This presentation includes etiology, pathogenesis, grading and sequelae of acne.

1. ETIOPATHOGENESIS OF
ACNE VULGARIS
DR.SMRUTI R

2. ACNE VULGARIS
DEFINITION:
Acne is a chronic ,self limiting ,inflammatory
disease of the pilosebaceous units, manifesting
generally in adolescence with pleomorphic
lesions like comedones , papules, pustules
nodules and cysts and these may lead to
scarring.

3. EPIDEMIOLOGY
 Typically Occurs Around Adolescence
 Peak Incidence –A) Males – 16-19 Years
 B) Females 14-17 Years
 Sex – Males > Females ( Androgenic Activity)
 Genetic Factors Influence The Susceptibity To Acne.
 Can Present In Neonate, Can Persist Beyond
Adolescence In Susceptible Individuals

4. PATHOGENESIS OF ACNE -
1. Hormonal regulation
2. Sebaceous Hyperplasia With Seborrhea
3. Altered Cornification And Differentiation
4. Colonization Of The Duct By Microbial Flora
5. Inflammation And Immune Response
6. Other Factors

5. HORMONAL CAUSES-
• Increased Sebum Secretion Can Be Due To –
1. Hormonal regulation –
a) Increase Sebum Production – Androgens , ACTH, Alpha
MSH, GH , Prolactin, Thyroid, Melacortin, EGF,IGF-1.
b) Decrease sebum production – Estrogen norprogesterone
Drugs like 5alpha reductase inhibitors, ranitidine,
cimetidine flutamide spironolactone.
2. Decreased SHBG Increase In Free Androgen
Availability
3. Increased Target Cell Response.
4. Increased Receptors And Androgen Binding Capacity Of
Target Cells.

6. SEBACEOUS HYPERPLASIA AND SEBORRHOEA-
 COMPOSITION OF SEBUM –
1. Triglycerides and free fatty acids (57.5%)
2. Wax esters ( 26%)
3. Squalene (12%)
4. Cholesterol esters (3%)
5. Cholesterol (1.5%)
 Lower levels of linoleic acid → accumulation of cornified
cells .
 FFA is important in causation of inflammation.

7. ALTERED CORNIFICATION AND DIFFERENTIATION -
 Increased sebum secretion and irritation by lipids
cause decrease in IL 1a and decreased linoliec acid.
 Abnormal proliferation and differentiation of ductal
keratinocytes.
 Adhesion of hyperproliferating ductal keratinocytes k/a
“retention hyperkeratosis”.
These lead to formation of the microcomedone which is
the precursor of all acne lesions.

8. COLONIZATION OF THE DUCT BY MICROBIAL FLORA
• Organism Like P.Acne, P Granulosum, P.Ovale, Staph.
Epidermidis Produce Lipases.
• Hydrolysis Of Triglycerides To FFA .
• Debris Attract PMLs & Activation Of Complement
Cascade.
• Engulfment Of Organism By PMLs.
• Further Liberating Hydrolytic Enzymes & Damage To
Follicular Wall .

9. INFLAMMATION-
 Increase In IL-1, K-6 And K-16 Activate Keratinocyte.
 Il -2 , Il-8 And TNF –Alpha Contribute To Inflammation
 LTB4 Induces Recruitment And Activation Of PMNL And
Monocytes
 Elevation Of Antibody Titre To P.Acne.
 IgG1 And IgG3 Are Increased In Moderate Acne.
 IgG2 Increased In Moderate To Severe Acne.
 Activation Of TLR-2 Triggers Inflammatory Cytokine
Responses In Acne.

10. OTHER FACTORS-
• Hot & humid climate (tight clothes ,cooks, coal mines,
chemicals )
 Emotional stress.
• Dietary factors – high glycemic load carbohydrate diet as
chocalate, ice-cream, fat rich diet , milk (iodine and low omega -
3 fatty acid )
• Drugs – anabolic steroids, corticosteroids phenytoin lithium
isoniazid anticancer drugs
• Smoking.

11. GRADES OF ACNE (PILLSBURRY’S CLASSIFICATION)
 Grade I (MILD): comedones (open or closed), occasional
papules.
 Grade II (MODERATE): papules, comedones, few pustules.
 Grade III (SEVERE): predominant pustules, nodules,
abscesses.
 Grade IV (CYSTIC): mainly cysts, abscesses, widespread
scarring.

12. SEQUENCE OF EVENTS -
SEBACEOUS CELLS
P.ACNE IMMUNE REACTIONS
MICROCOMEDONS P.ACNE IMMUNE REACTIONS
INFLAMMATORY LESIONS
CLOSED COMEDO AND OPEN COMEDONS
A) SEBUM ACCUMULATES
B) FOLLICULAR ENLARGES
C) KERATINOUS MATERIAL BUILDS UP
1) HYPERPOLIFERATION
2)KERATINOCYTE GRANULES INCREASE
3)DISTURED DESQUAMATION
FOLLICULAR KERATINOCYTE

13. THANK YOU