OXYDATIVE STRESS IN THE PATHOGENESIS OF

ACNE VULGARIS

Indah Yulianto., Yulianto D.,Moerbono M.,Prasetyadi M

DEPARTMENT OF DERMATOLOGY,
MEDICAL FACULTY OF SEBELAS MARET
UNIVERSITY/dr. MOEWARDI GENERAL HOSPITAL
SURAKARTA
THE AETIOPATHOGENESIS OF
ACNE IS MULTIFACTORIAL
Oil Production :
Stagnant behind
impaction
 SEBUM PRODUCTION

Increased sebum Sebum lipid-rich material

Production does not Contains
Correlate with Triglyceride & linoleic
Acne severity acid

Androgen stimulates enlargement

Of sebaceous glands
Increase sebum production
Where it all begins

Large sebaceous gland

Small hair follicle
Acroinfundibulum
site of focal nerrowing
site of blackage
 THE COMEDO

Keratinocyte proliferate
And stick together

PMNs migrate to site

Bacteria multiply and as part of
colonize follicle inflammatory
response
Androgen Metabolism of Sebocyte
 INFLAMMATION
Main Causes :
IL-1,Il-8, IL-10,TNF-
& other cytokines and
signal molecules produced
by keratinocyte,sebocyte and
immune system cells due to
FAs, P acnes,ROS
T cellular & humoral
immune response:
early Lymp infiltarte CD4 + -
CD8+
Recruitment neurophil/leucocyte
Macrophag activation
Complement activation
P acnes antigen Response to P acnes
(GehA,other due to HLA-DR to
enzymes,chemotactic Langerhans cells and
factors,HSP ) and basal
mitogen production
keratynocytes,persisten
ce of P acnes in
macrophages antibody
production etc
 Hormone production :
Adrenal/gonadal androgens (tetosteron, etc) due to
neuroendocrine factoers : puberty, hiperandrogenic woman,
diet induced hyperinsulinemia, etc
Hormone effect in
CRH stress, and orther.
the sebacceous
follicle Sebacecaous follicle sensibility :
Andogen and CRH receptors

5 -reductase activity (tetosteron DHT (more active))

Nervus Additional comedogenic factors :

stimulation (SP), Cosmetic, drugs (corticoids, androgens,
stress, etc vitamin B, lithium, etc), autosomal-dominant
inhereted familiar traits,etc

Sebum production : Ductal plugging (hypercornification)

Proliferation and differentiation of sebocytes Ductal keratinocytes of the follicle :

( sebaceous galnds hypertrophy ) * Proliferation and differentiation
Accumulation of lipids and granules
Sebocyte lipogenesis and secretion Packing ( desmosomes,
tonofilaments, etc)
 Nervus Additional comedogenic factors :
stimulation (SP), Cosmetic, drugs (corticoids, androgens,
stress, etc vitamin B, lithium, etc), autosomal-dominant
inhereted familiar traits,etc

Sebum production :
Ductal plugging (hypercornification)
Proliferation and differentiation of sebocytes (
sebaceous galnds hypertrophy )
Ductal keratinocytes of the follicle :
* Proliferation and differentiation
Sebocyte lipogenesis and secretion
Accumulation of lipids and granules
Packing ( desmosomes,
tonofilaments, etc)
Hipercornification
Hypodesquamation

Comedo P. Acnes
* Duct colonization and biofilm formation
Plug formation,
accumulation of sebum,
cell debris, and IL-I

Anaerobis

TAGsGlyserol + Fas
(95 % GehA; 5%
sebocytes, ec )
 Accumulation of lipids and granules
Packing ( desmosomes,
tonofilaments, etc)
linoleic acid Hipercornification
Hypodesquamation

Comedo P. Acnes
Impaired * Duct colonization and biofilm formation
epidermal Plug formation,
barrier accumulation of sebum,
cell debris, and IL-I

Anaerobis FAs
Water influx
TAGsGlyserol + Fas
(95 % GehA; 5%
sebocytes, ec )
Inflamation
Cellular anf Humoral immune
response :
Early Lymphocyte infiltarte (
P acnes CD4+ > CD8 +)
* Recruitment of Neutrophiles/
Acnes Lipase (GehA)
Production of propionic and other acids Leukocyt
Other enzymes : proteases, Macrophage activation
Hyaluronidases, etc Complement activayion :
HSP, surface proteins, and others classic and alternative
Antigens, chemotactic factors, and mitogens pathways
 Anaerobis FAs
Water influx
TAGsGlyserol + Fas
(95 % GehA; 5%
sebocytes, ec )
Inflamation
Cellular anf Humoral immune response :
Early Lymphocyte infiltarte ( CD4+ >
P acnes CD8 +)
* Recruitment of Neutrophiles/ Leukocyt
Macrophage activation
Acnes Lipase (GehA) Complement activayion : classic and
Production of propionic and other acids alternative pathways
Other enzymes : proteases,
Hyaluronidases, etc Main Causes :
HSP, surface proteins, and others IL -1, IL-8 ,IL-10,TNF , and of
Antigens, chemotactic factors, and other pro-inflamatory cytokines and
mitogens signal molecu les produced by
kertinocytes, sebocytes, and immune
system cells due to Fas and other
irritants ( squalance peroxides produced
by P. acnes metabolization of sebum,
Sebaceous follicle damage neutrophile and other phagocyte
released hydrolases and reactive oxygen
species, cell-content from hydrolyzed
Keratynocytes damage and breakage of the follicle cells, Linoleic acid epithelium
comedo : barrier, keratin and hair effect on dermis,
Production of pro-inflamatory cytokines etc)
* Release of comedo inflamatory-irritant
content of dermis P. acnes antigens (GehA, other
P. granulosum enzymes, chemotactic factors, HSP, etc)
S. epidemidis and miogens production

Response to P. acnes antigens due

Pressure, friction, to HLA-DR of Langerhans cells, and
excessive Extension of inflamation to dermis basal keratynocytes, persistence of P.
scrubbing or acnes in macrophages, antibody
washing, etc (papules, pustules, cysts, nodules)
production, etc.