1. Acne
By Lee so hee

2. Burden of Disease Acne Most common skin disease
Can cause disfigurement and permanent physical scarring
Can cause emotional and psychological scarring as well

3. Burden of Disease
Acne
Social, psychological and emotional impairment reported to be similar to that associated with epilepsy, asthma, diabetes and arthritis
Scarring can lead to lifelong problems with self-esteem

4. Pathophysiology Acne: A Disease of Pilosebaceous Units
Exist all over body except palms and soles
Most concentrated on face, chest and upper back
Make sebum which maintains hydration of the skin and hair
Lined by keratinocytes
Contains hair follicle
병이 어떻게 생기고, 어떻게 진행되고, 결국 어떻게 되는가.....

5. Pathophysiology
Normal pilosebaceous unit:
Image courtesy

6. Pathophysiology Pathogenesis of Acne: Four key factors
Excess sebum production
Comedogenesis
Propionibacterium acnes colonization
Inflammation

7. Pathogenesis 1. Excessive sebum production
Due to sebaceous gland hyperplasia
Thought to be related to androgen activity, but precise role unclear
5α-reductase type 1 is present in sebaceous gland and converts testosterone to dihydrotestosterone (DHT)

8. Pathogenesis Comedogenesis:
Hyperproliferation of follicular epithelial cells
May be related to lower levels of linoleic acid in sebum
Prevents normal shedding of follicular keratinocytes
Leads to plugging of the follicle and creates a microcomedo
Lipid and cellular debris build up within the microcomedo
Exact mechanism not understood

9. Pathogenesis Microcomedo Earliest microscopic lesion
Characterized by follicular plugging
No bacteria or inflammation
Image courtesy of

10. Pathogenesis Microcomedones can evolve into: Noninflammatory lesions
Closed and open comedones
Can remain stable for long periods of time or turn into inflammatory lesions
Inflammatory lesions
acne pustules, papules, nodules and cysts

11. Pathogenesis Open and closed comedones
Open comedo – “blackhead” – follicular opening reaches skin
Dark discoloration is not dirt
Closed comedo – “whitehead” follicular opening remains beneath skin
Images courtesy of

12. Pathogenesis Propionibacterium acnes colonization
Anaerobic diphtheroid
Part of normal skin flora
Proliferates inside plugged follicle
Microcomedo fills with P acnes
Provokes an immune response through inflammatory mediators

13. Pathogenesis Inflammation – due to P acnes
P acnes hydrolyzes the triglycerides and creates free fatty acids
Fatty acids penetrate dermis causing inflammation
P acnes also secretes chemotactic and pro-inflammatory factors that recruit neutrophils and lymphocytes to follicular epithelium
Inflammatory cells surround follicle, diffuse through follicular wall and make enzymes that disrupt follicular wall

14. Pathogenesis Inflammation – cont.
Follicular wall ruptures and leaks lipids, fatty acids and bacteria into dermis
This causes more inflammation and characteristic acne lesions
Degree of inflammation may be dependent on individual immune response to P acnes

15. Pathogenesis

16. Epidemiology of Acne
J Am Acad Dermatol 1995 May;32(5 Pt 3):S6-14.

17. Epidemiology of Acne Subtypes of Acne Intrinsic Acne Extrinsic Acne
Acne Vulgaris – most common
Acne Fulminans
Perioral Dermatitis
Extrinsic Acne
Acne Cosmetica
Drug Induced
Childhood Acne
Acneiform Eruptions
Rosacea
Steroid Acne

18. Epidemiology of Acne Acne Vulgaris Peak incidence at puberty M>F
Close to 100% prevalence in teenage boys
Prevalence drops to <5% in adults age 35-44yrs

19. Epidemiology of Acne Acne Vulgaris in Women
As age increase, acne become more common in females than males
At age 40, found in 1% of males and 5% of females
70% of females have flare 2-7 days prior to menses
Pregnancy can cause flares or improvement
Look for PCOS in women with severe acne, irregular menses, hirsutism

20. Epidemiology of Acne Myths of Acne Vulgaris
Eating chocolate or rich/oily foods not associated
Skin is not “dirty” – aggressive cleaning does not help
No clear association with stress – may be from touching/picking at face while stressed
Sunlight never found to improve acne

21. Classification of Acne
Classification of Acne Vulgaris
No great classification system
Based on 1990 American Academy of Dermatology guidelines
Mild Acne – Few to several papules and pustules but no nodules
Moderate Acne – Several to many papules and pustules with a few nodules
Severe Acne – Numerous papules and pustules as well as several nodules

22. Classification of Acne
Classification of Acne Vulgaris
Can also classify based on type of lesion
Comedonal (Non-inflammatory)
Papulopustular or Nodulocystic (Inflammatory)

23. Topical Treatments Benzoyl peroxide
Generally considered first-line therapy
Inexpensive and available over the counter
Bactericidal
Has not been shown to induce bacterial resistance
Primary side effects are skin drying and irritation

24. Topical Treatments Superior to tretinoin, equal to Retin-A Micro
Retinoids: Normalize desquamation of the epithelium, preventing obstruction of the pilosebaceous outlet. Prevents formation of new comedones. Maximal response occurs over 12 weeks.
Adapalene (Differin)
Superior to tretinoin, equal to Retin-A Micro
Less irritation
Tazarotene (Tazorac)
Superior to tretinoin and adapalene in some studies
Most irritating

25. Topical Treatments
Antimicrobials: More effective for inflammatory lesions than retinoids. When used as monotherapy induction of microbial resistance is a major issue. Combination with benzoyl peroxide mitigates this problem.
Clindamycin (Cleocin)
Erythromycin
Sulfacetamide (Klaron)
Azelaic acid (Azelex)
There are preparations of clindamycin + benzoyl peroxide (BenzaClin) and erythromycin + benzoyl peroxide (Benzamycin) that are available

26. Oral Treatments
Antibiotics: Indicated for moderate to severe disease or in patients for whom topical treatments have failed
Erythromycin
Has become 2nd line because of microbial resistance
Tetracycline
Moderate to severe phototoxicity and GI intolerance
Cheap
Doxycycline
Minocycline
Potent acne medication
Generally reserved for doxycycline or tetracycline refractory cases because of rare but severe side effects
TMP-SMX

27. ORAL TREATMENTS Hormonal therapy OCs Useful adjunct in female patients
Decrease circulating androgens, thereby decreasing sebum production
Choose a formulation with progestins of low androgenic potential such as norethindrone (Norlutin), ethynodiol (Zovia), and norgestimate (Ortho-Cyclen)
Spironolactone
Best if used in combination with OCs

28. ORAL TREATMENTS Isotretinoin (Accutane)
Used to treat severe, nodulocystic inflammatory acne
Affects all four pathogenetic factors of acne: reduces size and secretion of sebaceous glands inhibits growth of P. acnes reduces inflammation normalizes differentiation of follicular keratinocytes
Only treatment that can suppress acne over the long-term and possibly induce permanent remission
40% have remission after one treatment, 40% have a mild recurrence that is responsive to medications that did not work previously, and 20% need retreatment

29. ORAL TREATMENTS Isotretinoin Continued Side effects
Extremely teratogenic (females must be on 2 forms of birth control during use)
Monthly monitoring of LFT’s and triglyceride levels is required
The link between isotretinoin and depression remains controversial

32. References
Chiu A, Chon SY, Kimball AB. The response of skin disease to stress. Arch Dermatol 2003;139: Feldman S, Careccia RE, Barham KL. Diagnosis and treatment of acne. Am Fam Physician 2004;69: ,