Corneum, stratum

Skin. The skin s unique molecular transport and barrier properties pose a challenge for transdermal dmg dehvery. Diffusion of dmgs through the stratum corneum, the outer layer primarily responsible for the skin s limited permeabUity, varies by dmg, by skin site, and among individuals. Until recently, virtuaUy aU dmgs appHed to skin were topical treatments. 

Emulsion components enter the stratum corneum and other epidermal layers at different rates. Most of the water evaporates, and a residue of emulsifiers, Hpids, and other nonvolatile constituents remains on the skin. Some of these materials and other product ingredients may permeate the skin others remain on the surface. If the blend of nonvolatiles materially reduces the evaporative loss of water from the skin, known as the transepidermal water loss (TEWL), the film is identified as occlusive. AppHcation of a layer of petrolatum to normal skin can reduce the TEWL, which is normally about 4—8 g/(m h), by as much as 50 to 75% for several hours. The evaporated water is to a large extent trapped under the occlusive layer hydrating or moisturizing the dead cells of the stratum corneum. The flexibiHty of isolated stratum corneum is dependent on the presence of water dry stratum corneum is britde and difficult to stretch or bend. Thus, any increase in the water content of skin is beHeved to improve the skin quaHty. 

The abihty to moisturize the stratum corneum has also been claimed for the presence of certain hydrophilic polymers, for example, guar hydroxypropyl trimonium chloride [65497-29-2] on the skin. By far the most popular way to moisturize skin is with humectants, some of which are Hsted in Table 12. It is claimed that humectants attract water from the environment and thereby provide moisture to the skin. 

Studies of the interactions between water and the Hpid constituents of the stratum corneum suggest that the supply of water per se is not responsible for skin quaHty and condition. Water vapor from lower layers provides a constant supply of moisture to the epidermis. Instead, the abiHty of the skin to retain the moisture is critical, and this abiHty depends on the HpidlameUar bilayers that occupy the spaces between the ceUs of the stratum corneum (44—46). 

Sweating, the other powerful heat loss mechanism actively regulated by the thermoregulatory center, is most developed in humans. With about 2,6 million sweat glands distributed over the skin and neurally controlled, sweat secretion can vary from 0 to 1 I7(h m ). The other, lesser, passive evaporative process of the skin is from the diffusion of water. The primary resistance to this flow is the stratum corneum or outermost 15 pm of the skin. The diffusion resistance of the skin is high in comparison to that of clothing and the boundary layer resistance and as a result makes water loss by diffusion fairly stable at about 500 grams/day. 

Some of the discomfort of warm environments, the perception of skin moisture, and the interactions of clothing fabrics with the skin may be due to the moisture itself. The skin s outer layer of dead squamous cells of the stratum corneum can readily absorb or lose water. With moisture addition, the cells swell and soften. With drying, they shrink and become hard. In this setting the skin s moisture may be better indicated or characterized by the relative humidity of the skin (RH i ) rather than skin wettedness,-" ... 

The skin is the largest organ in the human being. In particular, the surface layer of the outer epidermis, the stratum corneum, usually provides quite good protection against chemical compounds. Nevertheless, the skin is an important entry route for chemical compounds into the body. 

Reported studies have shown its anti-inflammatory effects and anti-oxidant action. It acts by thinning the stratum corneum, promoting epidermolysis, dispersing basal layer melanin and epidermal and dermal hyaluronic acid and collagen gene expression that increases through an elevated secretion of IL-6 [3]. 

It is a lipophilic compound which removes intercellular lipids that are covalently linked to the cornified envelope surrounding epithelial cells [3]. It also enhances penetration of other agents. Resorcinol (m-dihydroxy benzene) is structurally and chemically similar to phenol. It disrupts the weak hydrogen bonds of keratin [4]. Lactic acid is an alpha hydroxy acid which causes corneocyte detachment and subsequent desquamation of the stratum corneum [5]. 

Tretinoin 0.05-0.1% which is the most critical component of this regimen as it results in decreased stratum corneum thickness, increases the kinetics of epidermal turnover, and decreases corneocyte adhesion... 

Exfoliants such as glycolic acid or lactic acid result in decreased corneocyte adhesion and stimulate epidermal growth by disrupting the stratum corneum... 

