Mastic liposome treatment for shiny and impure skin

The water-insoluble oleoresin was made available for skin care application by stabilising it in a liposomal preparation. In this form, mastic inhibits the sebum production enhancing enzyme 5a-reductase type I in vitro. In clinical studies with volunteers suffering from oily skin and impurities it was shown that mastic visibly reduces pore size, shininess and the number of blemishes, which makes mastic an ideal active to treat impure skin. 

It is a common misconception that oily and impure skin is a problem that mostly teenagers have to face. In fact, many adults still struggle with skin impurities, or even suffer from new-onset problems long after puberty,1 which can take a toll on their confidence and emotional wellbeing. One main cause of these impurities is the overproduction of sebum by sebocytes of sebaceous glands situated in the hair follicles, which leads to a general oily appearance of the skin. Furthermore, high sebum production levels are associated with increased pore size.2 Obstruction of the sebaceous duct due to high sebum levels and hyperkeratinisation leads to comedo formation, which can result in a blackhead if the sebum plug is oxidised or a whitehead/microcyst if the whole canal is closed off by skin cells. Such a blockage can trap bacteria inside the duct, which are able to multiply by feeding off the excess sebum. These bacteria can cause inflammation and may lead to pustules and lesions. Greasy skin, comedones and enlarged pores all contribute to an impure appearance of the skin and share excess sebum production as a common cause. 

So what causes increased sebum production in the first place? The main regulator of sebum formation in the sebaceous gland is the hormone dihydrotestosterone (DHT), which is formed through the irreversible reduction of testosterone by the enzyme 5a-reductase.3 There are three isoforms of 5a-reductase (type I, II and III), with 5a-reductase type I being the isoform responsible for sebum production and the major isoform expressed in skin cells, especially in the sebocytes of the sebaceous glands.4 DHT binds to the same androgen receptor as testosterone but it possesses an up to ten times higher receptor binding affinity and potency for transcriptional activation of target genes that lead to sebocyte differentiation and sebum production.5 Therefore, preventing DHT generation by inhibiting 5a-reductase type I results in reduced sebum production and clearer skin.