The hair follicle and sebaceous glands continually undergo dynamic remodelling in a cyclical manner involving tightly coordinated sequences of cell proliferation, differentiation and death of cells. Sebaceous glands are clustered by the side of a hair follicle, into which they discharge their secretion - sebum.

Their short duct is lined by stratified squamous epithelium. Sebum is created by the total breakdown of the cells and may lubricate the hair shaft, shield the skin from drying and moisture, and avoid microbial infection.

View on the Cause of Acne is Changing

Modern research is changing the classical view of acne as caused by Propionibacterium acnes bacteria to an approach of acne as an inflammatory disorder. In this view androgens, regulatory neuropeptides, hormone receptors, and environmental factors are portrayed as factors able to interfere with the biological cyclical dynamic breakdown of devitalized cells into sebum inside the sebaceous follicles. Interruption of discharge of sebum to the surface of skin leads to obstruction of the ducts (microcomedones) and then enlarged comedones that become inflammatory lesions.

The acne inflammation goes through certain stages. Pro-inflammatory lipids, chemokines (molecules released by cells at the site of injury or infection which originate intracellular signals which stimulate cell motion, and cytokines (cell-secreted proteins that modify 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 appearance of acne lesions. Propionibacterium acnes is not originally involved but may mediate later inflammatory episodes leading to worsening of the lesions.

Immune System Affects Acne

Acne usually appears in people whose skin has suffered a variation in its natural immunity. Some people have higher levels of constitutive, natural immunity in the skin and some may also have a much powerful response to external stimuli, and that depends vaguely on genetic factors related to excess androgen activity in puberty, that trigger sterile inflammatory phenomena.

Acne is initiated by an inflammatory signal to the neural system without involvement of bacteria in its initiation. During puberty sebum secretion is exacerbated and the first flow of sebum through the previously empty duct can originate forces of enough magnitude that damage the pilosebaceous gland. The body responds with the production of inflammatory molecules to stimulate cell division and quickly recover the lining of the inner surface of the ducts.

Causes of Acne Lesions

At the same time, the sebum in the distal orifice of the sebaceous gland duct and/or the hair follicle leads to the creation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On exposure to oxygen, the comedone turns dark originating what is commonly referred to as a black head. The water content of the comedone is eliminated by evaporation and osmosis into the adjacent horny layer (keratin) of the surface epidermis leading to a hardening of the comedone, starting at the external surface. The comedone may become attached to the keratin and thus "moored" to adjacent elements of the skin. The comedone becomes changed chemically, as well as physically, thus becoming an element which is foreign to the body. This status of "foreignness" provokes a further inflammatory response, including immune activities and other responses of several defense systems, specially those associated with granulocytes and macrophages.

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