Disorders of Sebaceous Gland

Anatomy and physiology

• In humans, pilosebaceous units or pilosebaceous follicles are found on
all skin surfaces, except palms and soles

• Each comprises a duct, which ends in the dermal papilla, a hair fiber (or
pilus) produced by the dermal papilla, a sebaceous gland and its
associated sebaceous duct

• The duct supports and protects the hair fiber and also drains sebum
produced by the sebaceous gland and carries it to the skin surface.

• Three types of pilosebaceous units may be distinguished

histologically: the terminal follicle, the vellus follicle, and the sebaceous
follicle
• The pilosebaceous duct is lined by a stratified, squamous
epithelium consisting of keratinocytes

• Sebaceous glands form from the outgrowths of the outer root

sheaths of hair follicles and are clearly visible by the 15th
week of fetal life

• They consist of either a single lobule (acinus) or a collection

of acini

• The sebaceous duct is lined by a thin epithelium consisting

mainly of a basal and granular layer

• The glands are separated from the dermis by a connective

tissue capsule, consisting of fine collagen fibers, fibroblasts,
and a capillary plexus
• The cells of sebaceous glands, called sebocytes, which are
modified keratinocytes

• Sebum is an oily liquid containing triglycerides, free fatty

acids, wax esters, squalene, and a little cholesterol produced
by the gland, modified by bacteria that hydrolyze
triglycerides to produce free fatty acids

Composition of Sebum
Function of sebum
• The lipid film both controls moisture loss from the epidermis
and protects the skin from fungal and bacterial infection

• The sebaceous gland has also been shown to secrete

vitamin E into the upper layers of facial skin

• This mechanism may in part serve to protect skin surface

lipid and the upper stratum corneum from harmful oxidation
 Acne vulgaris: overview
Definition:
Multi-factorial disease characterized by abnormalities in
sebum production, follicular desquamation, bacterial
proliferation and inflammation.

Prevalence:
 85% adolescents experience it
 Prevalence of comedones (lesions) in adolescents
approaches 100%
 affects 8% of 25 - 34y yr olds, and 3% of 35-44yr olds
 Overview

 Acne vulgaris is one of the common cutaneous disorder

 10 percent of all patient encounters with primary care

physicians

 Pts can experience significant psychological morbidity

and, rarely, mortality due to suicide.

 Important that physicians are familiar with Acne Vulgaris

and its treatment.
 Overview

 affects all races and ethnicities with equal significance

 Darker skinned patients at increased risk for developing

post-inflammatory hyper-pigmentation and keloids.
 Contributory Factors
• Acne may develop de novo in adulthood.

• Post-adolescent acne predominantly affects women

(76%):
-hyperandrogenous
-family history in half
-premenstrual flares in older women

• Adolescent acne has a male predominance

• Most pts with acne likely have glands locally hyper-
responsive to androgens.

• Other factors can cause increased androgen production

• Higher serum levels of DHEA-S are found in pre-pubertal

girls with acne

• Acne tends to resolve in the third decade as DHEA-S

levels decline

• Medication induced
 Medications that can cause acne

• Disulfiram
ACTH
• Azathioprine
Halogens
• Barbiturates
Iodides
• Isoniazid
Steroids
• Lithium
Cyclosporine
• phenytoinB2,6,12
Vitamins
 Pathogenesis:

Acne vulgaris is a disease of

pilosebaceous follicles.

Factors:
•  Retention hyperkeratosis.

•  Increased sebum production.

•  Propionibacterium acnes
within the follicle.

• Inflammation
 Initial pathogenesis (reason unknown):

follicular hyperkeratinization

proliferation +
decreased desquamation of keratinocytes

hyperkeratotic plug
(microcomedone)
 Pathogenesis

Sebaceous glands enlarge

Sebum production increases

Growth medium for P. Acnes

plugs provide anaerobic

Lipid-rich environment
 Pathogenesis

Bacteria thrive

Inflammation results (IL-1α, IL 8,12,TNF)

Chemotactic factors attract neutrophils

Depending on conditions

Non-inflammatory Inflammatory papule/

open/closed comedones pustule/nodule
Acne pathogenesis

(IL-1α, IL 8,12,TNF)
Acne pathogenesis
 Classification
• Grade 1 — Mainly comedones with an occasional small
inflamed papule or pustule; no scarring present
Mild
• Grade 2 — Comedones and more numerous papules and
pustules (mainly facial); mild scarring

• Grade 3 — Numerous comedones, papules, and pustules,

spreading to the back, chest, and shoulders, with an Moderate
occasional cyst or nodule; moderate scarring

• Grade 4 — Numerous large cysts on the face, neck, and Severe

upper trunk; severe scarring
 Terms/Definitions
• Microcomedone:

hyperkeratotic plug made of sebum and keratin in follicular canal

 Closed comedones (whiteheads)

closed comedo
(a whitehead):

Accumulation of sebum
converts a microcomedo
into this
Closed comedones (whiteheads)
 Open comedo (blackhead)

open comedo
(a blackhead):
when follicular orifice is
opened + distended.

