Unformatted text preview: Acne Vulgaris Acne vulgaris -A disease of the pilosebaceous
unit. ei“Y (eªY) Zi“Y eq‡m ei“Y
(eªY) nq ? A normal pilosebaceous
unit A normal sebaceous gland
The sebaceous gland is found throughout the skin,
except palm and sole and is androgen dependent.
The glands predominantly found in scalp, face, neck and
trunk (hair bearing area), They occur in association with hair follicles and share a
common channel of exit from the skin, known as
pilosebaceous duct. A normal sebaceous gland It does not secrete until puberty, apart from
temporary activity during infancy, probably caused by
adrenal androgen of maternal origin.
During the course of evolution, the gland becomes an
unnecessary component of skin like the appendix. Main constituents of sebum Constituents of sebum ( oil ); A mixture of
2. Cholesterol ester
4. Wax esters ACNE VULGARIS Acne vulgaris is a self-limiting disease of the
The cause is multifactorial.
Clinical lesions range from non-inflammatory
comedones to inflammatory papules, pustules,
nodules and cysts. Incidence of Acne vulgaris
Acne vulgaris occurs worldwide, affecting 90%
of the people at sometimes in their life.
The age of onset is at puberty.
Contrary to popular belief, acne is not confined
to teenagers. It may continue into 3rd and 4th
decades of life. Incidence of Acne vulgaris Acne is commoner and more severe in male
than in female, relating to its androgen activity.
Heredity also plays a role. If patient’s mother
and father had bad acne, the patient may too. Types of acne lesions A. Noninflammatory lesions (comedones ):
1. Closed comedone ( whitehead ) :
when a trapped sebum and bacteria stay
below the skin surface, a whitehead is formed.
2. Open comedone ( blackhead ) :
when a trapped sebum and bacteria open to the
surface and turn black due to oxidation of
melanin. White head and Black head Types of acne lesions
B. Inflammatory lesions:
Scars do not occur in all patients; severe inflammation
may lead to scar formation. Various types of scar may occur, including atrophic
scars, so-called ice-pick scars which are common on the
checks & hypertrophic or keloid scars on the chest and
back. PATHOGENNESIS OF ACNE Pathogenesis of Acne Vulgaris is multifactorial:
Four key factors are responsible for the
development of Acne:
1. Follicular epidermal hyperprolifaration.
2. Excess sebum excretion.
3. Presence and activity of Propionibacterium acne.
4. Inflammation. Diagram to show suggested events in the
pathogenesis of acne. PATHOGENNESIS OF ACNE 1. Follicular epidermal hyperprolifaration is the
first recognized event in the development of
Currently 3 leading hypothesis have been
proposed to explain why follicular epithelium
is hyperproliferative in individuals with Acne. PATHOGENESIS OF ACNE a. Androgenic hormone is the initial trigger.
b. Change in lipid composition have been
implicated in the development of AV.
c. Inflammation is the 3rd hypothesized factor
incriminated in comedone formation.
(IL-1 alfa –a proinflammatory cytokine). Pathogenesis of Acne 2. Excess sebum excretion is another key factor for the
development of acne and is predominantly androgen
contd--- Pathogenesis of Acne
Androgens (from the testes, ovaries, adrenals & sebaceous
glands themselves) are main stimulants of sebum
excretion, although other hormones (e.g. thyroid hormones
& growth hormone) have minor effect too.
Increased target organ sensitivity ie sebaceous gland
This may be caused by 5 alfa-redctase activity being
higher in the target sebaceous gland than in other
parts of the body. PATHOGENNESIS OF ACNE 3. Presence and activity of Propionibaterium acne.
Proximal to the follicular outlet obstruction, sebum
and keratinous debris accumulate. This leads to
the formation of the dilated sac of lipid that is
called a comedone.
This provides an attractive environment for the
growth of anaerobic bacteria, specially P. acne.
Contd.. Pathogenesis of Acne (contd.) 3. Presence and activity of Propionibaterium acne.
