The skin is constantly exposed to DNA-damaging environmental perturbations and requires
biological mechanisms to protect against and repair the damages:
Increasing of epidermal layers.
DNA-cell repair mechanisms and apoptosis.
Antioxidant and enzymatic protection.
Melanin production stimulation.
The photodamages induced by UVRays are signals that increase melanogenesis. An excess of Reactive Oxygen Species, such as Superoxide anion, stimulates melanocytes metabolism.
1. PIH, post inflammatory hyperpigmentations
Inflammation plays a main role in induced hyperpigmentations:
- Even the most common cause of hyperpigmentation: sunlight exposure of skin, is more likely a postinflammatory response to UV damage to skin (Gilchrest et al., 1998; Abdel-Malek and Kadekaro, 2006).
- This results through several mechanisms. Among them is direct stimulation of melanocytes by inflammatory mediators such as IL-1-α, endothelin-1, and/or stem cell factor (Sriwiriyanont et al., 2006).
These cells are often retained in the upper dermis . Thus, PIH can be a very long-lived problem for the skin.
2. Actinic lentigos
Melasma is often attributed to UVR exposure, pregnancy, oral contraceptives, deseases, some cosmetic formulations.
Regenerativ protocols associated to dermatological treatments.
- Interfering with the pathways that synthesize melanin.
- Powerful Antioxydant action, to interfer with Anion Superoxide.
- Decreasing the melanine transfer to the top most layers of the skin.
Significant improvement of the pigmentation.
PROTOCOL IN INTEGRATIVE
BEFORE and AFTER
new approch in Melasma treatment
- Hight Protection from oxydative stress, control of melanogenesis.
Many international studies have demonstrated the efficacy of topical treatment with Tranexamic acid, on melasma.The results indicate that TA inhibits melanin synthesis not by acting directly on melanocytes, but by inhibiting melanogenesis activators.
Tranexamic Acid appears to be as effective as topical hydroquinone.
RED LIGHT 633NM IN