Antimicrobial activity against P.acnes of free fatty acids have been demonstrated that lauric acid has the strongest antimicrobial activity compare to that of palmitic acid or oleic acid [23]. Antimicrobial effects of free fatty acids, lauric acid, palmitic acid and oleic acid on P. acnes were compared [23].

Lauric acid one of the typical fatty acids found in the human sebum, shows stronger antimicrobial activity than benzoyl peroxide whle not inducing any cytotoxicity to human sebocytes [24]. However of drawback of lauric acid is its poor water solubility. It requires a solvent such as dimethylsulfoxide (DMSO), which is very irritant to the skin. Incorporation of lauric acid in liposomal form, whichh enhances its absorption, has eliminated us of DMSO [23].

Another category of topical treatments are plant based extracts and oils, namely, Leptospermum scoparium or manuka oil, from the tea tree family yet still a distinct plant with more robust antimicrobial properties. Its main constituents are leptospermone, calamenene, falvesone, cadine-3,5-diene and α-copaene with wide bactericidal and bacteriostatic effects on a range of gram positive, more prominent effect, and gram negative bacteria and fungi, among them, C. acnes (MIC=0.211 and 0.055 reported by two different studies) and S. epidermidis (MIC=1.40) whose dysbiosis recognized in pathogenesis of acne vulgaris.

Cell lysis of staphylococcus aureus with concentration of manuka oil as low as 1.5% have been shown with β-triketone known as the accountable constituent. Other plant oils with antibacterial effect on C. acnes have been studied and reported, thyme with MIC=0.016, cinnamon with MIC=0.016, and rose with MIC=0.016 are among the most notables. Certain amalgamations of essential oils demonstrated synergism and vigor to pulverize pathological microorganisms with propitious safety profiles and encouraging applicability to attenuate acne.

Marine extracts from kelp and algae have been novel focus of several studies for their polemic antimicrobial properties, albeit their bioactives against C. acnes and S. epidermidis appears as provably substantial avail. Among the plethora, fucofureckol-A from the kelp Eisenia bicyclis was found to be most remarkable with MIC of 32-128 μg/ml and in combination with erythromycin significantly reduced to 1μg/ml. On the other hand, glycolipids of marine algae, as cardinal element, were demonstrated with antioxidant and antimicrobial traits with two major biogenic groups of neutral galactolipids and sulfolipids. Galactolipids of brown algae Fucus evanescens was discovered accountable for inhibitory efficiency against C. acnes with MIC of 50μg/ml with montogalactosyldiacylglycerol as effectual compound.

Topical timolol has been subject of some late studies in an effort to broaden the acne treatment armamentarium  for its vasoconstricive, antiangiogenic and anti inflammatory effect while precedent research did not add up to a supportive pattern for  propronolol. Timolol, a not selective β-blocker demonstrates inhibitory impact on matrix mataloproteinases, MMP-2, MMP-9 and IL-6 while carrying a more favorable safety profile. A study of 114 patients of acne vulgaris and rosacea with no control cohort for eight weeks has shown efficacy of timolol in control of acne and rosacea, largely, due to its reach in thwarting inflammation and vasoconstriction-led decrease in sebum production.

Tretinoin is another topical modality that could be used to treat acne vulgaris. This derivative of Vitamin A is keratolytic and may cause a form of dermatitis called retinoid dermatitis. It could be combined with antibiotic to address other etiologies involved in formation of acne lesions. One of these combinations is tretinoin-clindamycin that one study indicates its increased efficacy. Another retinoid combination is with benzoyl peroxide that one study suggests its efficacy [25]. New retinoids(adapalene) have shown to have anti-inflammatory effects which aims to another mechanism in development of acne, inflammation (increase in IL-1 and TNF). This reserves use of retinoids in management of inflammatory lesions as well as previously-explained non inflammatory acne.

Oral Treatment:

Isotretinoin is among oral medications used in severe cases of acne through concurrent reduction in hyperkeratinization and associated inflammation [26]. Isotretinoin has a profound impact on sebaceous gland size and function, thereby decreasing serum level of more active androgens [27]. The marked sebostatic effect of isotretinoin may not be be the sole explanation for its mechanism of action [28]. Retin-A tretinoin (topical form of isotretinoin) is among acne modalities to get rid of breakouts especially when other forms of therapy has failed. Tretinoin is a prescribed drug and an skin irritant particularly in liquid form with extensive adverse effect profile. Cold climates and exposure to sunlight cause marked irritation. Retin-A (tretinoin) precipitates antikeratinization and prevents formation of the comedones.

