ACNE VULGARIS

• Acne vulgaris is a self-limited disorder of the

pilo- sebaceous unit that is seen primarily in
adolescents.
• While the course of acne may be self-limiting,
the sequelae can be lifelong, with pitted or
hypertrophic scar formation.
 ETIOLOGY AND PATHOGENESIS
• These key elements are: (1) follicular
epidermal hyperproliferation, (2) excess
sebum production, (3) inflammation, and (4)
the presence and activity of Pro-
pionibacterium acnes.
 A. Microcomedo
• Follicular epidermal hyperproliferation results in the formation of a
microcomedo
• The epithelium of the upper hair follicle, the infundibulum, becomes
hyper- keratotic with increased cohesion of the keratinocytes
• The excess cells and their tackiness result in a plug in the follicular ostium.
• This plug then causes down- stream concretions of keratin, sebum, and
bacteria to accumulate in the follicle
• hese packed concretions cause dilation of the upper hair follicle producing
a microcomedo.
• The stimulus for keratinocyte hyperproliferation and increased adhesion is
unknown. However, several proposed factors in keratinocyte
hyperproliferation include: androgen stimulation, decreased linoleic acid,
increased interleukin-1 (IL-1) α activity, and effects of P. acnes.
Dihydrotestosterone (DHT) is a potent androgen that may play a role in
acne
 B. Comedo
• The second key feature in the pathogenesis of acne is excess sebum
production from the sebaceous gland.
• Components of sebum— triglycerides and lipoperoxides—may play a role
in acne pathogenesis. Triglycerides are broken down into free fatty acids
by P. acnes, normal flora of the pilosebaceous unit. These free fatty acids
promote further bacterial clumping and colonization of P. acnes, incite
inflammation, and may be comedogenic.
• Lipoperoxides also produce proinflammatory cytokines and activate the
peroxisome proliferator-activated receptors (PPAR) pathway, resulting in
increased sebum.
• Androgenic hormones also influence sebum production through actions
on sebocyte proliferation and differentiation.
 C dan D
• The microcomedo will continue to expand with densely packed keratin,
sebum, and bacteria.
• Eventually this distension will cause follicular wall rupture. The extrusion
of the keratin, sebum, and bacteria into the dermis results in a brisk in
ammatory response.
• The predominant cell type within 24 hours of comedo rupture is the
lymphocyte. CD4+ lymphocytes are found around the pilosebaceous unit,
while CD8+ cells are found perivascularly.
• One to two days after comedo rupture, the neutrophil becomes the
predominant cell type surrounding the burst microcomedo.
• P. acnes also plays an active role in the process of inflammation. P. acnes is
a Gram-positive, anaerobic, and microaerobic bacterium found in the
sebaceous follicle. Adolescents with acne have higher concentrations of P.
acnes compared to nonacne controls.
 CLINICAL FINDINGS
• History :
- Hyperandrogenism should be considered in the female
patient whose acne is severe, sudden in its onset, or
associated with hirsutism or irregular menstrual periods.
- Drug-induced acne may be caused by: anabolic steroids,
corticosteroids, cor- ticotropin, phenytoin, lithium, isoniazid,
vitamin B complexes, halogenated compounds, and certain
che- motherapy medications, particularly with epidermal
growth factor receptor (EGFR) inhibitors
• CUTANEOUS LESIONS :
- The primary site of acne is the face and to a
lesser degree the back, chest, and shoulders.
• The lesions may be either noninflammatory or
inflammatory.
• The noninflammatory lesions are comedos, which
may be either closed (whiteheads) or open
(blackheads).
• The open comedo appears as a at or slightly raised
lesion with a central dark-colored follicular impaction
of keratin and lipid. Closed comedones, in contrast to
the open comedones, may be difficult to visualize.
They appear as pale, slightly elevated, small papules,
and do not have a clinically visible orifice (Fig. 80-3A).
• Scarring can be a complication of both noninflammatory and
inflammatory acne. There are four general types of acne scars:
o (1) ice pick,
o (2) rolling,
o (3) box-car, and
o (4) hypertrophic
 TREATMENT
The mechanism of action of the most common treatments for
acne can be categorized in the following categories as they relate
to the pathophysiology:
• Correct the altered pattern of follicular keratinization.
• Decrease sebaceous gland activity.
• Decrease the follicular bacterial population,
• particularly P. acnes.
• Exert an anti-inflammatory effect.