Liposkin® Cream

Today's understanding of the pathogenesis of acne is constantly evolving. However, the identified key pathogens include follicular hyperkeratinization, microbial colonization by propionic bacteria, and complex inflammatory mechanisms involving both innate and acquired immunity. In addition, studies have shown that neuroendocrine regulatory mechanisms, diet, genetic and non-genetic factors can all contribute to the multifactorial process of acne pathogenesis.

VITAMIN D IN VULGARIS ACNE
Acne is the most common skin disease and affects up to 80% of adolescents and young adults. Acne can be associated with permanent scarring which has a significant negative effect on the psychology, social relationships and quality of life of acne patients.

The pathogenesis of acne is multifactorial and includes sebaceous gland hyperplasia and hyperpigmentation, Propionibacterium acnes hyperplasia and local inflammation. In addition to the role of P. acnes in acne inflammation, pro-inflammatory cytokines such as interleukin 6 (IL-6) and IL-8 also play a role, while the induction of 5-lipoxygenase and cycloxygenase-2 signaling pathways in sebaceous cells leads to the production of pro-inflammatory lipids. Also, the parent metalloproteinases (matrix metalloproteinases, MMPs, collagenases, gelatinases, stromelysins, matrylicins) are endopeptidases that produced by various cells such as keratinocytes and sebaceous cells, and play a central role in the remodeling of the parent substance during inflammation.

Vitamin D induces the expression of antimicrobial peptides such as catalystin and β-defensin in neutrophils, monocytes and natural killer (NK) cells. Sebaceous cells in vitro express the vitamin D receptor (VDR) and have the necessary enzymes for the synthesis and metabolism of the biologically active metabolite of vitamin D, 1,25-Dihydroxyvitamin D3 (1,25 (OH) 2VitD3), also known as calcitriol. Also, 1,25 (OH) 2VitD3 reduces the lipogenesis of sebaceous cells in vitro, with applications in acne.