Acne, the most common of all skin disorders and the bane of almost
every adolescent face, is caused due to various biological factors
mostly related to the function of the sebaceous glands.
Acne develops from the combination and intertwining of several
complex biological processes. Evidence suggests the involvement
of sebaceous hyperplasia or excessive sebum production by the
sebaceous glands, follicular hyperkeratinization, colonization
of the hair follicle by Propiobacterium acnes, as well as immune
reactions and discharge of chemical inflammatory mediators into
Relation of acne to sebaceous glands
The sebaceous glands are situated in the hair follicles and the
epidermis and found all over, especially in the area of the face
and scalp, but not on the palms or soles of the feet. Sebaceous
glands are a holocrine secreting tissue and its most important
function is the secretion of sebum, the excess of which manifests
as the development of acne. Sebum is a lipid rich fluid which
is released onto the surface of the skin when mature sebocytes
in the sebaceous glands rupture. The sebum is made up of cholesterol,
fatty acids, fatty alcohols, glycerides, wax esters and sterol
Increase in sebum secretion reaches its peak on the fist week
after birth in infants. After this the sebum secretion subsides
and only rises again at around 9 years of age and continues to
reach another paek at about 17 years of age. This is the reason
behind infant acne and adolescent acne respectively. Acne in childhood
develops into severe acne in adolescence.
The sebaceous gland functions associated with acne are proinflammatory
lipids, locally produced cytokines, periglandular peptides, neuropeptides,
and substance P, which is release at the endings of nerves in
the sebaceous glands.
The function of androgens in acne development
Androgens bring about the differentiation in sebaceous glands.
The sebaceous glands are vital areas where active androgens are
formed. The role of androgens in the pathogenesis of acne has
been proven both clinically and through experimental evidence.
Androgens are produced in the sebaceous glands from the adrenal
precursor hormone - primarily dehydroepiandrosterone sulfate (DHEAS).
The occurrence of acne during pre puberty is related to the heightened
levels of serum DHEAS, which is also a precursor for testosterone.
The rise in DHEAS is associated with an increase in sebum production
and development of comedonal acne and severe inflammatory acne
Hormones and acne
Hormones are thought to have a tremendous impact on the development
of acne. They also act on the hyperkeratinization of hair follicles,
which also helps lead to acne. Growth hormones that are secreted
in the pituitary glands may also be involved in the manifestation
of acne. So acne mostly occurs in the adolescent years when there
is high secretion of the growth hormone and the serum levels of
the somatomedians or growth factors are highest and the excess
of which leads to seborrhea and acne. Estrogen, glucorticoids
and prolactin in women influence sebaceous gland function and
therefore have effect on the development of acne.
Neuropeptides and acne
Corticotrophin releasing hormone from the nerves of the skin
and sebocytes are produced and discharged when the cutaneous nervous
system senses stress and damage of skin and deals with the cell
damaging signals in this manner. The nerves near the sebaceous
glands of acne sufferers release this neuropeptide substance.
Acne as a primary inflammatory disease
It is now accepted that acne vulgaris is an inflammatory disease,
which occurs as an immune reaction to the P. acnes bacteria. Follicular
hyperkeratinisation leads to a change of the hair follicle make
up with consecutive proliferation of bacteria, chiefly Propionibacterium
acnes, in the hair follicle. This leads to further increased production
of the pro-inflammatory cytokines and tumour necrosis factor [alpha]
by T cells and keratinocytes, which gives rise to yet more proliferation
of bacteria. In response, follicular keratinocytes produce hypergranulosis
similar to the impermeable skin outer layer, resulting in the
formation of microcomedones. These microcomedones are more simply
described as small lumps of dead skin and oils mixed together – the
seeds for the subsequent plugging of the hair follicles and the
development of acne. Further inflammatory responses lead to the
development of increasing degrees of severity in inflammatory
forms of acne.
Sebaceous lipids responsible for acne formation
Sebaceous lipids secreted by the sebaceous glands are also responsible
for the development of acne. The lipid mixture is made up of squalene
and wax esters, triglycerides and cholesterol. The sebaceous lipids
are functional in three dimensional skin surface lipid organization
and also synthesize free fatty acids on the skin surface. The
stimulation of sebaceous glands by androgens during puberty leads
to a rise in lipid synthesis and the formation of acne. These
lipids have pro-inflammatory properties, which lead to acne development.
The lipids are also food for the bacteria and so the increase
in lipids present also promotes the proliferation of P. acnes.
Treatments aimed at controlling acne should therefore take into
consideration all these biological factors so as not only to reduce
sebum production and Propionibacterium acnes, but also try and
control pro-inflammatory lipids in sebum and inhibit accumulation
of inflammatory cells around the hair follicles.