1. Acne Vulgaris
TSMU

2. Definition
Acne vulgaris, more commonly referred to simply as
acne, is a chronic inflammatory disorder of the
pilocebaceous unit.
characterized by:
 abnormalities in sebum production
 follicular desquamation
 bacterial proliferation
 inflammation

3. Overview
 Acne vulgaris is the most common cutaneous disorder.
 It affects more than 17 million Americans.
 Patients can experience significant psychological morbidity
and, rarely, mortality due to suicide.
 Important that physicians are familiar with Acne Vulgaris and
its treatment.
 affects all races and ethnicities with equal significance.
 Darker skinned patients at increased risk for developing
post-inflammatory hyper-pigmentation and keloids.

4. Etiology
Acne is polygenic and multi-factorial. Four main pathogenetic
factors contribute to the disease:
• Propionibacterium acnes and Staphylococcus epidermidis
colonisation. :
bacteria found deep in follicles and stimulate the production
of pro-inflammatory mediators and lipases.
• Inflammation and immune response. Inflammatory cells and
mediators efflux into the disrupted follicle, leading to the
development of papules, pustules, nodules, and cysts.
• Sebaceous gland hyperplasia and excess sebum production.
• Abnormal follicular differentiation.

5. Propionibacterium Acne
Propionibacterium acne is a gram-positive, non-motil rods relatively
slow growing typically aerotolerant anaerobic gram positive bacterium

6. Staphylococcus epidermidis
• S. epidermidis is a very hardy microorganism, consisting of
nonmotile, Gram-positive cocci, arranged in grape-like clust-
ers.is part of human skin flora and consequently part of human
flora. Although S. epidermidis is not usually pathogenic,
patients with compromised immune systems are often at risk
for developing acne.

7. Pathophysiology
• The initial step in the development of acne is the formation of
the microcomedo.Follicular keratinocytes that exhibit increas-
ed cohesiveness do not shed normally, leading to retention
and accumulation.
• Androgens stimulate enlargement of sebaceous glands and
increased sebum production, and the abnormal keratinaceo-
us material and sebum collect in the microcomedo.
• This leads to a build-up of pressure, and whorled lamellar
concretions develop. At this stage, a non-inflammatory
comedo may be seen clinically.

9. • This micro-environment allows the proliferation of bacterium,
which is part of the normal flora of follicles. This gram-positive
rod has low virulence but is capable of metabolising
triglycerides and releasing free fatty acids.This metabolism,
as well as its ability to activate complement, produces pro-
inflammatory mediators, including neutrophil chemo-
attractants.
• With increased pressure and recruitment of inflammatory
mediators, the microcomedo may rupture and release
immunogenic keratin and sebum, thus stimulating an even
greater inflammatory response

10. • Depending on the specific inflammatory cells present,suppur-
ative pustules or inflamed papules, nodules, or cysts may
develop. If a sufficient amount of inflammation and tissue
damage results, post-inflammatory hyperpigmentation and
scarring may result.

12. Clinical Manifestations:
• Closed comedone (whitehead) - a clogged follicle.
Whiteheads usually appear on the skin as small, round, white
bumps.
• Open comedone (blackhead) - a plugged follicle that opens
and turns dark at the surface of the skin. Blackheads do not
indicate the presence of dirt.
• Papules - inflamed lesions that appear as small, pink bumps
on the skin.
• Pustules (pimples) - inflamed pus filled lesions that are red at
the base.
• Cysts and nodules - large, inflamed, pus filled lesions deep
under the skin that can cause pain and scarring.

13. • Local symptoms :
include pain
tenderness.
• Systemic symptoms :
most often absent
Severe acne with associated systemic signs and symptoms
such as Fever, Psychological impact on any patient

14. Closed comedones (whiteheads)
Accumulation of sebum converts a microcomedo into this.

15. Open comedones (blackhead)
when follicular orifice is opened and distended.
Melanin + packed
keratinocytes + oxidized
lipids  dark colour

16. Whitehead and blackheads

17. Pustules
inflamed pus filled lesions that are red at the base.

18. Cysts
• Cysts:
when follicles rupture into
surrounding tissues, resulting
in papule/pustule/nodule.

19. Classification
• Classification system generally as follows
• Type 1 — Mainly comedones with an occasional small inflamed
papule or pustule; no scarring present
• Type 2 — Comedones and more numerous papules and pustules
(mainly facial); mild scarring
• Type 3 — Numerous comedones, papules, and pustules, spreading
to the back, chest, and shoulders, with an occasional cyst or nodule;
moderate scarring
Type 4 — Numerous large cysts on the face, neck, and upper trunk;
severe scarring

20. Diagnosis
• Complete history
• Pay attention to endocrine function
- Rapid appearance with virilization/menstrual irregularity
• Complete medication list
• Physical exam:
- Location - scarring
- Lesion type - keloid
- pigmentation

21. LABORATORY EXAMINATION
No laboratory examinations required. If there is suspicion of
an endocrine disorder, free testosterone, follicle-stimulating
hormone, luteinizing hormone, and DHEAS should be deter-
mined to exclude hyperandrogenism and polycystic ovary
syndrome.
majority of acne patients, hormone levels are normal.
Laboratory examinations
transaminases(ALT, AST), triglycerides, and cholesterol
levels may be required if systemic isotretinoin treatment is
planned
DHEAS - Dehydroepiandrosterone

22. DIFFERENTIAL DIAGNOSIS
• Comedones are required for diagnosis of any type of acne.
Comedones are not a feature of acne-like conditions and of the
conditions listed below.
• Face - S. aureus folliculitis, pseudofolliculitis barbae, rosacea,
perioral dermatitis.
• Trunk -Malassezia folliculitis, “hot-tub” pseudomonas folliculitis,
S. aureus folliculitis, and

23. Treatment
The goals of pharmacotherapy for acne vulgaris are to reduce
morbidity and to prevent complications.
Medication: Benzoyl Peroxide Antibiotics,Topical and Oral
retinoids
Benzoyl Peroxide :
Benzoyl peroxide is a first-line treatment for mild and
moderate acne vulgaris due to its effectiveness and mild side-
effects

24. Antibiotics:
• Topical and systemic antibiotics used in the treatment of
acne vulgaris are directed at Propionibacterium acnes.
They also have anti-inflammatory properties.
 Minocycline
 Doxycycline
 Tetracycline

25. Retinoids:
• These agents decrease the cohesiveness of abnormal hyperproliferative
keratinocytes, and they may reduce the potential for malignant degene-
ration. They also modulate keratinocyte differentiation.
 isotretinoin
 Tretinoin topical
 Adapalene
 Tazarotene

26. Alternative treatments
• Phototherapy with blue and red light emitted from special
fluorescent lights, LEDs, lasers, or dichroic bulbs.
• Photodynamic therapy involving intense blue or violet light,
• zinc, teat tree oil, heat therapy, salt water therapy are all
used for treating acne.

27. Prognosis
Acne of any severity usually remits spontaneously by the
early to mid-20s,but a substantial minority of patients,
usually women, may have acne into their 40s.