Acne and Acne related

disorders
Disorders of sebaceous glands and
Rosacea

.Omar Abdulaziz Al-Sheikh, M.D

College of Medicine
King Saud University
 Objectives
Acquiring knowledge of the etiology and
pathogenesis of acne and acne related disorders.
Understanding the disease spectrum and various
types of clinical presentations.
Knowing the differential diagnosis of acne and
related disorders.
Acquiring knowledge of the therapeutic options
and their indications.
to be familiar with the etiology, clinical types and
treatment of rosacea.
:Definition
Is a chronic inflammatory disorder of the
pilosebaceous apparatus of certain body
area (Face> Torso > rarely the Buttocks),
resulting in greasiness and polymorphic
skin eruption.
Incidence:
Acne affects all skin types, the male and
female ratio is virtually the same but tends
to be more severe in males.

85% affects the age group 12 24 years

8% affects the age group 25 34 years
3% affects the age group 35 44 years
Etiology:
1. Genetic Aspect, (Acne runs in family)
other example: the case of severe acne
that is associated with XXY syndrome.
2. Occupation (Environmental, Mechanical)
e.g. exposure to acnegenic mineral oil
(Pomade acne), dioxin
3. Drugs Oral and topical Hydrocortison
(Steroid acne), Lithium, Hydantoin,
contraceptives
4. Endocrine Factors (Recalcitrant Acne,
POD/s, MARSH Syndrome) .
Pathogenesis: ( three main steps
recognized and hypothesized)

1. Follicular Hyperkeratosis (the cause not

fully understood) theory suggest:
deficiency in Linoleic acid,
the effect of 5-a reductase enzyme on
converting Androgen (Testosterone)
hormone to the active acnegenic and
potent (Dihydrotestosterone) DHT,
the direct effect of Interleukin-1 on
follicular hyperkeratosis
Fig 1 Fig 2

Fig 3
Perifollicular
Hyperkeratosis histology
Seborrhoea is a common feature between
patients with acne.

2. Abnormal production of abnormal sebum

increasing the ratio of wax ester to
cholesterol and cholesterol ester and is
believed to be the response of sebaceous
glands to DHEA
3. Colonization of the affected unit with
bacteria Propionibacterium acne
and yeast named Malassezia furfur
Fig 4 Fig 5

Malassezia furfur Propionibacterium

acne
 P acne is a potent activator of complement
via classical pathway
Fig 6 Fig 7
Propionobacterium acne lipases act on sebaceous fatty
acid (Triglycrides) to release irritant free fatty acid and
low-molecular- weight peptide an extra cellular factor
that penetrate the follicular wall and stimulate
Polymorphs and Lymphocytes initiating inflammation

Fig 8
 Hydrolytic enzymes released from the
activated complement antibodies complex
together with exoenzymes produced from
P acne cause rupture of follicular wall

Fig 9
 Once the wall is damaged Various agents
(prostaglandin-like substance, amino acid,
short chain fatty acids) that are produced by
the inflammatory cells and P acne extrude to
the dermis causing more inflammation
Clinical features: (Acne and acne
related Disorders)

1. Acne Vulgaris:
Papules: (Less than 0.5 cm)
Comedones (Open Blackheads or closed
Whiteheads)
 Open Comedones (Blackheads)
Fig 10 Fig 11

Open Comedones
Closed Comedones (Whitehead)
Fig 12 Fig 13

Closed Comedones
 Inflammatory papules
Fig 14 Fig 15

Inflammatory
papules
 Pustules :
Fig 16 Fig 17

Pustules
 Nodule (more than 0.5 cm)
Fig 18 Fig 19

Nodule
 Cystic acne: the cysts are usually
large 1-4cm
Fig 20
Fig 21
2. The nodules and cysts could be
associated with sinuses as in Acne inversa

Acne inversea (Hidradenitis suppurativa a

misleading name) because it is considered by
some to be a disorder of apocrine gland (Sweat
gland) but In my opinion Acne inversa affects
primarily the Pilo Seb. Unit and affect secondarily
the sweat gland, hence the correct name Acne
inversa rather than Hidradenitis suppurativa is
preferred.
Fig 22
3. Neonatal Acne and Infantile Acne

Neonatal acne: cause unknown but some

believed is due to passing of
Transplacental androgen other suggest the
role of Mlalassezia furfur and sympodalis .
affect 1 in 5 mainly inflammatory
comedones on nose and cheeks affect new
born between the 1st and 6th week of age
Fig 23
 Infantile Acne: affect males more than
females, usually between 3 and 6 months
of age, and tend to be severer than the
neonatal one and believed to be due to
Endogenic androgen from the infants
gonads.
Fig 24
4. Recalcitrant Acne

Affect Women and associated with (Adrenal

hyperplasia "11-B- or 21-B hydroxlase
deficiencies) acne is usually nodulocystic
5. Acne Fulminans

