Epidermis regeneration

Although the epidermis regenerates readily over an intact or partly intact dermal bed, it is well-known that de novo synthesis of the dermis does not occur spontaneously [65, 66], Likewise, even though the rat sciatic nerve is regenerated spontaneously across a 5-mm gap or occasionally across a 10-mm gap (provided that the cut ends of the nerve are inserted in a saline-filled rubber tube), no such regeneration is spontaneously observed across a 15-mm gap [67,68]. The appropriate use of collagen-GAG matrices leads to synthesis both of skin, complete with dermis and epidermis [79, 80, 84] and of new sciatic nerve [83]. It is this ability to induce de novo synthesis of nearly physiological tissue... 

The post-peel mask cream contains retinol microencapsulated in a cyclodextrin. Vitamin A is involved in the processes of cell division and differentiation that help the epidermis regenerate after the peel from the cells of the basal layer. 

The product should only be applied to the face. There is a large number of pilosebaceous units here that help the epidermis regenerate properly. 

Epidermis Regeneration Cellular proliferation No scar Superficial wounds... 

Epidermis The cellular outer layer of skin, about 0.1 mm thick, which protects against moisture loss and infection. An epidermal graft, for example, cultured epithelium or a thin graft removed surgically, requires a dermal substrate for adherence onto the wound bed. The epidermis regenerates spontaneously following injury, provided there is a dermal substrate underneath. 

Due to the relative ease of oxidation of the parent compound, common delivery forms in cosmetic formulations and clinical trials are vitamin E acetate (a-TAc, structure in Fig. 15.7a) and vitamin E phosphate. These forms are expected to permeate and to regenerate free active a-TH through enzyme-catalyzed hydrolysis activities in skin. Although a-TAc is readily hydrolyzed by esterase action to vitamin E upon oral ingestion, no consensus as to the extent of bioconversion of topically applied a-TAc has been reached. Two published studies demonstrate bioconversion up to 10-15% in the viable epidermis [35] including the basal layer [36]. These and other studies show no detectable metabolism of a-TAc in stratum corneum [37]. 

It must be stressed that the primary mechanism of many topical irritants (e.g., organic solvents, corrosives) is the impairment to the stratum corneum barrier properties discussed earlier. If the stratum corneum barrier is perturbed, a feedback response may be initiated whereby regeneration of the barrier occurs. This reaction is mediated by cytokines (especially TNF-a) originating locally within the epidermis. However, additional responses to these inflammatory mediators may in themselves launch an irritation response mediated by the keratinocytes. Thus, regardless of the initiating mechanism, the sequelae to many irritants is the same, making the definition of unique dermal computational toxicology models difficult. 

A chemical peel is a skin treatment intended to visibly improve the structure of treated tissue by the external application of a caustic solution. It can simply accelerate the natural processes of exfoliation, but can also completely destroy the epidermis and a more or less large proportion of the dermis, essentially by protein coagulation or lysis. The effect of any peel reaches the dermis, directly or indirectly and to varying depths, where the processes of regeneration are induced to a greater or lesser degree, depending on the molecule or molecules used and the application procedure. 

The basic protocol for ETCA is intended to reach the basal layer of the epidermis or the Grenz zone. There are (many) other deeper protocols but they are not as straightforward as ETCA and the risk of complications is relatively much higher. ETCA is not necessarily a light peel it can be used to reach all depths, from the basal layer of the epidermis to the reticular dermis, depending on the protocol used. The relatively superficial action of the ETCA solution (basic protocol) strongly stimulates the skin regeneration... 

An application of dansyl chloride accumulates in the epidermis and stains the skin. It is possible to measure the rate of disappearance of this coloration after the application of different hydroxy acid solutions at a constant pH. The rate at which the color disappears is correlated with the rate of cell replacement, and therefore provides information on the stimulation of epidermal turnover and on the capacity of the acid to stimulate skin regeneration. TCA (which is not a hydroxy acid), at 0.5%, stimulates skin renewal up to 50%, lactic acid (at 4%, pH 3) stimulates up to 34%, acetic acid (3%, pH 3) up to 30%, and pyruvic acid (4%, pH 3) up to 23%. Partial neutralization of these solutions, to pH 5, quite clearly reduces the rate of renewal, and neutralizing these same solutions to pH 7 takes away all of their clinical effectiveness. 

Chronic use of AHAs seems to allow the dermis and epidermis to thicken gradually and regenerate after an initial period of flaking that, in contrast, thins the epidermis and requires the daily use of effective sun protection. 

Sometimes, all that is needed for the skin on the hands is to rebuild the dermis and epidermis. This type of skin regeneration is perfectly suited to Easy TCA (ETCA) two examples of this treatment are shown in Figures 19.2 and 19.3. 

After a deep peel, the body takes 4-6 weeks" to regenerate a structurally normal skin. During these 6 weeks, the skin appears very red, as the many newly formed blood vessels are showing through an incomplete, thinned and pale epidermis. Six weeks is usually the minimum time that erythema lasts after a phenol peel. After this time, inflammation may persist and the skin can still appear red for several more months. 

The keratinocyte reserves allow rapid and easy regeneration of the epidermis. The retractile myofibroblast system is not stimulated. There is no risk of scarring. 

Skin repair after a peel to the reticular dermis is slower, as all the basal layer keratinocytes have been destroyed and the skin can only rely on the differentiated keratinocytes of the pilosebaceous units and the intradermal excretory ducts of the sweat glands. To repair the dermis, the sebocytes in the pilosebaceous units must dedifferentiate, and horizontal growth is required to close the skin quickly. Next comes a phase of vertical growth whose purpose is to regenerate a physiologically sound epidermis that will maintain homeostasis and restore the vital barrier function after the keratinocytes have differentiated into corneocytes. 

The majority of the skin s immune defenses are found in the deep layers of the epidermis and dermis. An intraepi-dermal peel lets in many xenobiotic microorganisms, but all of the skin s defenses remain viable and usually stop any local infection from developing. After an intraepidermal peel, skin regeneration is very rapid and there is not really enough time for infection to set it. Intraepidermal peels are usually repeated once a week or every 2 weeks. Each intraepidermal peel stimulates the skin s regenerative capacities, and the skin finds it more and more easy to resist infection. Therefore, these peels do not increase the risk of infection (or only very little). The risk of herpes is not increased. 

The drawback to using creams when the epidermis is regenerating is that skin debris builds up and forms a base for the infection underneath the occlusive layer. The... 

It is generally accepted (but not officially specified) that botulinum toxin should be injected at least 1 week before a peel. The obvious advantage of this prior injection is that the toxin blocks muscle movements and allows the dermis and epidermis to regenerate on a smooth base . Eight days after the toxin has been injected, its effect is complete and the peel can be applied without any risk of the toxin being moved or diluted. 

LIVING OR VIABLE EPIDERMIS renewal or regeneration time (rf viable epidermis average time required for a basal cell to reach the stratum corneum... 

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