These bacteria produce lipase that hydrolyze the
sebaceous lipids, resulting in the release of free
fatty acids, which defuse through the follicular
wall & create dermal inflammation that we call a
‘spot’ or ‘zit’. Pathogenesis of Acne 4. Inflammation may be a primary or a secondary
Most of the evidence to date suggests a
secondary inflammatory response to p. acne.
However, IL-1-alfa expression have been
identified in microcomedone, and it may play a
role in the development of acne. Acne Vulgaris moderately severe Closed comedones, inflammatory papules on the checks, chin
and forehead. Inflammatory papules, papulo-pustules,
irregular depressed on the checks and
forehead Papulo-pusturar and cystic
lesions on the checks. Large cystic lesions and several closed comedones
on the check with irregular scars. Irregular shaped pitted scars
on the check caused by acne Acne vulgaris.
Note comedones, papules and pustules. Acne vulgaris.
Note the closed (white) comedones and open (black)
comedones. Acne vulgaris.
Nodular and nodulo-cystic acne. Acne vulgaris.
Scaring occurs in some individuals and it is permanent. Acne keloids.
Acne may result in scarring and occasionally keloids,
especially on the shoulders and front of the chest. Nodulocystic acne.
Large, inflamed nodules, cysts and scarring occur.
Isotretinoin has revolutionized treatment. Treatment of acne with isotretinoin. Treatment of acne.
Dryness of the mucous membranes is a universal side
effect of isotretinoin, but teratogenicity is the most
serious hazard. Infantile acne (milk spots).
Transplacental maternal adrenal androgens stimulate
the infantile sebaceous glands and produce acne. It
disappears spontaneously within 3 to 6 months. Post adolescent female acne.
Papules and pustules occur, particularly on the chin,
cheeks and jaw, which may be deep and painful and
worse premenstrually. Pomade acne.
Greases used for the hair may spread onto the forehead
and occlude the pilosebaceous orifices. This is common in
blacks. Steroid Acne
lesions on the back
of a young man on
Note the absence
of comedones and
scars. Steroid Acne Steroid Acne with hypertrichosis Acne Myths Versus Facts
Myths: Blackheads are caused by dirt.
Fact: They (open comedones) are black because of
oxidation of melanin.
Myths: Frequent facials are beneficial.
Fact: Professional facial (a form of facial beauty
treatment) or at-home scrubs are not generally
recommended because they tend to aggravate acne. Acne Myths Versus Facts
Myths: Cosmetics, particularly oil-based preparations,
‘clog pores’ and cause acne.
Fact: Their use very rarely cause adult acne. More
commonly, cosmetics can be irritants and may cause
Myths: Acne should disappear by the end of
Fact: Some women have acne that persist well past
adolescence. Acne Myths Versus Facts Myths: Acne is caused or worsened by certain foods
such as chocolates, sweets, and greasy food.
Fact: Acne is not significantly influenced by diet.
Myths: A dirty face exacerbates acne; so, scrubbing
the face daily will help to clear it up.
Fact: Scrubbing the face with acne will irritate and
redden the already inflamed area. Acne Myths Versus Facts
Acne is due to ‘hormonal imbalance’.
Hormones are normal in vast majority.
In acne, sebaceous glands are unusually sensitive to
androgens due to an enhanced target organ sensitivity.
This is due to increased activity of an enzyme 5alfa-reductase
present in the sebaceous gland.
The enzyme converts testosterone to more potent 5alfadihydrotestosterone.
This binds to specific receptors in the sebaceous glands,
increasing sebum excretion. Acne Myths Versus Facts Myths:
Acne is related to sexual behavior.
