Acne, though not deadly, still requires treatment. Acne is a common
skin disorder and an annoying problem for both teenagers and adults, caused
by biological factors affecting the functions of the sebaceous glands.
Acne is the result of the interrelationship of many various biological
processes. It seems that sebaceous hyperplasia (excessive sebum production
by the sebaceous glands), follicular hyperkeratinization, colonization
of the hair follicle by Propiobacterium Acnes, immune reactions, and discharge
of chemical inflammatory mediators into the skin are involved with the
Acne and the sebaceous glands
Sebaceous glands are glands responsible for releasing sebum, the oily
substance excreted from the chest, face, neck and back areas. Sebaceous
glands are attached to hair follicles in the epidermis and are a holocrine
secreting tissue. Sebaceous glands excrete sebocytes, which when mature
forms sebum. Excess sebum is the main cause of acne, and is made up of
cholesterol, glycerides, fatty acids and alcohols, sterol esters, and wax
Sebum secretion has three noted peaks in a person’s lifetime: (1)
during the first week after birth; (2) at around nine years of age; and
(3) at 17 years of age. This is why acne seems to attack more frequently
and aggressively on infants and adolescents. It has also been found that
a child suffering from acne develops more severe attacks in adolescence.
Sebaceous gland functions associated with acne include locally produced
cytokines, periglandular peptides, neuropeptides, proinflammatory lipids,
and substance P, which is released at sebaceous gland nerve endings.
Androgens in acne development
Androgens have been proven clinically and through experimental evidence
to play an important role in the pathogenesis of acne. Androgens bring
about the differentiation in sebaceous glands, and are produced therein
as well. The adrenal precursor hormone – primarily dehydroepiandrosterone
sulfate (DHEAS) – produce androgens in the sebaceous glands. Heightened
levels of serum DHEAS, which incidentally is also a precursor for testosterone,
is a cause of acne during pre-puberty, and is associated with the increase
of sebum production and development of comedonal and severe inflammatory
Androgen is found in the vital areas of a sebaceous gland. It serves as
the pathogenesis of acne. The adrenal precursor hormone is the one responsible
of the production of androgen in the sebaceous gland. Dehydroepiandrosterone
sulfate (DHEAS) is related to the serum which is said to be a precursor
for the testosterone. In other words if the serum increases the surely
the DHEAS will also increase. When both of the serum and the DHEAS rise
then we will be facing a severe case of inflammatory acne and of the comedonal
acne. This is where the acne problem would be called an inflammatory disease.
Hormones and acne
Aside from sebaceous glands, hormones are also a factor in acne formation
by acting on the hyperkeratinization of hair follicles. Acne occurs mostly
during the adolescent stage due to the high secretion of growth hormones
during this stage, and the serum levels of the somatomedians (growth factors)
once again reach its peak. Women also have a tendency to suffer more acne
problems than men due to estrogen, glucorticoids and prolactin.
Neuropeptides and acne
When the cutaneous nervous system senses stress and skin damage, the nerves
near the sebaceous glands of acne sufferers release a neuropeptide substance
to deal with the skin damaging signals. This substance is composed of a
corticotrophin-releasing hormone from the nerves of the skin, and sebocytes.
Acne as a primary inflammatory disease
Acne vulgaris is today accepted as an inflammatory disease occurring as
an immune reaction to the P. acne bacteria. When bacteria proliferates
in the hair follicle, follicular hyperkeratinisation results and leads
to the formation of Propionibacterium acnes. In this event, the production
of pro-inflammatory cytokines and tumor necrosis factor [alpha] by the
T cells and keratinocytes increases. It leads to an even greater increase
of bacteria and creates small lumps (microcomedones) on the skin composed
of dead skin cells and oil. Microcomedones worsen and aggravate inflammation,
leading to severe acne formation.
Sebaceous lipids responsible for acne formation
The sebaceous glands also secrete sebaceous lipids that facilitate acne
development. These lipids are composed of squalene and wax esters, triglycerides,
and cholesterol. These sebaceous lipids are functional in three-dimensional
skin surface lipid organization, and synthesize free fatty acids on the
skin surface as well. During puberty, the stimulation of sebaceous glands
causes a rise in lipid synthesis and, consequently, acne development. Bacteria
also feed on these lipids, promoting their growth and propagation.
These biological factors should be taken into account when considering
acne treatment. As well as reducing sebum production and Propionibacterium
acnes, pro-inflammatory lipids in sebum should be controlled to hinder
the accumulation of inflammatory cells around the hair follicles.