Keloidal Wound Healing Model
This model is a combination of scientific research and clinical results taken from actual scar management cases. It is believed that from a keloidal model a more general and comprehensive wound healing model can be developed. Discussions of keloidal wound healing model can cover not only more serious chronic wound phenomena such as deep burns, skin graphing and decubitus ulcers, but also cosmetic concerns such as hyper and hypo-pigmentation, stretch marks, atrophic, acne scarring and wrinkles. The ultimate goal for ReJuveness scar management protocols is scarless wound repair using safe, inexpensive and noninvasive products.
Healing of skin is a deceptively complex process that involves multiple interactions of intercellular cascades, intercellular signaling with growth factors, injury signals and other cytokines, extracellular matrix dynamics, as well as the proliferation, migration and differentiation of numerous cell types. Problematic healing sequelae seen in keloid and hypertrophic scarring is a daunting problem, both as a basic science issue as well as a clinical entity. Although there are significant gaps in our understanding of the mechanisms involved, keloidal scarring once thought of as a post scarring proliferation disorder is now being understood as chronic wound or incomplete or dormant healing phenomena.
Keloids are fibro-proliferative disorders which seem to remain in the early stages of wound healing. Early stage wound healing symptoms such as redness, itchiness, swelling are coupled with increased Trans Epidermal Water Loss (TEWL that is four times higher than normal scars and skin) as well as quadrupled squamation or stratum corneum turn over rates and a four fold increase in electric conductivity in the area covering keloiding when compared to normal scars, atrophic scras and skin. On the cellular level keloid patho-physiology could be characterized by predominance of adhesive activity with a fourfold increase in the rate of fibronectin biosynthesis. High thrombospondin-1 levels associated with imbalanced urokinase plasminogin levels and high TGF-B1. There are many other interesting abnormal cellular events in keloids which at times have a tendency to confuse and defy understanding. The particular keloid model being presented here will concentrate on the surface cell receptor called CD36 and first it multilegand function rafting cholesterol and ceramides from the dermis to the epidermis and the lamellar bodies in order to remodel and reestablish a new healthy functioning stratum corneum. The second function of CD36 to be discussed will be of its analogue SRB1 (scavenger receptor beta 1) in the natural defense of malaria. The correlation between the proclivity of keloid formers to have actual presence, familial or genetic origins in tropical areas of the world and the action of silicone sheeting on keloids to raise CD 36 presence proposes a whole new mechanism of action of the positive effects of silicone sheeting on keloids and hypertrophic scars. The fifty year old mystery of how silicone sheeting reverses keloids can then be applied to a general theory of wound healing. This then raises questions of the positive effects of silicone sheeting on the wide range of skin concerns from chronic hard to heal wounds such as deep burns and decubitus ulcers to superficial scars, stretch marks, hypopigmentation, and stretch marks.
Another component and by no means least to be discussed is the irregular distribution of lipids and fats in keloids and as well as the migration of calcium as a major signal transducer in wound healing. Here the balance between collagen and collagenase will be covered.