Melanin + packed
keratinocytes + oxidized
lipids  dark colour
Open comedo (blackhead)
Whitehead and blackheads
 Papule,Pustules,Nodule

When follicles rupture into

surrounding tissues, resulting
in papule/pustule/nodule
Acne Conglobata
• Severe nodular acne with more
involvement of the trunk than the
face. Coalescing nodules, cysts,
abscesses, and ulceration;
occurs also on buttocks.
• Spontaneous remission is long
delayed
Acne Fulminans
• Teenage boys (ages 13 to 17).
• Acute onset , severe cystic acne
with concomitant suppuration
and always ulceration,malaise,
fatigue, fever, generalized
arthralgias,leukocytosis, and
elevated ESR
Pomade acne
• Pomades are greasy
preparations used to defrizz
curly Negroid hair.
• The rash is similar to cosmetic
acne and consist predominantly
of many non-inflamed lesions
around the forehead and other
areas where greasy pomades
may extend onto the hairless
skin
• Granulomatous/lymphoedematous
acne
• This is sometimes reported as solid
facial oedema in association
with acne
• Solid symmetrical or asymmetrical
facial oedema is likely to be due to
pre-existing hypoplastic lymphatics.
Occupational acne
Oil and tar acne
• This acneiform eruption occurs in
areas of skin that are in contact
with oils and crude tars
Chloracne
• This variant is part of a syndrome
that follows exposure to certain
toxic, chlorinated hydrocarbons.
• Chloracne lesions consist of Chloracne
multiple comedones; inflammatory
lesions are infrequent
Acne Excoriée
• Mild acne, usually in young
women, associated with
extensive excoriations and
scarring due to emotional and
psychological problems
(obsessive compulsive disorder)
SAPHO Syndrome
• Synovitis, acne, acne fulminans,palmoplantar pustulosis,
hidradenitis suppurativa, hyperostosis, and osteitis

PAPA Syndrome
• Sterile pyogenic arthritis,pyoderma gangrenosum, acne
An inherited autoinflammatory disorder
 Diagnosis

• Complete history
• Pay attention to endocrine function
- Rapid appearance with virilization/menstrual irregularity
PCOS and other syndromes
• Complete medication list
• Physical exam:
- Location - scarring
- Lesion type - keloid
- pigmentation
 Treatment of Acne Vulgaris

• Depends on type of clinical lesions

• Choose vehicle for topical tt. Accrding to pt’s skin type

(gel for oily, cream for dry skin)

• Microcomedone matures in 8 weeks

• Therapy must continue beyond this time frame

• Considerable heterogeneity in the acne literature, and no

clear evidence-based guidelines are available
 Comedonal acne

Process
Increased sebum + abnormal desquamation

• To reduce sebum production no other effective rx apart

from hormonal therapies or oral isotretinoin

• Hence Rx of abnormal keratinization is most effective

 Comedonal acne

Topical retinoids:

• Normalize keratinization
• only agents that affect terminal differentiation of follicular
epithelium.
• initial drugs of choice

 All transretinoic acid (tretinoin): C/I in pregnancy.

 Adapalene gel (no studies for pregnancy)
 Isotretinoin (tazoretene) : keratolytic, C/I in pregnancy
Issues with topical retinoids

• Photosensitivity – use in pm, sunscreen

• Local irritation – start lowest strength.

• Pustular flare during first few wks of Rx sign of

accelerated resolution.
Other topical agents:

• Useful when topical retinoids not tolerated

 Salicylic acid (promotes desquamation)

 Azelaic acid (antimicrobial, reduces hyperpigminetation)
 Gycolic acid
 Sulfur in OTC rx (keratolytic)
Mechanical removal of comedones

• Useful adjunct to topical rx

 Mild to moderate inflammatory acne

• Benzoyl peroxide: (antimicrobial, anticomedonal,

pregnancy risk C)

• Topical antibiotic

• Combination of both

• Combination rx more effective than mono in increased

inflammatory lesions.
 Mild to moderate inflammatory acne

Topical antibiotics
• Eliminate P. Acne
• Reduce inflammation

 Clindamycin
 Erythromycin
 Tetracycline
 Metronidazole
 Azelaic acid
 Moderate to severe acne

• If topical Rx not effective  oral isotretinoin

 oral antibiotics
 hormonal rx

• Oral isotretinoin
• Reduces sebaceous gland size/sebum production
• regulates cell proliferation and differentiation
• Effect last 1 yr after cessation
• Only med altering course of A. Vulgaris
 Moderate to severe acne
oral isotretinoin
• Adverse effects can be severe:
• Inc TG, teratogenic, bone marrow suppression,
hepatotoxicity, top 10 drugs for suicide/depression
reports.
• FDA practice rules:
2 negative pregnancy tests before rx
Pregnancy test each month (bring pt in)
physicians need authorization before prescribing
Pregnancy risk pts must use 2 contraceptive for at least
1 mo prior to rx. (manufacturer—must commit to 2 contracept.)
• Monitoring parameters: CBC w/ diff, ESR, glucose, Chol,
TG, LFT, CPK
• Obtain baseline, then regular intervals.

• LFT 1-2 x week until response to rx

• Lipids 1-2 x week until response to rx.
 Moderate to severe acne
• Oral antibiotics

-Tetracycline - erythromycin
- minocycline - TMP-SMX
- doxycycline - clindamycin

• Given daily over 4-6 mo, with taper.

 Moderate to severe acne:
• Practices to reduce resistance

• Use antibiotics if absolutely necessary

• Concomitant use of Benzyl peroxide may reduce

resistance

• If antibiotics are stopped and need to be restarted,

prescribe the same antibiotics
 Moderate to severe acne
• Hormone rx
• Unresponsive acne
• Send for Gyn eval if hirsutism/menstrual irregularities.
• Consider adult onset congenital adrenal hyperplasia,
ovarian/adrenal tumour, Cushing’s dz /syndrome, PCOS
(hirsutism, acne, irregular menses, acanthosis nigrans, insulin resistance)

• Anti-androgens (spironolactone, flutamide, ketoconazole,

cimetidine)
• Estrogen
• Min 3-6 mo of rx
Treatment algorithm for acne
Classifi cation of acne vulgaris and acne fulminans with therapeutic results
Thank You