Neither too little nor too much sex makes any
Masturbation do not cause acne. ( Thank goodness ! ) A.V treatment is multipronged-attacking four mechanisms which lead to
acne. 1 3
3 2 4 Topical Acne Medications
1. Retinoids (comedolytic & anti-inflammatory)
(Tretinoin, Isotretinoin, Adapalene, Tazarotane) 2. Antibiotics (anti-bacterial & anti-inflammatory)
(Clindamycin, Erythromycin, Benzoyl peroxide) 3. Azelaic acid (20% cream)
(antibacterial, anti-inflammatory & reduce proliferation of
Keratinocytes >inhibits formation of comedones) Oral Acne Medications
(Tetracycline, Doxycycline, Clindamycin
Erythromycin, Azithromycin) 2. Hormonal agents
c. Birth control pills
(2mg cyproterone acetate & 0.035 mg ethinylestradiol) 3. Isotretinoin Principle of treatment of acne vulgaris Type of acne Topical Agents Mild acne Retinoids
Benzoyl peroxide Moderately
severe acne Retinoids
comedonic) Benzoyl peroxide Systemic Agents Not necessary Not necessary Principle of treatment of acne vulgaris
Type of acne Topical Agents Moderately
severe acne Retinoids
peroxide + Antibiotics
inflammatory) Severe acne Systemic Agents Surgical / physical agents
Treatment of comedones:
Treatment of inflammatory nodules:
Treatment of inflammatory lesions:
1450-nm laser Surgical/physical agents Treatment of scarring:
*Filler substances Ref.
Goodheart”s photoguide of Common Skin
Disorders. Ref. Goodheart”s photoguide of Common Skin Disorders. (Patient education) The most important aspect of a successful acne treatment
programme is patient compliance.
At the initial visit, instructions should be given verbally and
on a written sheet that reinforces what was said.
The patients are best able to comply if medications are
used twice daily so that medications schedule can be
centered on an already established daily habit such as
tooth brushing. (Patient education)
Patients with acne are often depressed and needs
sympathetic counseling and support.
They will eventually improve as the treatment continues
-need to be stressed.
They may be informed that dramatic improvement may not
occur overnight and they may experience 40%
improvement after 4 months and 80% improvement after 8
months. (Patient education)
Patient should not have inappropriate expectations. Acne, in
most cases, can be controlled but not cured.
Acne remits spontaneously with time. For individual patient,
there is no way to predict in advance when they will
‘outgrow’ their acne.
Patient may express concern over the long –term use of oral
antibiotics, but they should be reassured that this is a safe
practice. (Patient Handout) Acne can be aggravated by a number of things:
Emotional stress may worsen.
Hair pomades and greasy cosmetics tend to clog pores
and may worsen acne.
Pricking or squeezing of pimples is harmful and may led
Hard scrubbing of the skin, too much exposure to the
sun often make acne worse.
Acne usually runs in families. (Patient Handout) Sweating
Sweating appears to worsen acne in 15% of acne sufferers.
Humidity may also worsen the condition.
Estrogen is usually helpful for acne control but Progesterone
may make acne worse.
It is common for all women to have an acne flare up days
before their periods. ( Progesterone) (Patient Handout) Use only your bare hands to wash. Washcloth is irritating.
Washing itself does not clear breakout since dirt does not
cause acne, so there is absolutely no need to scrub.
Washing with worm water, rinse with cold.
Gently pad dry. Rubbing the skin is irritating. Further Acne Facts
Because acne is a visible disease, patients may
suffer from anxiety, impaired self-image,
depression, employment insecurities, social
withdrawal, self-destructive behavior and suicidal
Acne tends to improve temporarily during summer.
Fall and winter acne flare-ups are quite common
often influenced by mood swings. (Patient Handout) A gentle cleansing must precede treatment in order to prevent
Look for the terms ‘oil-free’ and ‘non-comedogenic’ when
selecting a facial cleanser. You are on a right tract when
references to ‘mild’, ‘non-irritating’ and ‘non-overdrying’ are
mentioned as well.
Wash your face twice daily, morning and evening. Excess
washing can cause irritation. Further Acne Facts
Acne, Hirsuitism and irregular menstruation may be
associated with hyperandrogenism and/or
Adult acne is often more persistent than teenage
The two Hs – hormones & heredity- underlie
teenage acne and not the proverbial -bad diet and
dirty face- the two Ds. Further Acne Facts
Severe, unremitting, scaring acne is more prevalent
Skin care should be kept simple and gentle with the
use of mild soaps and harsh soaps are to be
The treatment of acne is suppressive, not curative !
