Among topical anti acne preparations benzoyl peroxide is the most well known, regarded an effective vehicle for inflammatory acne treatment which targets prominently bacterial colonization. Bacteria that normally live on the skin, cutibacterium acnes and staphylococcus epidermidis, also play a role in acne development. The bacteria known as Cutibacterium acnes, C.acnes, are responsible for causing acne through affecting multiple factors including lipogenesis which occurs in sebaceous glands. Staphylococcus aureus and anaerobes may get secondarily involved. However, all follicular micro-organisms may, under appropriate highly local conditions, increase or prolong the pathological state in a specific follicle. These bacteria produce substances that cause inflammation,which, in turn, makes efficacy of topical preparations such benzoyl peroxide for acne more challenging. They also make enzymes, which dissolve the sebum (oil from oil glands in the skin) into irritating substances. These substances also make the inflammation worse. Among topical acne treatment only a few show evident antibacterial effect. Benzoyl peroxide for acne also have been approved as an adjunct to oral antibiotics in new treatment paradigm for acne in patients with moderate to severe disease. A randomized double blind controlled study advocated clinical efficacy of a combination of adapalene and benzoyl peroxide in treatment of inflammatory acne which provides with substantiation the idea of multiple-agent approach to moderate to severe acne.
Homage to skin’s microbiome increasingly gain more grounds in medical community with focus on acne vulgaris. The physiological interactions between commensal bacteria and the skin has been subject of number of recent studies. The conventional view of C.acnes colonization as the main culprit in acne vulgaris has been undergoing harsh criticism and substituted by the idea that dysbiosis in skin’s microbiom is a trigger for inflammation and subsequent events. More research is called for to conceive the symbiotic and antagonistic dialogue between C. acnes and S. epdiermidis and indiscriminate eradication of skin’s microbiome using topical or systemic antibiotics may be cleaved to caution. Such dynamics are growing pivotal in that how immune compliance to bacterial colonization occurs and what elucidate inflammation when bacterial overgrowth does not utterly occur. For instance, hypoxia in occluded follicle alters C. acnes metabolites to short fatty acids, a milieu more amenable to propel TLR-2 receptors to initiate an inflammatory response by IL-6, IL-8 and TNF-alpha.
This antibacterial element was probably the first proven effective treatment for skin breakouts, acne and comedones. Free-radical oxygen is released upon administration and oxidizes bacterial proteins in sebaceous follicles, decreasing the quantity of irritating free fatty acids and of anaerobic bacteria. It also has keratolytic and comedolytic effects. Use of benzoyl peroxide for acne seems to be most effective for inflammation. The arising question is whether generated radical oxygen species, ROS, with use of this agent would deleteriously affect skin cells? This idea hypothesizes concurrent use of anti oxidants in any skin care which employs benzoyl peroxide to combat bacterial colonization axis of acne vulgaris to attenuate cytotoxicity and skin’s damage associated with use of this modality.
The idea of viewing epidermis as a live organ with changing dynamism rather than dead corneocytes has been more widely prevailing in scientific community over the past few years which enunciates constant regulation and transformation of lipid composition of the skin not only by keratinocytes and sebocytes yet by skin’s microbiome and its commensalism. C. acnes can produce short chain fatty acids from glycerol in anearboic condition such as what happens with occluded folicle in acne to fight inflammation and their ferocity against pathogens changes directly with a shorter length of the fatty acid. Likewise, S. epidermidis lowers pH of the skin lipids and maintain an acidic milieu around the corneocytes. Sphingosines are another group of lipids whose depletion correlates well with colonization of S. aureus. The existence of ceaseless dealings between skin’s lipids and its bacteria may pervade all future research and spawn development of novel means to control acne vulgaris, this more comes to light once antibacterial agents such as benzoyl peroxide for acne treatment are reckoned.
