Breakouts - Acne is an inflammatory skin disorder

Acne is an inflammatory disorder of the pilosebaceous follicles.

The hair follicle and sebaseous glands continually undergoes dynamic remodeling in a cyclical manner involving tightly coordinated patterns of cell proliferation, differentiation and death of cells. Sebaseous glands are clustered by the side of a hair follicle, into which they discharge the 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, protect the skin from drying and moisture, and prevent bacterial infection.

Ongoing research is modifying the classical view of breakouts as caused by Propionibacterium acnes bacteria to a perception of breakouts as an inflammatory disorder with androgens, hormone receptors, regulatory neuropeptides, and environmental factors being agents able to interrupt the natural cyclical dynamic breakdown of dead cells into sebum within the sebaceous follicles. Interruption of discharge of sebum to the surface of skin leads to occlusion of the ducts (microcomedones) and then enlarged comedones that become inflammatory lesions.

Pro-inflammatory lipids, chemokines (molecules released by cells at the site of injury or infection which give rise to 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 act as mediators for the initiation of acne lesions.

Propionibacterium acnes is not initially involved but may mediate later inflammatory events leading to worsening of the lesions.

Variation in the innate immunity of the skin predisposes to acne. 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 such depends indirectly on hereditary factors related to excess androgen activity in puberty, that trigger sterile inflammatory phenomena.

What Triggers Acne During Puberty?

Acne is initiated by an inflammatory signal to the neural system without involvement of bacteria in its initiation. During puberty sebum production is exacerbated and the first flow of sebum through the previously empty duct might create shear forces of sufficient magnitude that injure the pilosebaseous gland. The body responds with the release of inflammatory molecules to promote cell division and quickly restore the lining of the inner surface of the ducts.

At the same time sebum at the external orifice of the sebaceous gland duct and/or the hair follicle leads to formation of a dry "plug" (comedone) which obstructs the flow of sebum. On exposure to oxygen, the comedone turns dark forming what is commonly referred to as a "black head".

The water content of the comedone is reduced by evaporation and diffusion into the adjacent horny layer (keratin) of the surface epidermis resulting in 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 modified chemically, as well as physically, thus becoming a material which is foreign to the body.

This state of "foreignness" provokes a further inflammatory reaction, including immune reactions and other responses of various defense systems, particularly those associated with granulocytes and macrophages.

If the inflammatory reaction and the immune and other defense responses are effective in eliminating or containing the effects of the comedone, further progression of acne manifestations do not occur. Frequently, however, the immune and other defense reactions are not effective in terminating the acne process at this stage and the process progresses partly or wholly as described below.

While the comedone is obstructing the outlet of the duct, the sebaceous glands can continue to form sebum, which accumulates in the duct and in the glands, distending both. The distension and the resulting pressure lead to further intensification of the inflammatory reaction in the adjacent skin and subcutaneous tissues and produce additional swelling (edema), redness (erythema), discomfort, and a mass, which includes the obstructed and thefore encysted sebaceous gland ("redhead", "pimple", or acne papule).

Frequently, the defense mechanisms are not adequate to terminate this process promptly at the acne papule stage and it continues to progress as outlined below.

The above conditions favor the growth of bacteria, and the resultant infections involve the duct, the sebaceous glands and the surrounding tissues, usually in that order. The onset of the infection produces further inflammatory changes, thereby initiating a vicious cycle causing continued and/or increased obstruction of the outflow of the sebum, which in turn leads to more pressure, more inflammation and continued or progressive infection.

This leads to the formation of the acne pustule. The immune and other defense mechanisms having been inadequate to prevent these conditions from arising, frequently fail to arrest or reverse the process early in the acne pustule stage and it persists or progresses further.

Obstruction with or without infection leads to the formation of cysts. Infection of a cyst results in the formation of an abscess which leads to local tissue destruction. If this destruction of tissue has involved the connective tissue elements of the skin or subcutaneous tissues to a sufficient degree, healing is frequently accompanied and/or followed by scar formation.

The scars in acne can vary from minimal to extensive and severely disfiguring problems which are permanent sequallae of acne. While the process by which acne arises and lasts for an indefinite time may and frequently does come to a halt as a result of treatment or spontaneously, the scars persist for life unless they are removed.

An inflamed lesion can sometimes completely collapse or explode, severely inflaming the surrounding skin, and sometimes destroying neighboring follicles. These lesions are called nodules or cysts:

Nodule	Cyst
When a follicle breaks along the bottom, total collapse can occur, causing a large, inflamed bump that can be sore to the touch.	Sometimes a severe inflammatory reaction can result in very large pus filled lesions or cyst. This type of acne should be treated by a dermatologyst.

BIOSKINCARE is a biological skin care product for teenage acne that has no side effects. It works because it not only controls bacteria by boosting the production of the skin's own antimicrobials, it also unclogs pores through the action of enzymes that digest the keratin and sebum that plugs hair follicles. In fact it releases the amino-acid components of damaged skin proteins for their use in regenerating healthy cells which prevents and heals acne scarring.

It also moisturized the skin and eliminates redness quickly. It can be used in conjunction with medicines like isotretinoin (Accutanee & other brands prescribed for very severe acne) to avoid their dreaded side effects on the skin and to start healing scarring and stregthenning the skin while taking the medicines, for it does not interact with them.

Last modified: July 18, 2009

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What Parents of Teenage Boys Say Or Recommend?

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What Parents of Teenage Daughters Say Or Recommend?

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