Be patient………and don’t expect results
overnight ! Types of Acne
1. Infantile acne
Infants below the age of three months may develop facial acne.
They have elevated plasma adrenal androgens of maternal
origin. 2. Senile acne
Occurs in individuals over the age of 50 years. Comedones
localized to the temples and forehead. 3. Acne Cosmetica
Cosmetics were considered to be a major cause of adult acne in
With the exception of very greasy, occlusive products, cosmetics
are infrequent etiologic agents for acne. Types of Acne
4. Steroid acne
Sudden onset (usually within 2 weeks of starting high-dose
systemic or potent topical corticosteroid therapy).
Occurrence at any age.
Trunk is more commonly affected than face.
Not necessarily limited to the sebaceous gland rich areas.
Monomorphic presentation. Rarity of cyst formation.
Absence of true comedones. Types of Acne
5. Pomade acne.
6. Acne Mechanica.
7. Occupational acne.
8. Tropical acne
9. Acne with facial edema.
Acne uncommonly associated with a peculiar
inflammatory edema of mid-third of face. 10. Acne aestivalis.
Monomorphous, papular lesion occur after sun
exposure, mostly in women. Types of Acne
11. Acne fulminans ( acute febrile ulcerative acne )
12. Excoriated acne
Common in females.
The patient excoriates, scratches and plays with skin of
acne lesions so that even the smallest lesion may be
There is some associated mental stress or personality
disorder. Types of Acne
13. Acne Conglobata
Characterized by comedones, papules, pustules, nodules,
cysts and burrowing intercommunicating abscesses.
Healing results in an admixture of depressed and keloidal
Occurrence at a latter age and chronic unremitting course.
Prolonged antibiotic therapy guided by c/s.
The use of isotretinoin produces dramatic results and is now
the treatment of choice in dose of 2 mg/ kg/ day for 20
A combination of systemic steroid and isotretinoin produces a
better response. 1. ( May-2005) Define acne vulgaris. Write down the
pathogenesis (Jan-2008) and treatment (Jan-12;
Sep-2008; Jan-2008) of acne vulgaris. 2. Name 6 skin lesions found in Acne vulgaris (Jan2009). 6. A 23-year-old girl had few scattered small papules like
closed comedones (whiteheads) and pustules for last 3
years on face. During last 3 month she developed small
papules, monomorphic in nature. She had history of
applying topical steroid on face for last 4 months.
Q. What is the (1) diagnosis and (2) management? 5. A 19-year-old girl had inflammatory papules,
pustules with open and closed comedones on
both the cheek and forehead for last two years. Q. What is the (1) diagnosis and (2) management? 1. A 20 years old college girl presented with
comedones and papulo-pustular lesions on her face
and forehead about 6 months ( July-2008).
a. What is your clinical diagnosis?
b. Name 3 topical preparations for the patient.
c. Name 3 systemic drugs with doses and duration.
d. Give 2 advices. 8. Acne Vulgaris is disease:
__a) of sweet gland. __b) Commensales of epidermis is related. __c) Black head and yellow head comedon are present. __d) Clinically comedon,papule,nodule and cyst are
present in all patients. __e) Tetracycline is the safest and cheapest drug of
choice. 62. ‘Steroid acne’ differs from acne vulgaris: a. By absence of comedones b. By absence of pustules c. In its distribution d. In its outcome e. In no way at all 144. The following factors are operative in the
causation of acne: a. Excessive secretion of the sebaceous glands b. Bacterial infection c. Abnormal hormones d. Emotional tension E. Over-work 13. Clinical features of acne vulgaris includes
___a) White head.
___b) Hardening of skin
___d) Black heads.
___e) Herald patch. 145. The following drugs given systemically can
also control acne vulgaris: a. Antibiotics b. Androgens c. Oestrogens d. Corticosteroids e. Chlorquine THANK YOU ...
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