Though the acne or pimples are very common among
adolescence or young adults, it is better classified as a disease rather than a
physiological phenomenon due to inflammatory component and scarring it can
cause.
It is a common disease with more than 90% of the
people experiencing it sometime or other in their lifetime. Age of onset is
between 14-17 years among girls and 16-19 among boys.
Severity of acne is usuallny more among males due to
androgen activity. Genetic factors influence the susceptibility to acne.
Causes
1. Alteration
in the pattern of keratinization within the sebaceous follicle
2. Level
of circulating sex hormones, especially androgens
3. Quantity
and quality of sebum production
4. Colonization
by follicular microbial flora
5. Immunological
factors
6. Environmental
factors
Alteration in the pattern of keratinization
The comedones which are the primary lesions of acne
are formed by increased production as well as accumulation of keratin in the
sebaceous follicles. The stimulus for this may be androgens or the irritating
effect of sebum. It is found that the prepubertal girls with inflammatory and
comedonal acne have significantly higher levels of androgens. The acceleration
in the sebum secretion or its composition may irritate keratinocytes of
infundibulum leading to release of inflammatory substances.
The hyperkeratinization leads to decreased barrier
function which in turn makes it susceptible to inflammatory agents. Horny plug
debris become inflammatory and trigger acne. Increased hydration of comedones
causes obstruction of sebum outflow. This mechanism is the cause of tropical
acne and premenstrual flare of acne.
Circulating sex hormones
Androgens increase sebum secretion and cause sebaceous
gland hyperplasia while estrogens suppress sebaceous gland activity. When there
is increased androgen-estrogen ratio there is increase in acne.
Quality and quantity of sebum
Excess sebum secretion and sebaceous gland hypertrophy
is seen in acne patients. At the same time there is difference in the
composition of sebum too is responsible for inflammation. High levels of wax
esters and squalene are found in sebum of acne patients.
Follicular microbial flora
The resident bacterial flora like P.acnes,
P.granulosum, p.ovale and Staphylococcus epidermidis play important role in the
production of acne. Lipases released by these bacteria cause follicular
hyperkeratosis and even rupture of follicles. The materials thus released
attract neutrophils and inflammation sets in.
Immunological factors
Various immunological phenomena take place in acne
prone skin the details of which are beyond the scope of this article.
Environmental factors
A hot and humid environment aggravates acne due to
ductal hydration. The occupations involving exposure to such environments make
the persons with pre existing acne more susceptible to acne flares. Emotional
stress and strains of various types are known to worsen the condition while
natural light often improves acne. External applications of oils, pomades and
other comedogenic chemicals cause acneiform eruptions.
Diet plays a role in pathogenesis of acne. Sugar rich
diet causes hyperinsulinemia which results in androgen synthesis leading to
comedone formation. Diet induced hyperinsulinemia increases insulin like growth
factor (IGF-1) causing unregulated growth of follicular epithelium, sebum
production and synthesis of androgens from gonads.
Similarly, this insulin like growth factor (IGF-1) is
increased on intake of milk and diary products. Milk contains IGF-1 and induces
endogenous production as well. Milk also contains androgens. Iodine and low
omega fatty acids content of milk also seems to be responsible for acne
formation in high glycemic load diet.
Sequence of events
Microcomedo is the first lesion formed due to
increased keratinization leading to blockage of sebaceous canal resulting in
retension of sebum and initiation of inflammatory reaction. Increase in
bacterial flora increases inflammation. Further retention of sebum and release
of enzymes causes rupture of the gland. The spread of sebum in dermis adds to
the inflammation causing areas of accumulation of fluid, pus and glandular
debris. Scar forms on healing the pattern of which is determined by the size
and pattern of lesion and individual susceptibility.
Clinical
features
The lesions of acne are seen on face, chest, back,
shoulders and upper arms. Comedones or the early lesions of acne are chiefly of
two types-open and closed. Open comedones represent follicles with dilated
follicle.the black dot is caused by oxidization of melanin, transmission of
light through compacted epithelium and presence of certain lipids. Closed
comedones are small papules without surrounding erythema. There are several
subtypes like macrocomedones, sandpaper comedones and submarine comedones all
of which do not easily respond to topical therapies.
Grading of acne
Grade 1(mild): comedones, occasional papules
Grade 2(moderate): comedones, many papules, a few
pustules
Grade 3(severe): predominantly pustules, nodules and
abscesses
Grade 4(cystic): mainly cysts and abscesses
,widespread scarring
Oily skin is always associated feature and seborrhoeic
dermatitis also may coexist. Premenstrual flare and postmenstrual improvement
is common. Sequelae include hyperpigmentation and various types of scars.
Psychological
impact of acne
Patients with severe acne and scarring have shown wide
range of psychological abnormalities like depression, suicidal ideation,
anxiety, embarrassment, body dysmorphic disorder and social inhibition.
Treatment
Aims of treatment
1.
To reduce follicular bacterial
population , reduce lipases
2.
To remove follicular obstruction
3.
To reduce inflammation
4.
To reduce sebaceous gland activity by
blocking androgen stimulation.
General
measures
1.
Avoid usage of acnegenic drugs, oils,
cosmetics.
2.
Stress control.
3.
Rule out hormonal abnormalities.
4.
Regular face wash with proper
cleansing agents.
5.
Dietary restrictions as per the
personal observation, balanced diet.
Treatment
modalities
1.
Mild involvement: Benzoyl
peroxide/salicylic acid/azelaic acid topically.
2.
Mild to moderate involvement: Benzoyl
peroxide/ tretinoin/adapalene/tazarotene/clindamycin topically.
3.
Moderate to severe involvement:
a.
Oral antibiotics like doxycycline,
minocycline, lymecycline, azithromycin etc.
b.
Isotretinoin
4.
Cystic acne:
a.
Aspiration of cyst or intralesional
injection of steroid.
b.
Systemic antibiotics.
c.
Dapsone.
d.
Isotretinoin
5.
Adjunctive therapies like comedo
extraction, chemical peels, microdermabrasion, laser and light therapies.
6.
Acne surgeries like draining cysts,
punch grafts, resurfacing with laser, cryosurgery, dermarollers, fillers.
[ Reference: IADVL textbook of
dermatology]