Salicylic acid (ortho hydroxybenzoic add) is a beta hydroxy acid agent. It is a lipophilic compound which produces desquamation of the stratum corneum via removal of intercellular lipids [3] (see salicylic acid section). Given its keratolytic effects, it has become an increasingly popular superficial peeling agent. Salicylic acid peels induce injury via thinning or removal of the stratum corneum. In addition, salicylic acid potentially enhances the penetration of TCA. 

Hematoxylin/eosin stains of biopsies of back skin taken 24 h post-chemical peeling, a Glycolic acid peel 70%. Note stratum corneum necrosis... 

Epidermal melasma mcreased melanin in the basal, suprabasal and stratum corneum layers. Clinically, melasma... 

All humans experience intrinsic aging. Typically, it is characterized by smooth, relatively atrophic, finely wrinkled or lax skin. Histologically, the stratum corneum is normal. However, the epidermis is atrophic and there is flattening of the dermo-epidermal junction. Dermal features include decreased thickness, loss of elastic fibers, and a decrease in the biosynthetic capacity of fibroblasts [i, 2] (Table 15.1). 

Stratum corneum normal thickness (basket weave pattern), epidermis thinned, atrophic, flattened rete ridges... 

Superficial chemical peels, including salicylic and glycolic acids, and Jessner s peels target the stratum corneum to the papillary dermis. These agents can be safely used to facilitate the resolution of PIH (Figs. 16.2,16.3,16.4 and 16.5). To assess for variability in response and limit further PIH, when possible, chemical peels should be initiated at the lower concentrations and titrated to higher concentrations if necessary to increase efficacy while minimizing side effects (see Darker Skin Section). 

In addition, data obtained from infrared, thermal, and fluorescence spectroscopic studies of the outermost layer of skin, stratum corneum (SC), and its components imply enhancer-improved permeation of solutes through the SC is associated with alterations involving the hydrocarbon chains of the SC lipid components. Data obtained from electron microscopy and x-ray diffraction reveals that the disordering of the lamellar packing is also an important mechanism for increased permeation of drugs induced by penetration enhancers (for a recent review, see Ref. 206). 

Fig. 2.3.9 A time series of profiles showing the is shown by the lowest trace. The inset shows ingress from right (stratum corneum) to left the advance of the glycerine front against the (viable epidermis) of glycerine into human skin square root of time from which Fickian in vitro. The skin before application of glycerine diffusion is inferred.

Preliminary studies, which have repeated many of the in vitro experiments in vivo, reported that the differentiation between stratum corneum and viable epidermis is at least as good, if not better in vivo and that many of the other experiments are similarly reproduced [16]. 

Since dermatophyte hyphae seldom penetrate into the living layers of the skin, instead remaining in the stratum corneum, most infections can be treated with topical antifungals. Infections... 

Fungal skin infections are primarily caused by dermatophytes such as Trichophyton, Microsporum, and Epidermophyton. Trichophyton rubrum accounts for more than 75% of all cases in the United States.36 To a lesser extent, Candida and other fungal species cause skin infections. With tinea infections, the causative dermatophyte typically invades the stratum corneum without penetration into the living tissues, leading to a localized infection. 

Since dermatophyte hyphae seldom penetrate into the living layers of the skin, instead remaining in the stratum corneum, most infections can be treated with topical antifungals. Infections covering large areas of the body or infections involving nails or hair may require systemic therapy. Patients with chronic infections or infections that do not respond to topical therapy are also candidates for systemic therapy. 

Let us consider how the skin is structured to better understand how this tissue performs some of its vital functions. Consider the cross section of the skin sketched in Fig. 1. This illustration shows the readily distinguishable layers of the skin, from the outside of the skin inwards the 10 pm thin, fully differentiated, devitalized outer epidermal layer called the stratum corneum the 100 pm thin live, cellular epidermis and the 1000 pm thin (1 mm thin) dermis. Note that all the thicknesses specified here are representative only, for the actual thickness of each stratum varies severalfold from place to place on the body. Dispersed... 

The outermost layer of the skin appearing in the exploded epidermal sketch of Fig. 1(b) represents the stratum corneum (the horny layer). The principal barrier element of the skin, it is an essentially meta-bolically inactive tissue comprised of acutely flattened, stacked, hexagonal cell building blocks formed from once-living cells. These cellular building blocks are... 

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