The Inflammatory Cause of Acne
The hair follicle and sebaceous glands regularly undergo dynamic remodelling in a cyclical way involving tightly coordinated patterns of cell multiplication, differentiation and death of cells. Sebaceous glands are clustered near a hair follicle, into which they discharge their secretion - sebum.
Their short duct is lined by stratified squamous epithelium. Sebum is formed by the total breakdown of the cells and may lubricate the hair shaft, shield the skin from drying and moisture, and prevent bacterial infection.
View on the Cause of Acne is Changing
Modern research is modifying the old view of acne as caused by Propionibacterium acnes bacteria to an approach of acne as an inflammatory condition. In this view regulatory neuropeptides, androgens, hormone receptors, and environmental factors are portrayed as factors able to interfere with the biological cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Blockage of emission of sebum to the surface of skin leads to occlusion of the ducts (microcomedones) and then bigger comedones that become inflammatory lesions.
The acne inflammation goes through certain stages. Pro-inflammatory lipids, chemokines (substances produced by cells at the site of damage or infection which give rise to intracellular signals which promote cell motion, and cytokines (cell-produced proteins that affect the expression of growth factors as well as migration of white blood cells to an injured site and fibroblast proliferation), seem to work as promoters for the initiation of acne lesions. Propionibacterium acnes is not originally involved but may mediate later inflammatory events leading to worsening of the lesions.
Immune System Affects Acne
Variation in the innate immunity of the skin predisposes to acne breakouts. Some people have higher levels of constitutive, innate immunity in the skin and some may also have a much stronger response to external stimuli, and that depends indirectly on genetic factors related to excess androgen activity in puberty, that cause sterile inflammatory phenomena.
Bacteria does not initiate acne; the real cause is an inflammatory signal to the neural system. During puberty sebum secretion is exacerbated and the first flow of sebum through the previously empty duct might originate forces of sufficient magnitude that damage the pilosebaceous gland. The body responds with the production of inflammatory molecules to promote cell division and quickly recover the lining of the inner surface of the ducts.
At the same time, the sebum in the external orifice of the sebaceous gland duct and/or the hair follicle leads to the formation of a dry "plug" (comedone) which blocks the continued flow of sebum. On exposure to oxygen, the comedone turns dark forming what is usually known as a black head. The aqueous content of the comedone is eliminated by evaporation and diffusion into the adjacent horny layer (keratin) of the surface epidermis leading to a hardening of the comedone, starting at the upper surface. The comedone may become attached to the keratin and thus "moored" to adjacent elements of the skin. The comedone becomes modified chemically, as well as physically, thus becoming a material which is strange to the body. This status of "foreignness" initiates a further inflammatory reaction, including immune reactions and other responses of various defense systems, specially those related to granulocytes and macrophages.
You can now clear acne and remove the related scars with topical application of an all natural treatment for acne lesions. When treating the acne inflammation, this natural acne product works with your body without bieffects.
Published November 20th, 2007