Etymology

The word “Acne” was invented in ancient Greece. Some
theories claim that the word Acne comes from the Greek word “Akme” which means
a point or a spot. Early Greeks recognized acne as a ‘Tavoot’ and associated it
with puberty.In 2nd AD the meaning of acne appear to be widened to
include the height or culmination of growth and development and thus ‘Puberty’.

We Will Write a Custom Essay Specifically
For You For Only $13.90/page!


order now

The Roman physician Pliny and Celsus used the word
‘Varus’ for the ailment. Cassius in 3rd AD explained that since this
ailment is related to puberty, it is kown by the name of ‘Akmas’.

Till the 5th century AD, the use of the
acne was considered as misrepresentation of the word acme.But with works of
Emperor Justinians physician, Aetius, it indicates that the word acme was
misprinted. Its use became obsolete until the 1800’s, when ‘Acne’ regains a
place in medical dictionaries.

Willan and Bateman (1813 AD) divided acne in the
sense of Ionthoi or Vari into 3 types: Simplex, Punctata an Indurata on the
basis of 3 types of lesion which occur.

A fourth member of this group of disease they call
Acne Rosacea which they agree is the gutta rosacea of the older physicians.

In 1840 AD, fuchs for the first time divided acne
into acne vulgaris, acne mentagra and acne rosacea. This was the first use of
the term ” Acne Vulgaris”

                                 

Acne vulgaris is a chronic disease of the sebaceous
follicles characterized by polymorphic skin lesions. These include open and
closed comedones, macules,papules, nodules and pseudocysts.29(AE till, V
Gauldon. WJ Conliffe, KT Holland. The cutaneous microflora of adolescent,
persistent and late onset Acne Patient does not Differ. Br. J. dermatol : 2000;
142(5) :885-92.)

Acne vulgaris is one of the commonest skin disease
with a point prevalence reaching 100% among adolescents. Although it is usually
a condition of adolescence, acne vulgaris affects 8% of 25 to34 year old and 3%
of 35 to 44 years old age group.7(John Redman coxe. The Writings of Hippocrates
and Galen Epitomised from the original Latin translation. 1846: Lindsay and
Blakister(Philadelphia): P99, 179)The peak incidence of acne is in
the mind to late teens.30(W Mitchell Sams Jr. Peter J Linch. Principles and practice
of dermatology. 2nd edition Churchill livingstone ; 1996; Pp801-2.)

It is slightly more common in boys than in girls,
the severe forms of acne are much more common in boys. The incidence is similar
in male and females until the mid20s, thereafter, acne is more prevalent in
females,but the severity and frequency are markedly decreased.30Hormonal
factor are probably responsible for the higher incidence of acne in post
adolescent women than men.31(Jay H Stein. Internal Medicine. 5th ed. Mosby
Publication; 1998 ; Pp 1304-5.)

 

PATHOGENESIS OF ACNE VULGARIS

# Incresed sebum excretion

#Abnormal keratinisation

#Activity of the follicular microflora

#Inflammation

 

 

Host factors such as heredity,environment and
emotional state also contribute to the development of acne lesion.31(Jay H Stein.
Internal Medicine. 5th ed. Mosby Publication; 1998 ; Pp 1304-5.)

 

Increase sebum excretion

Adult levels of sebum output are an absolute
prerequisite for the development of the disease.40(Gred Plewig,
Albert M Klingman. Acne and Rosacea. 2nd ed. Springer-Verlag Heidel
berg (Germeny): 1993: Pp, 39-43.) The onset of acne, especially the
comedonal type at puberty seems to correlate with onset of androgenic hormone
stimulation and may be the first sign of pubertal maturation and may be the
first sign of pubertal maturation in girls, preceding pubic hair and breast
development.30(W Mitchell Sams Jr. Peter J Linch. Principles and practice
of dermatology. 2nd edition Churchill livingstone ; 1996; Pp801-2.)

Acne frequently begins in the prepubertal or early
adolescent period with an increase in adrenal androgen leading to an increased
production of sebum with puberty and gonadal development, androgen production
increases even further.Androgenic hormones( gonadal and adrenal) stimulate both
enlargement and increase activity of sebaceous glands on the face neck and
upper trunk.

Althuogh testosterone levels are normal in most acne
patient, local conversion to the end organ effector dihydrotestosterone(DHT)
may be increased in acne bearing skin.7(John Redman coxe. The Writings of Hippocrates
and Galen Epitomised from the original Latin translation. 1846: Lindsay and
Blakister(Philadelphia): P99, 179.)This local conversion is by the
enzyme 5 alpha reductase.A cytoplasmic receptor for the local hormone DHT has
been demonsterated in human skin.A complex is formed between DHT and this
receptor and is then transferred to the nucleus where it promotes gene
expressions as a direct response to hormone stimuli.This initiates the
biochemical reactions leading to the manifestation of the androgenic
stimulation.

It has been shown that the conversion of
testosterone to DHT was up to 30 times greater in acne bearing skin than in
normal skin from the corresponding areas.Plasma level ofs of testosterone are
normal in most acne patients.40(Gred Plewig, Albert M Klingman. Acne and Rosacea. 2nd
ed. Springer-Verlag Heidel berg (Germeny): 1993: Pp, 39-43.) Individuals
with acne have higher rates of sebum production and often the severityof acneis
proportional to the amount of sebum production.7(John Redman coxe. The Writings of Hippocrates
and Galen Epitomised from the original Latin translation. 1846: Lindsay and
Blakister(Philadelphia): P99, 179) Sebum acts in partnership with
bacteria to produce keratinisation and hence blockage of the pilosebaceous duct
and comedo formation.42(Anitha S Pakula, Lawrence D Neinsteria. Adolescent Health
care: A practical guide. 2002; Pp442-3.)Sebum alter the environment
in the follicle via three mechanism;

1 It accumulates behind the micrcomedone

 

causing follicular dilatation.

2 It provides a substrate for bacterial lipases that
produce free fatty acids from triglycerides in sebum.

3 It may contribute to abnormal follicular
keratinisation.The sebum form patient with severe acne is often relatively
deficient in linoleic acid, an essential fatty acid required for normal
epithelial differentiation.31(Jay H Stein. Internal Medicine. 5th ed. Mosby
Publication; 1998 ; Pp 1304-5.)

 

2 Abnormal keratinisation

Retention hyperkeratosis of the acro infundibulim of
sebaceous follicles is a primary event in the pathogenesis of acne vulgaris.The
follicular epithelium becomes hyper plastic and a horny impaction is formed.

The cause of the hyperproliferation of keretinocytes
and the abnormalities of differentiation and desquamation are unknown. It is
likely that hyper responsiveness to the stimulation of sebocytes and follicular
keratinocytes by androgen lead to the hyperplasia of the sebaceous glands and
the seborrhoea that characterize acne.31(Jay H Stein. Internal Medicine. 5th
ed. Mosby Publication; 1998 ; Pp 1304-5.)

 

Abnormal follicular keratinisation prevent the loss
of epithelial cells normally carried out of the follicle by the flow of sebum.
The epithelial cells adhere and trap sebum and bacteri in the infra
infundibular portion the follicle.The cohesiveness of follicular epithelial
cells is though to be related to a decrease in membrane coating granules.It is
these lytic enzymes that allow normal differentiation to occur.31(Jay H Stein.
Internal Medicine. 5th ed. Mosby Publication; 1998 ; Pp 1304-5.)

 

Downing
and co workers postulated a linoleic acid deficiency of the follicular
epithelium. The concentration of linolic acid and acylceramide in the sebum of
acne patient is lower than in