC, called natural desquamation, has strongly attracted many skin researchers because this is the process which regulates the condition of the skin. It is for this reason AHAs have become the ultimate clinical remedy to correct dehydration, assist in cell regeneration, increase lamellar organelle activity (I call these the water babies of the SC), compact SC for younger looking skin, increase restoration of rete ridges at the dermal/epidermal junction, and a multitude of other benefits for skin rejuvenation stemming from SC activity.
In the late 1980s, when I started using AHAs and other peeling modalities, the marketing metaphor describing acid and professional exfoliation end point achievement illustrated the ‘brick and mortar’ theory. Given this, how many aestheticians actually understand this hypothesis and how it applies to responsible and professional skin practice?
Dr. Elias, et al, originally conceived the rhetorical expression of the ‘brick and mortar’ model, referencing the SC in the early 1980s. According to his epiphany, the vision he perceived was cellular ‘bricks’ sealed and kept together by the lipidic ‘mortar’ of the SC. Although several aspects of SC morphology and function can be explained on this basis, one major difference noted concerning the SC cohesion and desquamation, is the principal factor responsible for maintaining attachment between corneocytes. These are actually not the lipids, but are desmosomes and corneodesmosomes. It is their progressive degradation that actually leads to the liberation of these cornified cells at the skin surface and also becomes the direct mechanical and/or enzyme effect of professional desquamating (peeling) products when applied to the SC.
The desmosomes of the SC are rivet-like structures that provide SC cohesion and integrity. However further upward in the SC the desmosomes are modified configurations and termed corneodesmosomes due to their relationship with the corneocytes. Corneodesmosomes, the modified desmosomes of the SC, are largely responsible for the strong corneocyte cohesion and crucial for a proper barrier function of the epidermis.
Their degradation at the epidermal surface is of major importance for a “normal desquamation” process. The most marked difference between corneocyte and the parent keratinocyte is that the former are largely devoid of cellular organelles, which degrade during their formation. As a result, the corneocytes are only capable of catabolic reactions.
In understanding the world of the SC corneocyte, this resident is localized within the hydrophobic lipid lamellae and requires a mechanically stable structure of specialized proteins. This unambiguous covering is identified as a ‘protein cage’ known as the cornified envelope (CE), which encapsulates the corneocyte. It is the specialized proteins linked by specific y-glutamyl-e-lysine and y-glutamyl-polyamine isopeptide bonds that results in each corneocyte being enclosed by a protein shell that is really a macromolecule. The major adhesive components of corneodesmosomes are two glycoprotein’s, mainly desmoglein 1 (Dsg1) and desmocollin 1 (Dsc1). Synthesized and secreted by granular keratinocytes, corneodesmosin is also an adhesive glycoprotein, located in the extracellular part of the corneodesmosomes, which is a 529-amino-acid long, glycine, and serine rich protein.
Keeping this skin science in mind, we as professionals must understand that during a professional treatment all of these indigenous constituents are removed and require replenishment via SC ‘identical’ serums. One critical application step to initiate, especially after a peel, mask, or enzyme treatment when the corneodesmosomes structures are dissolved and corneocytes removed.
Depletion of these substances also occurs when daily cleansing, exfoliation, and masks are an integral part of prescribed skin care. Your client should be instructed to put back into the skin what has been removed at least twice a day. No doubt you recall the ‘tight’ feeling experienced after cleansing. This is due in part to the removal of these lipids and amino acids. Incorporating a replenishing serum is a critical step to rebuilding the infrastructure of these inner cellular substances and structures, essential to cellular health and principal to a balanced, healthy skin.
Dry skin is a complex phenomenon in which the skin can feel rough, taut, itchy, and visibly look ‘dry’ due to the appearance of macroscopic flakes (non-nucleated corneocytes) or scale build-up on the skin surface.
To understand dry, dehydrated skin, you must first understand the processes taking place both in the epidermis and the SC, but particularly within the superficial layers of the SC because this is ultimately where dry skin manifests. Dry skin results from a perturbation in the process of desquamation. In healthy, hydrated skin, desquamation is a carefully regulated process in which the surface corneocytes are shed in careful balance with the underlying formation of new corneocytes at the stratum granulosum/corneum boundary. Desquamation is not only responsible for maintaining SC thickness, but by ensuring a continual turnover of corneocytes it also protects against the ever-present damaging effects of the environment.
Water content is vital to SC balance and desmosomal degradation is inhibited under dry skin conditions as compared to a moist environment. A dry skin displays impaired barrier function as indicated by increased TEWL and diminished water-holding capacities. Both of these biophysical anomalies can be related to altered composition of the lipids of the SC. While not the primary defect, the impaired barrier repair function (BRF) and surface roughness associated with dryness may render the skin more susceptible to irritation and sensitivities.
Lipids are as critical to the function of the SC as gas is to an automobile. Restoration of barrier function is accompanied by re-accumulation of lipids within the SC interstices.
