XII November 2017 N 8 SKIN WHITENING Maurizio Ceccarelli & Coll. Protocol for skin pigmentation treatment. The skin responds to injury by increasing the thickness of the stratum corneum and pigmenting. The damage activates p53, which results in the production of pro-opiomelanocortin by the keratinocytes. The POMC is fragmented into smaller peptides. One of these is MSH. The MSH acts on the specific receptor of the melanocyte. This leads to a cellular response with DNA reading relating to the synthesis of tyrosinase. The enzyme is synthesized in an inactive form.
Once released, the tyrosinase protein must acquire a spatial arrangement that makes it active in its enzymatic role. To allow this, the protein must be bound to a sugar with a glycation process. Once activated, tyrosine converts the amino acid tyrosine into melanin. Dark melanin (eumelanine) and red melanin (feomelanine) are synthesized. In particular, tyrosinase is liberated from the Golgi Reticulum, within particular structures, melanosomes. These begin their migration into the cell while synthesize, inside them, melanins. The movement, active process along the cytoskeletal proteins, allows melanosomes to move, inside the cell towards the periphery of this, along the dendrites.
Arriving at the end of the dendrites, the melanosomes pass, for an active process, in keratinocytes. This tells us that, normally, melanin produced is eliminated through regular epidermal exfoliation. But if the damage is particularly important, the spread of melanin occurs not only in the epidermic but also in the dermis. In this case, it can not be eliminated naturally and must be removed. Let's see now how to treat melanin accumulation. Today, we infiltrate melanin accumulation with a 300 mg solution of Ascorbic Acid, mixed with 1 ml of Lidocaine. It infiltrates below the accumulation, very superficially.
Ascorbic acid, as a reducing agent, transforms dark melanin (oxidized) into light melanin (reduced) by clarifying pigmentation. Additionally, ascorbic acid enters the cellular antioxidant system by reducing the damage from free radicals of oxygen. Ascorbic acid also acts as a slowing action in melanogenesis, reducing the function of tyrosinase. As said, infiltration is carried out very superficially under the pigmentation. We carry two sessions, spaced one week apart. Then wait for a month, the result will occur and, if necessary, repeat the treatment.
We treat both the local accumulation of melanin, and the skin color of the high phototypes. For dark skin, the treatment is performed every two weeks, forever (pigmentation is genetic). The protocol also reduces possible pigmentation following traumatic treatments such as the use of Plexer, Laser, Radiofrequency, Peeling. We know that when we do a trauma on the skin we induce an inflammatory response. The inflammatory response results in a new stimulation of melanogenesis.
More phototype is high and most important is the melanic reaction to injury and, therefore, the risk of a negative response to traumatic treatment. Indeed, in predisposed subjects, a treatment performed to eliminate a melanic deposit may induce a new pigmentation response worse than the initial one. Inflammatory response induces the induction of a new melanogenesis. Indeed, the damaged keratinocyte liberates plasminogen which becomes plasmin. Plasmine activates phospholipase and cascade of ecosyanoids, with inflammation.
Post Traumatic Skin Treatment prevents pigmentation that can result in traumatic skin treatment. The protocol provides the block of inflammation, induced by the treatment, using tranexamic acid, which blocks the activity of plasmin. We apply on the area a mix formed by a vial of tranexamic acid and the Aeglexa Night cream containing active ingredients that reduce the degree of injury. The damage induces release of ROS and inflammatory cytokines. The Aeglexa line as a strength Astaxanthin, the most potent scavenger of ROS currently on the market, blocking the start of the damage.
Contains Laminaria Ocroleuca that blocks inflammatory cytokines released from keratinocyte damage. It contains Macrocistis Pyrifera and Sanguisorba officinalis capable of blocking the action of the metal proteinase site activated that destroy the skin matrix. We discharge the patient prescribing at the morning, sun block to avoid the stimulus pigmentary of sunlight. And in the evening, the Aeglexa Night Cream that allows you to act on the various stages of melanogenesis in order to slow down the pigmentation response. The Aeglexa Night Cream contains active ingredients useful to slow down the pigmentation due to inflammatory damage.