Among topical retinoids, adapalene, a more receptor-selective retinoid, shows the best tolerability/safety profile followed by isotretinoin and tretinoin [29]. Retin-A differs from benzoyl peroxide and topical antibiotics in having no or a controversial effect on Porpionibacterium.acnes and causing no direct effect in surface free fatty acids. Tretinoin seems compelling against microcomedones (a blackhead) compare with other treatment modalities provides a rationale for its use in most forms of acne. This agent is particularly helpful in reducing non-inflamed lesions and comedones thereby indirectly reduces the number of inflamed blemishes by correcting the follicular hyperkeratosis.

This drug is a powerful exfoliant and can cause tenderness, redness and scaling. Antibiotics may be used in moderate to severe cases of acne. Tetracyclin, Erythromycin and Clindamycin are more commonly used. Their potential side effects and development of resistance discourage their use for long term and renders them not a proper choice in acne maintenance therapy [30]. Use of medicinal plants and herbal preparation have been widely exercised in topical treatments or in and oily skin care no significant avail as in most cases outcomes not measured and treatments not standardized.

Hormonal antiandrogen modalities the androgen-metabolizing cells of pilosebaceous unit, i. e. follicular kertinocytes and sebocytes, with a reduction of the sebum secretion rate of 12.5 to 65% [31]. Prescription of hormonal antiandrogen acne medications is limited to female patients who present additional signs of peripheral hyperandrogenism or hyperandrogenemia. In addition, females with acne tarda, persistent acne recalcitrant to treatment, parallel with contraception as a requirement for a systemic isotretinoin treatment, can be treated with hormonal antiandrogens [31].

Treatment guidlines and a note of precaution in pediatric population


Topical and systemic antibiotics have been the mainstay of acne management protocol for over 50 years. Incidence of antibiotic resistance in acne has continued to rise across the globe from 20% in 1978 to 72.5% in 1995 [32]. Antibiotic resistance in acne represents a significant international public health concern because resistance can occur in more pathogenic bacteria than P. acnes, and an increase in pathogenic P. acnes has been reported [33]. Emerging antibiotics resistance of P. acnes is a ground for attention and a reminder of a need to modify the current acne guidelines [34]. Furthermore acne vulgaris is not primarily a bacterial infection and other pathological factors, if not more significant, appear to be equally substantial. Thus, treatment with modalities which address pathologies other than bacterial side of acne pathology are more gravely called for.

Products that may cause irritation are widely used for control of acne with the potential to reduce treatment adherence [35]. Topical retinoids often cause severe local irritation called retinoid dermatitis [36]. Cytotoxicity associated with tretinoin and benzoyl peroxide [37] demand a new therapeutic approach, in particular a different regimen as maintenance treatment. New modalities with safer side effect profile seem to be more promising in maintenance and may require incorporation into therapeutic guidelines.

A note on Acne severity

It is of note that global grading system and lesion (papule, pustule, comedone) counts are equally reproducible methods of grading inflammatory acne which significantly contributes to follow up of any regimen to control comedones[38].

Mild form: Comedones, whiteheads and blackheads, few papules or pustules seen. An open comedone is defined as a non-inflamed follicular opening containing a keratotic plug that appear black, a blackhead [39]. The closed comedone, whitehead, contains less compact keratinous material and has a narrow follicular orifice [40]. Topical agents are indicated only. Benzoyl peroxide, topical clindamycin, topical erythromycin, or a combination [41] could be used.

Moderate acne: Papules and pustules frequently seen, One nodule may be occasionally found. Topical as well as systemic agents, if no response withing eight weeks, may be started. Topical tretinoin or adapalene, systemic tetracyclin are most frequently used.

Severe: Nodules and cysts commonly found. Even presence of a few of these type categorized as severe. Presence of cysts requires treatment with systemic agents such as isotretinoin (first line) or anti-androgenic agents even though some more recent studies suggest a trial of topical treatments. Scarring can be counted as severe acne.

(a), skin affected by P. acnes


(b), skin affected by P. acnes after application of lauric acid


Effect of lauric acid against Propionicbacterium. acnes has been demonstrated. See resolution of inflammation on the right after injection of lauric acid into the skin. On the left the skin is not treated with lauric acid [24].

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