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Acne
is a chronic inflammatory disorder that occurs in the adolescent as well
as the adult. It involves a variety of lesions originating from the pilo-sebaceous
follicle. Pilo-sebaceous follicles exist all over the body: the face,
thorax and back. These are the primary seat of polymorphic juvenile acne
and contain a great number of them.
A) There
are three types of follicles:
- Vellus
Follicle: represented by a tiny hair and a tiny gland. This type of
follicle, although responsible for surface oil, plays no part in the
acne process.
- Sebaceous
Follicle: the fine hair lies within a wide canal filled with keratinized
cells. The sebaceous gland is large and multi-lobulated.
- The sebaceous
follicle plays the key role in acne formation, and is found in great
numbers on the face, back and chest.
- Terminal
Hair Follicle: the thick hair fills the canal of the follicle completely.
This type of follicle does not develop acne.
B) The Sebaceous
Gland
The size of the sebaceous gland enlarges as the gland produces more sebum.
In an acne case the sebaceous gland, which on normal skin is approximately
1/10 mm. large, increases in size up to four times. For example, in acne
conglobata, the most severe type of acne, it is not uncommon to find oil
glands which are enlarged ten times. In aged skin, oil glands can enlarge
due to atrophy rather than oil secretion - in fact, the amount of oil produced
decreases with age.
C) Sebum
Sebocytes are produced within the sebaceous glands and form the sebum
which, together with horny cells, are responsible for comedo-formation.
The lipids produced by the sebocytes take approximately one month to come
to the skin surface.
Some of the components of sebum are: free fatty acids, triglycerides,
esters, squalene, glycerides and cholesterin. Bacteria and micro-organisms
such as staphyloccocus corinebacterium acne, as well as pityrosporum (fungus),
are part of the natural flora of the pilosebaceous canal. In case of acne
they produce lipase (enzymes) and split glycerides and triglycerides into
free fatty acids. This, in turn, is irritating and can produce an inflammation
of the follicular epithelium.
Pathogenic Factors
- Obstruction
of follicular orifice with keratinized cells, sebum and debris.
- Hypersecretion
of sebaceous gland.
- Increased
production of free fatty acids due to bacterial activity.
- Formation
of micro-comedones, closed or open comedones.
- Comedone-created
pressure on follicular wall, which ruptures.
- Seepage
of dead cells and sebum into dermis results in papule, pustule and/or
nodule formation, depending on the depth of injury.
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