II. Pathophysiology: Overview
- Acne Progression (4 step process)
- Images
- Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)
III. Pathophysiology: Androgen Mediated Sebum Production
- Causes
- Adrogen-mediated sebum over-production
- Increased Sebaceous Gland sensitivity to normal androgen levels
-
Sebum composition
- Triglycerides
- Cholesterol esters
- Waxes
- Fatty Acids
-
Sebum Effects
- Drains to skin surface via pilosebaceous canal
- Excellent growth medium for Cutebacterium acnes (previously Propionibacterium acnes)
IV. Pathophysiology: Keratinous Obstruction of sebaceous follicle outlet
V. Pathophysiology: Comedones form from keratin and sebum collection
- Open Comedones (Black heads)
- Combination of sebum and keratin
- Melanin gives them the black color
- Seldom become inflamed
- Closed Comedones (White heads)
- Do not communicate with the skin surface
- Block pilosebaceous canal
- Encourage Anaerobic Bacteria to grow
- Propionibacterium acnes fuels inflammatory process
- Lipase secretion lyses Triglycerides
- Free Fatty Acids fuel local irritation
- Closed comedones progress to inflammatory lesions
VI. Pathophysiology: Bacterial Colonization of trapped sebum
- Cutebacterium acnes (previously Propionibacterium acnes) Bacteria colonizes sebum
- P. acnes secretes a Lipase that hydrolyzes sebum
- Converts Triglycerides into free Fatty Acids
- Free Fatty Acids irritate local cells