The action of benzoyl peroxide on sebum excretion is questionable. It has been shown that it reduces sebum synthesis. Benzoyl peroxide for acne has been employed with a dramatic effect on cutaneous bacteria, reducing by 2 log cylcles the number of skin surface Propionibacterium acnes and Staphylococcus epidermidis so that it must be counted as first line modality in acne treatment and may be used in mild to moderate forms of acne, while its adjunctive use has been leveraged in severe acne treatment in association with oral agents to abridge likelihood of bacterial resistance. One study on ductal bacteria confirms that benzoyl peroxide reduces colonization in the duct. This property renders Benzoyl Peroxide for acne an effective topical modality. Benzoyl peroxide also may have an anti-inflammatory effect since a reduction in number and size of inflamed lesions is observed early in treatment. Treatment of acne with benzoyl peroxide with adapalen or other agents has been suggested by several studies. Benzoyl peroxide is also been suggested for treatment of mild rosacea.
Skin irritations and mild dermatitis may be seen. Dryness and scaly skin are not uncommon. Benzoyl peroxide for acne is associated with skin irritation and may cause contact dermatitis in certain individuals and its concentration and mode of of preparation also play a significant role in its harshness once the final product is applied to the skin. So skin irritation could vary from one product to another with the same concentration of benzoyl peroxide.
Incubation of the skin bacteria P.acnes, staphylococcus aureus and staphylococcus epidermidis with lauric acid (C12:0), found abundantly in palm oil, yielded minimal inhibitory concentration (MIC) values against the bacterial growth over 15 times lower than those of benzoyl peroxide. The lower MIC values of lauric acid indicate stronger antimicrobial properties than that of benzoyl peroxide. Lauric acid is among the skin surface lipids, byproduct of cleavage of sebaceous triglycerides and also found naturally as a free fatty acid of sebum. While lauric acid is mainly active against gram positive bacteria, sphingosine and dihydrosphingosine, found in stratum corneum, liberated from ceramides by action of ceramidase, antibacterial effect spans a wider range, gram positive as well as gram negatives.
While benzoyl peroxide is notorious for its bactericidal impact, its stimulating effect on fibroblasts which leads to more production of oxygen free radicals enchant curious minds. Triggered fibroblasts by benzoyl peroxides shore up more proliferation of fibroblasts and help with wound healing and prevention of acne scars. Another aspect of this picture is inflammation itself that is the initial mechanism in wound healing and once protracted scar tissue evidenced by lack of fetal scar tissue without inflammation.
There are three major therapeutic goals for acne which are forcibly addressed in evidence-based skin care: Resolve existing acne, prevent scarring, and suppress the development of new clinical lesions by treating and preventing the development of subclinical microcomedones. Our skin care is aimed at these objectives. Benzoyl peroxide, alpha and beta hydroxy acids, and azelaic acid are appropriate therapeutic options for use in maintenance therapy. Those agents that demonstrate the best cutaneous tolerability, are easily integrated into patients’ lifestyles, and are associated with potential therapeutic dividends such as “skin-repairing” effects offer the highest potential for patient adherence. Despite well-recognized role of propionibacterium acnes in pathogenesis of acne, non-antibiotic treatments in maintenance and suppression of non-inflammatory comedones becomes widely acceptable. It is of note that inflammation is intrinsic to the course of an acne lesion and it unrelentingly exists in all stages of acne vulgaris.
This treatment kit, an skin care regimen which has been bioengineered to respond to the four causes responsible in development of acne and substantially based on plant-derived and herbal treatments. Increased sebum excretion is controlled during the day by “Day Effect”, an element of our acne kit, and overnights by the treatment serum. Depletion of essential fatty acids (linolenic acid) is associated with sebaceous gland hypertrophy and hyperkeratinizaton of the ducts, two features relevant to acne even cystic lesions. “Day Effect” and Acne serum by providing the skin with essential fatty acids regulate sebum excretion. This regulating cream also targets bacterial colonization. “One-Step Cleanser and Toner” is an aimed polyphenol-rich vehicle toward bacterial colonization in acne.
“Day Effect”, sebum regulator, keeps fighting bacterial colonization during the daily activities while controls skin’s secretions concurrent with moisturization. Acne inflammation which is far greater in cystic form, is controlled by extracts and essential oils of Chamomile, Lavender Sage, Licorice root and Green tea present in these serums such as treatment serum, “Day Effect” and “One-Step Cleanser and Toner”. Bioflavanoids, Green tea extract and alpha lipoic acid help to mitigate stratum corneum changes as a result of depletion of its antioxidants