Mechanisms
of development and strategies to treat
Treatment
should be aimed at achieving clearance
of acne, prevention of scarring and, where necessary, relief
from any psychologic stress resulting from the acne. Early treatment
of acne may be commenced in the disease process in order to prevent
scarring and it is important to select appropriate therapies according
to the clinical signs and psychologic disability. Coming up with
a protocol for adult acne cure requires understanding of acne mode
of development. Although, the precise mechanisms of acne are not
known, it is clearly accepted that there are these four major etiological
factors involved in development of acne:
1. An increased sebum
production
2. Ductal
hypercornification (hyperproliferation of ductal epidermis)
Hypercornification is overproduction of epithelial cells lining
follicles (sebaceous ducts, these ducts conduct sebum to the skin).
Hypercornification may result in closure of the ducts and cause
comedone and acne
3. Bacterial colonization
of the duct with Propionibacterium
acnes (see photo)
4. Further production
of inflammation in acne sites
Acne
and sebum generation: Several
factors influence sebum production, but it is predominantly
hormonally stimulated. In treatment of acne androgens, and their
influence must be considered. Androgens especially from the testes
and adrenals, stimulate the sebaceous gland directly and influence
acne inflammations. Estrogens exert a variable inhibitory effect
in pharmacological doses. Sebum excretion is significantly greater
in patients with cystic
acne and attempts pharmacologically to reduce the sebum excretion
are a logical approach to its topical treatment.
The sebaceous glands
( part of sebaceous follicles ) are under endocrine control and
so it is not surprising that sebum production shows change according
to age and sex of an acne patient. Sebum production is dramatically
greater than that in females in normal individuals as well as acne
patients. There is an increase in sebum generation with a peak at
about age 40. Any approach to control androgens appear to be relevant
to adult acne since the sebaceous follicle ( Sebaceous glands are
located in the dermis (the middle layer of skin) and secrete oil
onto the skin.
) is an organ targeted by androgens.
Hyper
proliferation of ductal
epidermis is associated with development of adult acne. A possible
stimulus to pilosebaceous duct hypercornification could be hormones,
in particular androgens. Within the duct, variations in the lipid
composition have been put forward to explain comedone ( a initial acne lesion ) formation, which could be either closed (whiteheads, see photo) or open (blackheads, see photo). Such variations include an increased concentration
of squalene, squalene oxide, and certain fatty acids. A decrease
in the linloleic acid fraction of the skin surface lipids has been
shown in a patient with acne. Micro-organisms have also been implicated.
Skin
surfaces in the acne prone areas are colonized with Staphylococcus
epidermidis and Propionibacterium acnes. However, P. acnes appear
to be the main organism in acne and its elimination should be addressed
during the course of acne. Studies suggest that bacteria have nothing
to do with the initiation of comedogenesis.
However, P. acnes, in particular, may in some situations be important
in the initiation of inflammation. It is also quite likely that
they are involved in a perpetuation of inflammation once established.
The
adult acne inflammation is not, in most cases, an abnormal response
of the immune system. The inflammation represents a normal immune
and nonimmune response to foreign substances penetrating the dermis.
It is important for a patient on a blemish treatment to know that
acne is not infectious. In most cases the inflammation settles,
papules and pustules lasting about 3-14 days but larger lesions
persist longer. The larger and more actively inflamed lesions will
in some instances produce permanent dermal damage and result in
acne scars. Could acne be cured? Most treatments
target the present lesions and do not eliminate the underlying cause.
Relapses are very common and could be triggered by cauasative factors
among them stress and hormonal imbalance.
Manifestations
of acne
Patients
almost always demonstrate lesions on the face. Smaller percentages
exhibit acne on the back and on the chest. Acne lesions are divided
in two major groups. Inflammatory and non-inflammatory lesions.
Skin treatment of these two types of acne may vary. Non-inflammatory
lesions or comedones are subdivded into white heads and black heads.
White heads are closed comedones with some pathological changes
in pilosebaceous duct (hypercornification of the duct, which results
in closure of the follicle). Black heads or open comedones presents
as an obvious black lesion especially on the top.1-3 mm in diameter.
Accumulation of the melanin (skin pigment) in blackheads cause the
black color. There are many patients who have few or no black heads.
Manifestations of adult acne in form of white heads and black heads
is very common and they may be the starting point for an inflammatory
lesion.
Inflammatory lesions
such as papules, pustules, nodules, cysts, macules and scars are
among other manifestations of acne. Papules and pustules are more
superficial compare to the rest of inflammatory acne and their cure
takes a shorter period of time, 5-10 days. These pimples are caused
by blockage of oil glands. Papules are red lesions (pimples). Pustules
are similar to papules but with a central collection of white pus
at their top. Nodules are deep-seated structures and tend to remain
for as long as eight weeks before finally resolving. Cysts ( cystic
acne ) are not very common but when they occur they may reach
several centimeter in diameter. Cysts are tender, sensitive, deeper
and larger pimples filled with pus. Cystic
acne is considered a severe acne form and its treatment must
be consulted with a physician. Cystic acne cure may take longer
period of time and its recurrency is very likely.
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