Acne causes, bacteria proliferation & acne inflammatory reaction
 

Acne bacteria proliferation & the acne inflammatory reaction, cause and effect loop from improper outflow of increased sebum production.

Acne, in general, is caused by a profusion of factors. In general, there are four main factors that cause acne: genetics; hormonal activity; bacteria; and the inflammatory response.

Genetics is a prominent component as it is well known that if several members of the same family were affected with moderate to severe scarring from acne, then this heightens the risks of you contracting acne.

Acne and bacteria living in symbiosis in the hair follicles or canals

Another causative factor in acne is the presence of bacteria in the follicular canal. This is no big surprise, as an adult human being consists of ten times as many microbial cells as mammalian cells, and he she carries around approximately 1.25 kg of microbes. Furthermore, it has been estimated that we provide host for at least 1500 different microbial taxa that collectively contain more than 200 times as many genes as the human genome. Most of these organisms have not yet been grown in the laboratory, and so we know very little about them.

Not only our indigenous micro flora protect us against exogenous pathogenic microbes, but they also provide us with as much as 10% of our energy requirements, supply a range of vitamins, and play a key role in the development of our immune system and mucosal surfaces. But that is another story, for indigenous microbes can also be damaging to us when they go out of balance.

Within the follicular canal are bacteria which are indigenous to the follicular lining. Among the bacteria flora present are anaerobic, gram positive organisms called Proprionibacterium acnes. It is interesting to note that they are present in abundance in pathologically affected sites. They are reduced during oral antimicrobial treatment, and their absence from nonhuman animal skin is striking especially since animals do not exhibit acne vulgaris.

Hormones influence the outset of acne

As you hit the age of puberty your body begins to change in many different ways. Such changes include the production of more hormones, and one of its consequences is the activation of the sebum glands which create a skin lubricating fluid called sebum. Sebum protects your hair from drying out, prevents excessive moisture loss from the skin surface, keeps the skin soft, and inhibits the growth of certain microbes. Sebum glands reside inside your hair follicles (400-800 glands per cm2 in the face, forehead and upper chest) and sebum gets to the surface of your skin through your once clear skin pores.

The skin is composed of several tissues (epidermal, connective, nervous and muscular) and is one of the largest organs of the body in terms of its surface area (approximately 1.75 m2) and weight (approximately 5 kg.) It has a variety of functions. Chief among them is protecting underlying tissues from microbes.

The epidermis is a keratinised, stratified, squamous epithelium. Its thickness varies from 0.5 to 3mm. depending on its location and, being the outermost layer of the skin, it is obviously and important site for microbial colonization. The most common cell of the epidermis (comprising approximately 90% of all the cells of the skin) is the keratinocyte. New keratinocytes are constantly being produced in the stratum basale and, as they are pushed towards the surface, they undergo a process known as keratinization.

This involves the production of a protein, keratin, and the eventual death of the cell. The dead, keratinized cells (known as squames) comprise the outer layers of the epidermis (with lipids filling the intercellular spaces) and are gradually sloughed off - a process termed desquamation. It has been estimated that the skin surface of the average adult is composed of approximately 2 x 10 9 squames. It takes between 2 and 4 weeks for the transfer of a cell from the basal layer to the outermost layer and, as a result of this process, it has been estimated that the stratum corneum is renewed every 15 days.

The keratin present in the cells protects the underlying tissues from heat, chemicals, and microbes. Melanocytes are the next most common cells of the epidermis. These have long slender projections and produce brown-black pigment melanin which is transferred to keratonicytes where it absorbs ultraviolet light, thus protecting the skin from its damaging effects. The only other cells present in the epidermis are Langerhans cells (which are involved in the immune response to microbial invaders) and Merkel cells (which are associated with sensory neurons and are involved in the sensation of touch).

