The hair follicle and sebaceous glands continually undergo dynamic remodelling in a cyclical manner involving tightly coordinated patterns of cell multiplication, differentiation and death of cells. Sebaceous glands are gathered 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 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 disorder. In this view androgens, regulatory neuropeptides, hormone receptors, and environmental factors are portrayed being factors able to interrupt the biological cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Interruption 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 (molecules produced by cells at the site of injury or infection which originate intracellular signals which stimulate cell motion, and cytokines (cell-secreted 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 appearance of acne lesions. Propionibacterium acnes is not initially related but may mediate later inflammatory episodes 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 better levels of constitutive, innate immunity in the skin and some may also have a much powerful reaction to external stimuli, and that depends indirectly on genetic factors related to excess androgen activity in puberty, that trigger 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 load of sebum through the previously empty duct might originate forces of sufficient magnitude that injure the pilosebaceous gland. The body reacts with the release 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 external orifice of the sebaceous gland duct and/or the hair follicle leads to the formation of a dry "plug" (comedone) which obstructs the continued flow of sebum. On contact with oxygen, the comedone turns dark originating what is commonly known as a black head. The aqueous content of the comedone is eliminated by evaporation and osmosis into the adjacent horny layer (keratin) of the upper epidermis resulting in a hardening of the comedone, starting at the upper surface. The comedone may 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 a material which is foreign to the body. This status of "foreignness" provokes a further inflammatory reaction, including immune reactions and other responses of several defense systems, particularly those associated with granulocytes and macrophages.

You can now clear acne and erase the related scars with topical application of an all natural cream for scar tissue. When treating the acne inflammation, this natural acne product works with your body without bieffects.