Restoration of the SC requires increased availability of the major lipid components. Studies clearly demonstrate that epidermal cholesterol, FA (fatty acids), ceramide, and glucosylceramide synthesis are required individually for barrier homeostasis and prove three key lipids are required for permeability barrier that must be supplied together in proper proportion for normal barrier recovery. Homeostasis implies a balance between cell growth and cell death. This balance is essential for the development and maintenance of multi-cellular organisms. Homeostasis is controlled by several mechanisms including apoptosis, a process by which cells condemned to death are completely eliminated. Physiologic mixtures of topical lipids influence barrier function, not by occluding of the SC, but rather by contributing to the lipid pool within SG (Stratum Granulosum) cells.
The lipids found in normal SC consist mainly of a series of ceramides, cholesterol, and fatty acids. There are six representatives of ceramides in the human SC and the flexibility of this membrane relies on these lipids to keep the skin supple and hydrated. Important evidence exists that verifies water-soluble materials, such as free amino acids, organic acids, urea, and inorganic ions determine the water-holding properties of the SC and these materials have been identified as Natural Moisturizing Factors (NMF).
Lactic Acid, a natural organic acid, increases the NMF in skin required to support the restoration of the SC. The lactic acid NMF component is a valuable occupant for the SC because it contains scores of factors that increase the water holding capacity of the SC, while it reorganizes cells. The composition of NMF consists of, but is not limited to: 40 percent free amino acids, 12 percent lactate, 8.5 percent sugars-organic acids-peptides and other substances, potassium, calcium, magnesium, urea, etc.
Research of over 30 years has revealed that AHAs, most particularly lactic and glycolic acid, have many beneficial actions on the skin. It seems unlikely that the future will see discoveries of new major effects of AHAs on the skin since this ingredient has been studied so extensively and proven to be an important clinical resolution for dry, aging, acne, and pigmented skin. Instead, it is the vision of this author and many published scientists; clarification of their mechanisms of action should enable more effective targeting and optimal use of AHAs for the indication of dry skin along with other benefits.
When lipids are removed from the SC environment, the remedy is simple – although the constituents are complex–replenish these indigenous residents with efficacious fluids consisting of amino acid peptide complex, ceramides, hylauronic acid, and other native hydrating components. I cannot emphasize enough the importance of using the skin organ as the base for everything you do for a professional solution. This is an important point of difference. Anything that removes or compromises lipid balance of the SC, such as organic solvents, cleansers, peeling ingredients, microdermabrasion, cavitation, etc., induces the condition of dry skin which is characterized by a reduction in the water-holding function of the SC. Thus, as indicated, structural lipids mainly comprised of ceramides, play a significant role in the water holding properties of the SC and elucidate the role of ceramides as natural moisturizing factors and recovery of dry, irritated skin.
Another important ‘water’ element the skin required for dehydration recovery is hylauronic acid. Always look for a natural plant source made from microbial fermentation or vegetable ferments. This natural skin element is able to bind 1000+ times its weight in water and acts like a moisture magnet to maintain extracellular fluidity in the SC. Hylauronic acid (HA) acts as an intercellular ground substance and fills the space between the collagen and elastic fibers necessary to keep collagen hydrated. HA also promotes moisture retention and penetrates the skin’s surface with increased water absorption to assist in diminishing wrinkles, while treating dry, damaged skin. In addition, HA supports the natural protective mechanism of the skin and can eliminate active oxygen free radicals produced by ultraviolet radiation in the epidermis, and protect the skin from damage.
This ingredient is one of the more heavily researched substances in medicine with literally thousands of clinical trials focusing on it. HA acts as a lubricant by allowing fibers to pass over each other smoothly, thus making the tissue softer, pliable, healthier, and younger acting. This is the one significant reason HA is used to treat scarred tissue successfully.
In conclusion, although the SC has many functions, its ability is to serve as a protective barrier that prevents excess loss of fluids and electrolytes allows life in a terrestrial environment to spawn healthy cells for healthy skin. It is a savvy aesthetician who understands the physiology, anatomy, and histology of the SC. For it is only then that she can practice with the science, knowledge, and skill to liberate the SC from an imbalance and orchestrate the new generational development of dermal and epidermal cells for younger, supple, healthy skin.

Christine Heathman, Master Aesthetician, CME, LMT, is the Founder and CEO of Glymed Plus. With over 20 years of practicing clinical aesthetics, her experience with the medical profession is well established. As a licensed professional, she holds three licenses in aesthetics: one in California, a Master License in Utah, and one in Europe. As the Director of Education for the Gly-Med Institute of Skin Sciences in Spanish Fork, Utah, Heathman directs and provides the skin care professional with exceptional training. Her dedication to education is well established in the skin care industry and is known on a global basis for exceptional schooling in advanced skin care. For more information, please contact her at This email address is being protected from spambots. You need JavaScript enabled to view it..