Two important novelties in etiopathogenesis and therapy of acne

The reclassification from Propionibacterium acnes to Cutibacterium acnes was proposed in 2016. A standardized method to perform molecular typing of C. acnes, according to the degree of resolution needed (phylotypes, clonal complexes, single-locus sequence typing), has been recently suggested. In the first article of this supplement, the authors review the most recent data on C. acnes and its involvement in etiopathogenesis of acne. New findings on C. acnes have revealed that, contrary to what was previously thought, its proliferation is not the trigger of acne. A tight equilibrium between members of the skin flora and C. acnes phylotypes might play a more critical role in acne onset. Loss of microbial diversity can indeed lead to chronic inflammatory skin diseases. In particular, the presence of C. acnes phylotypes in patients with acne and healthy subjects is discussed: some C. acnes strains and unique genomic sequences seem to be associated with acne development and severity. In the same article, a review of the state of the art on virulence factors, the role and importance of biofilms in resistance of C. acnes to antibiotics and the relationships between phylotypes and antibacterial susceptibility are presented. The second article is on Myrtacine activity in acne. Myrtle (Myrtus communis Linnaeus 1753) belongs to the family Myrtaceae. More than 40 different varieties of myrtle are known. It grows in arid grounds, mainly in Sardinia, but also in Spain, Corsica, Greece, Tunisia and Algeria. The liqueur (‘mirto’) obtained from its fruits is famous. Myrtacine is an ethanolic extract of myrtle leaves. It contains 6% A and B myrtucommulones (or acylphloroglucinol), with antibacterial activity, and 15%–20% ursolic acid, with anti-inflammatory activity. An antiproliferative action has also been demonstrated: Myrtacine inhibits keratinocyte proliferation by 27% and 76% at 1 and 3 lg/mL, respectively. At concentrations ranging from 0.0001% to 0.03%, Myrtacine inhibits the proliferation of planktonic and non-planktonic P. acnes strains which are sensitive or resistant to erythromycin. This inhibition occurs at much lower concentrations than with benzoyl peroxide. On P. acnes biofilm, 0.1% Myrtacine has two complementary actions: (i) very rapid inhibitory action on biofilm formation, after 5 h of contact, and (ii) destruction of biofilm, after 1 min of contact. Furthermore, Myrtacine decreases the synthesis of proinflammatory mediators via the cyclooxygenase and lipooxygenase pathways, and the lipase activity. This anti-inflammatory action of Myrtacine was demonstrated by a sponsor-free, multicentre, prospective, randomized, parallel-group study in 164 patients with mild to moderate acne, who previously developed a retinoid dermatitis. One group of patients was treated with 0.2% Myrtacine and 4% nicotinamide (2 applications/day); the second group was treated with a moisturizer (2 applications/day). Patients treated with the Myrtacine /nicotinamide combination showed a statistically significant improvement in symptoms (pruritus, stinging and burning sensation) as well as signs (erythema, dryness and oedema). Good clinical results were observed also in patients with nodular acne. The Myrtacine study published in this supplement to JEADV demonstrates that (i) C. acnes colonization is high, but not significantly different, in both patients with mild to moderate acne and healthy control subjects, and (ii) phylotype IA is predominant in acne patients. In addition, the authors observed that a cream containing Myrtacine induced a decrease in acne severity according to the Global Acne Severity Scale (GEA), a decrease in non-inflammatory and inflammatory lesions, reduced porphyrin synthesis by C. acnes and a significantly reduced load of erythromycin-resistant strains of C. acnes.