Madecassic acid that reduces inflammation. Enoyl-phenylalanine which is an antagonist of MSH receptor. The receptor block prevents melanocyte activation and melanin formation. Acetylglucosamine which inhibits the glycation process necessary for the functional activation of tyrosinase. Dimethylmethoxy-chromanyl-palmitate, arctostphylos uva ursi leaf and azeloyl diglycinatel that act directly inhibiting the activity of tyrosinase. Niacinamide acts by slowing the movement of melanosomes to the periphery of melanocytes.
Aeglexa Night also contains active ingredients that help to repair the damage caused by the treatment Astaxanthin, a powerful ROS scavenger, maintains the FOXO3 function needed to resist the cell and keep it alive. Acetylglucosamine, as the precursor of hyaluronic acid. Proline, which is the precursor of collagen. Ceramides and Cholesterol, as precursors of the cell wall.
Recently new substances have been proposed for the treatment of hyperpigmentation. We see the Function of Succinic Acid. This substance acts on the slowing down of the melanogenesis process starting with the damage from ROS. It works by reducing the action of ROS directly. And indirectly, increasing the function of cell antioxidants (Superoxydodismutase, Glutathione Peroxidase and Catalase).
Succinic acid, such as acid, has a reducing action. This function allows to slow down the early stages of melanogenesis by reducing the oxygen function. The function of tyrosinase is also reduced by the chelation of copper, the active site metal. The chemical process of chelation allows to sequester a metal, by blocking the enzymatic function. Succinic acid, dicarboxylic acid, chelates copper by blocking the function of tyrosinase.
Dark melanin can be turned into light melanin with whitening of the skin. This can be achieved by reducing the oxidized (dark) melanin in reduced (clear) melanin with succinic acid. Tranexamic acid acts on postinflammatory hyperpigmentations. Inflammatory response induces the induction of a new melanogenesis. The damage determines the release of plasminogen from keratinocytes.
The plasminogen, transformed into plasmin, free arachidonic acid activating the inflammatory cascade. Tranexamic acid blocking the site of plasminogen lysine, avoids the formation of plasmin and the activation of the inflammatory process. The action of tranexamic acid is dosedependent. Concentrations between 1 and 5 mmol should be used. Succinic acid and tranexamic acid are included in the Whitening protocol for the spotd, for the genetically dark skin and for ano-vaginal bleaching. We prepare the bleaching solution by mixing 0.5 ml of ascorbic acid with 0.5 ml of succinic acid and 0.5 ml of lidocaine.
After injectable treatment, apply a decongestant mask for 15 minutes. Removed the mask, apply on the area a mix formed by tranexamic acid and Aeglexa Day Cream. We repeat the treatment once a month. We continue the treatment with a lightening peeling. Applying it once a week.
Between one session and the other, the patient uses, in the evening, Aeglexa Night Cream. Cream is applied every night. The protocol is also used in aesthetic gynecology for ano-vaginal bleaching. Pigmentation of the genital area has a function of protecting the area on a genetic basis. This means that the melanin is continuously produced independently of external stimuli. The treatment must be done in a continuous manner.
We clarify the dark melanin using the reducing action of ascorbic acid and succinic acid. Combine the treatment with the slowing down of melanin formation process. Practically, initially we perform the treatment injective accompanying it, then, with the topical treatment. We anesthetize the part to be treated with an anesthetic cream. Or, better, with the systemic use of Nitrogen Protoxide.
We use a bleaching solution with 0.5 ml of ascorbic acid, 0.5 ml of succinic acid and 0.5 ml of lidocaine. Injectable treatment with acid drugs causes an inflammatory response with subsequent hyperpigmentation. To slow this unwanted reaction we use tranexamic acid. After injectable treatment, apply a decongestant mask for 15 minutes. Removed the mask, apply on the area a mix formed by tranexamic acid and Aeglexa Day Cream.
The treatment is repeated once a month. We continue the treatment with a lightening peeling. Applying it once a week. Between one session and the other, the patient uses, in the evening, Aeglexa Night Cream.