The dermis has a far more complex structure and consists of 1) connective tissue containing collagen and elastin fibers giving the skin elasticity; 2) small finger like projections (papillae) which protrude into the epidermis and contain nerve endings sensitive to touch, heat and pain; 3) hair follicles; 4) arrector pili muscles - for controlling hair movement; 5) sebaceous glands; 6) sudoriferous glands; 7) nerves; 8) adipose tissue; and 9) capillaries and veins.

On the keratin lined follicle canal, where the sebaceous glands reside, Proprionibacterium acnes bacteria live in symbiosis, feeding on and transforming the sebum produced from the sebocytes cells before it reaches the surface. The nascent sebum is largely lipid in composition and also contains DNA, RNA, proteins, and other cellular components that result from the breakdown of sebocytes themselves. Proprionibacterium acnes are found only in sebaceous rich areas.

If the nutrients in the follicular canals increase due to an active and large sebaceous system and, sebum does not flow properly out of the canals, then colonization and high growth rates of Proprionibacterium acnes will form. The resident bacterial flora produces biologically active molecules such as histamine, extracellular enzymes, and peptides which may trigger the inflammatory reaction that characterizes acne vulgaris.

Since the follicular lining in the pilo-sebaceous unit is intact before puberty, it has been theorized that if colonization of Proprionibacterium acnes occurs in sufficient numbers, they produce antigenic molecules that promote the initiation of inflammation. Proprionibacterium acnes can produce proteinases, lipase, and hyaluronate lyase all of which may serve as the catalysts or initiators of the inflammatory infiltrate which are composed of neutrophils and lymphocytes.

The key factor in adolescence is hormonal, for at this stage androgens interact with receptors on the sebaceous glands and cause stimulation of the sebaceous gland to hypertrophy and hence form more sebaceous production of lipids and free fatty acids which distend the follicular canal. More specifically, there is evidence for increased peripheral metabolic conversion of the androgen testosterone to dihydrotestosterone at the level of the skin in people suffering from acne. It is further hypothesized that receptors on the sebaceous gland for the active androgen dihydrotestosterone can exhibit various degrees of sensitivity, and that a heightened sensitivity response may be partially or entirely genetically predetermined.

Basic lesion in acne is the comedone.

The basic lesion in acne is the comedo. On the exposure to oxygen the comedone becomes dark and forms what you know as a blackhead. The comedo is created by retention of layers of dead skin known as keratin in the lining of the follicles. In addition to hyperkeratosis (which is thickening or retained layers of keratin), there is an accumulation of sebum. The combination of the keratin and the sebum produces a plugging of the opening of the follicular canal, and papules are formed by inflammation around the comedones. Depending upon the degree of inflammation, pustules, cysts, nodules, granulomatous reactions, scars, and keloids may develop.

Inflammatory Response.

Airborne contamination and other toxic materials further aggravate the inflammatory reaction. As bacteria begin to proliferate within the clogged pore your immune system reacts by releasing granulocytes and macrophages, which are groups of white blood cells that eliminate the bacteria. The inflammation process is necessary to eliminate the continuing effects of excess bacteria and signal the body to repair the damage to tissues. Often times the immune response system can't stop the reproduction of acne bacteria due to lack of white blood cells or an impaired system.

Activity of the Sebaceous Gland.

When a comedone is blocking the outlet of the sebum ducts, the sebaceous glands continue to form sebum, which accumulates in the sebum canal increasing the comedone in size. The expansion in size results in pressure and leads to a further intense inflammation response in the surrounding skin and creates swelling, redness, discomfort, and a mass. (pimple, redhead, acne papule). Frequently your immune response system cannot act on the acne papule thus furthering the stage of growth and infection.

Growth of Acne Bacteria.

The above conditions encourage the growth of bacteria and result in infection within the duct, the sebaceous gland, and surrounding tissue. The commencement of the infection produces further inflammatory changes, therefore starting a cycle of accentuated obstruction of the outflow of sebum which leads to even more pressure, inflammation, and progressing infection causing cysts and pustules to occur. The effect on skin tissues caused by such infections is very damaging and the healing process usually results in a scar.

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January 05, 2009

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