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

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

View on the Cause of Acne is Changing

Ongoing 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 being agents able to interrupt the natural cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Interruption of emission of sebum to the surface of skin leads to obstruction 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 injury or infection which give rise to intracellular signals which promote cell motion, and cytokines (cell-secreted proteins that modify the expression of growth factors as well as migration of leukocytes to a damaged site and fibroblast proliferation), seem to act as mediators for the initiation of acne lesions. Propionibacterium acnes is not originally related but can 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 can also have a much stronger response to external stimuli, and that depends vaguely on hereditary 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 load of sebum through the previously empty duct might create forces of enough magnitude that damage the pilosebaceous gland. The body reacts with the production of inflammatory molecules to promote 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 blocks the continued flow of sebum. On exposure to oxygen, the comedone turns dark originating what is usually referred to as a black head. The water content of the comedone is eliminated by evaporation and diffusion into the adjacent horny layer (keratin) of the upper epidermis leading to a hardening of the comedone, starting at the external surface. The comedone can become attached to the keratin and thus "moored" to nearby elements of the skin. The comedone becomes changed chemically, as well as physically, thus becoming an element which is strange to the body. This state of "foreignness" provokes a further inflammatory response, including immune reactions and other responses of several defense systems, particularly those associated with granulocytes and macrophages.

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