Affect youngsters 13 17 years of age, very

severe with ulceration and puss discharge,
associated symptoms include (fever,
malaise, myalgia, arthritis and bone pain)
laboratory investigation shows ESR
Can be induced by starting the patient on
high dose of isotretinion (Roaccutane).
Fig 25
6. Acne Conglobata

Very severe Acne, Nodulocystic form with

abscess formation, affect Torso more than
the face, usually associated with XYY
Syndrome.
 Fig 26

Fig 27
7. Acne Agminata (Lupus Milliaris Disseminatus
Faciei)

Some believe it is form of Rosacea

(Granulomatous type), diagnosis is made
at Histological base, Caseating
Granulomata at the dermal level.
Fig 28
8. Acne as part of other syndromes

MARSH Syndrome (Melsma, Acne, Rosacea,

,Seborrhoeic eczema, and Hirsutism)
Acne Conglobata
Favre Racouchot syndrome elderly with elastosis
as part of Helioderma, sun exposure is a
predisposing factor.
Polycystic ovarian syndrome
Atrophoderma vermiculatum as part of so called
Ulerythema ophryogenes, in Noonan Syndrome ,
de Lange Syndrome , and
Rubinstein-Taybi Syndrome Not considered acne
9. Occupational
I Environmental

Chloracne rare forms of acne affect

patients exposed to Halogenated
Hydrocarbons or who ingested Chlorinated
Phenols (Dioxin)
Pomade acne or known as Oil Folliculitis
Acne Aestivalis or so called Mallorca Acne
Occupational
II mechanical acne

Folicullitis Nuchae or so called Acne

Keloidalis
Pseudofollicultis barbae
Acne excoriee as part of Psychodermatosis
 TREATMENT

Note: All medications used for the treatment of

acne act as:
1. Anti comedonal
2. Anti inflammatory
3. Anti microbial
Topical Keratolytic

Retinoid ( Retinoic acid 0.025, 0.05, 0.1%)

Adapalene (Differin 0.1%)
Salicylic acid
Benzoyl peroxide (peeling agent and
antimicrobial)
Azelaic Acid (10, 15, 20 %)
Topical Antibiotic

Topical clindamycin (Dalacin T)

Erythromycin
Mupirocin (Bactroban)
Sodium Fusidic acid (less significant in the
treatment)
Systemic therapy

Antibiotic (Macrolides and Tetracylines)

1. Tetracycline
2. Doxycycline
3. Minocycline (blue grey discoloration and
drug induced LE)
4. Azithromycin
 Systemic Retinoids :
Isotretinoin caps (Roaccutane): 0.5 1 mg/kg
The most effective drug for acne.
Indicated for severe forms (nodulocystic and fulminant) but also for milder
forms associated with scarring or with significant psychological impact.
Relapse is minimal with cumulative dose of 120 150 mg/kg.
Side effects include: cheilitis, dryness, alopecia (less frequent than with
acitretin), photosensitivity, xerophthalmia, decreased night vision,
keratitis, benign intracranial hypertension (incresed risk with concomitant
use of tetracyclines), photosensitivity, hypertriglyceridemia,
hypercholesterolemia, elevated liver enzymes, depression (controversial),
skeletal hyperostosis, myalgias.
Teratogenicity : Retinoid - induced embryopathy. Pregnancy category X.
Pregnancy must be prevented during treatment and for at least 1 month
after discontinuing the drug.
Other forms of therapy
Systemic steroid (Prednisolone): for acne fulminans and
intralesional steriods for cystic acne.
Photodynamic therapy i.e. Laser therapy and phototherapy (Less
significant)
SMT D002 is a new promising and potentially safe medication
(Oxybutynin chloride), it has successfully completed two Phase I
trials in healthy volunteers and believed to treat seborrhoea, a
symptom of Parkinson's disease and the primary cause of acne.
Topical formulation of the drug is currently being developed by
Summit company.
Hormonal therapy (Anti-androgen)
Spironolacton (Potassium sparing agent) and Metformin as
(Hypogylcemic agent) in treatment of PCOS (Polycystic Ovary
Syndrome) have good results on acne
 Rosacea
- A controversial topic in dermatology largely
because of its uncertain pathophysiology and
clinical variation.
- Erythema of the central face that has persisted
for months or more.
- Primary features: flushing, papules pustules and
telangiectases.
- Secondary features: burning, stinging, edema,
plaques, dry appearance, phyma, peripheral
flushing and ocular manifestations.
 Epidemiology
Common in caucasian population
Fair skinned individuals
women>men
Onset typically begins after age 30
 Etiology and pathogenesis
1) Vascular reactivity:
Rosacea is induced by chronic repeated triggers of flushing
exposure, they include:

1) Hot or cold temperature 7) Sunlight

2) Hot drinks
3) Spicy foods
4) Alcohol 8) Emotional
disteress
5) Certain cosmetics 9) Topical
irritants
6) Medications
 Etiology and pathogenesis
2) Dermal matrix degeneration and endothelial
damage
Inherent problems with vessels permeability
Delayed clearance of inflammatory mediators and
waste products
Photodamaged connective tissue (solar elastosis
is a common background on which rosacea
histologic features are superimposed
 Etiology and pathogenesis
The role of microbe induced follicle based
inflammation
Commensal organisms which reside in hair
follicles and sebaceous glands may trigger
folliculocentric inflammatory papules.
Demodex folliculorum (mite) or associated
bacteria (bacillus oleronius).
 Sub-type classification
Sub types were defined by the National Rosacea
Society (NRS) expert committee in 2002.
1) Erythematotelangiectatic : persistent erythema and
telangiectasias on the central face.
2) Papulopustular: papules and pustules predominate on
convex areas on a background of persistent erythema
3) Phymatous: patulous follicular orifices, thickened skin and
nodularity
Most often affect the nose (rhinophyma)
Almost exclusively in men
4) Ocular: Blepharitis is the most common feature (mebomian
gland dysfunction)
Conjuctivitis, iritis, scleritis, keratitis
Fig 29Erythematotelangiectatic
Rosacea
Fig 30 Papulopustular Rosacea
Fig 31 Rhinophyma
 Rosacea variants
Granulomatous rosacea: Rosacea
variant characterised by
monomorphic yellow brown or red
papules/ nodules located on the
cheeks and periorificial skin.
Granulomas on histology
The background facial skin is
otherwise normal
 Differential Diagnosis
Full and detailed history (including medications)is required,
Medications that induce flushing include : all vasodilators,
calcium channel blockers, nicotinic acid, morphine, amyl
and butyl nitrite, cholinergic drugs, bromocriptine,
tamoxifen, cyproterone acetate, systemic steroids and
cyclosporine.
Diagnosis is made clinically
Differential diagnosis include:
Seborrheic dermatitis
Steroid folliculitis/Perioral Dermatitis
Acne vulgaris
Erythromelanosis faciei and keratosis pilaris rubra
Lupus erythematosus
Lupus miliaris disseminatus faciei
 Treatment
Sunscreens
Avoidance of aggravating factors.
Topical medications include:
Metronidazole
Sodium sulfacetamide and sulfur
Azelaic acid
Benzoyl peroxide
Tretinoin
Erythromycin and Clindamycin
 Oral medications include:
Tetracyclines:
Tetracyclines are the most commonly prescribed
oral medications for the treatment of rosacea.
They act by their anti-inflammatory effects
Erythromycin (for children with granulomatous
perioral dermatitis)
Isotretinoin
 Laser and light therapy
Laser and Intense Pulsed light IPL is useful in
treating persistent erythema and telangiectasias
Pulsed dye laser (585 or 595 nm)
Potassium-titanyl phosphate laser KTP 532nm, for
superficial small telangiectasias.
Deep facial vessels require longer wavelengths :
Diode laser (810)
The long pulsed alexandrite laser (755nm)
Long pulse ND:YAG (1064nm)
 Treatment of Phymatous Rosacea
Early to moderate Phymatous changes could be
treated with Isotretinoin.
Advanced phyma is treated with surgery or
surgery followed by isotretinoin.
Scalpel tangential excision
Electrosurgery
Laser CO2 ablation.
Fig 1, 2 www.scf-online.com/.../keratinization38_e.htm keratinization of the duct of the hair
.follicle
open (Blackheads) comedones, Medical Encyclopedia www.nlm.nih.gov/.../ency/imagepages/2087.htm
Fig.3
Fig 4. Malassezia furfur www.doctorfungus.org/thefungi/Malassezia.htm Closed comedones
.Skin and allergy centre
Fig 5
Fig 6 www.ohiohealth.com/bodymayo.cfm?id=6&action=t... Mayo Foundation for Medical and
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Fig 7
Fig 8 bacterial colonization www.healthcaresouth.com/pages/acnewhatis.htm
Fig 9 Breakage of follicular wall www.healthyskinbydesign.com/acne.cfm papule
Fig 10 open comedones www.healthcaresouth.com/pages/acnewhatis.htm
Fig 11
Fig 12 closed comedones www.healthcaresouth.com/pages/acnewhatis.htmfig
www.dermalogix.net/acne/acne.html open and closed comedones schematic pictures
www.dermalogix.net/acne/acne.html proriobionacterium acne in pilosabaceous unit
www.healthyskinbydesign.com/acne.cfm. follicular hyperkeratosis in acne
Fig 13
Fig 14
Fig 15
Fig 16 www.healthyskinbydesign.com/acne.cfm pustule
Fig 17. Courtesy of Skin and allergy centre
Fig 18 www.healthyskinbydesign.com/acne.cfm nodule
Fig 19 nodule www.acnekil.com/What's_Acne/photo_gallery2.htm
Fig 20
Fig 21 Courtesy of Skin and allergy centre
Fig 22 Courtesy of Skin and allergy centre
Fig 23 www.adhb.govt.nz/.../BenignLesions.htm at neonatal dermatology benign lesions
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Fig 24 Courtesy of Polonia, second edition
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