Acne Vulgaris Pathophysiology

Acne Progression (4 step process)
1. Androgen Mediated Sebum Production
2. Keratinous Obstruction of sebaceous follicle outlet (Results in formation of comedones)
3. Bacterial Colonization of trapped sebum (with Cutebacterium acnes, previously Propionibacterium acnes)
4. Inflammatory reaction (Papules, Nodules and cysts)
Images
1. Lewis (1918) Gray's Anatomy 20th ed (in public domain at Yahoo or BartleBy)

Causes
1. Adrogen-mediated sebum over-production
2. Increased Sebaceous Gland sensitivity to normal androgen levels
Sebum composition
1. Triglycerides
2. Cholesterol esters
3. Waxes
4. Fatty Acids
Sebum Effects
1. Drains to skin surface via pilosebaceous canal
2. Excellent growth medium for Cutebacterium acnes (previously Propionibacterium acnes)

Abnormal follicular epithelium shedding
Pre-Puberty Sebaceous follicles
1. Lobulated glands empty into pilosebaceous canal
2. Follicles most dense on face, back and chest
3. Inactive until Puberty
Post-Puberty Sebaceous follicles
1. Androgen production increases
2. Stimulates sebaceous follicles to secrete sebum

Open Comedones (Black heads)
1. Combination of sebum and keratin
2. Melanin gives them the black color
3. Seldom become inflamed
Closed Comedones (White heads)
1. Do not communicate with the skin surface
2. Block pilosebaceous canal
3. Encourage Anaerobic Bacteria to grow
4. Propionibacterium acnes fuels inflammatory process
  1. Lipase secretion lyses Triglycerides
  2. Free Fatty Acids fuel local irritation
5. Closed comedones progress to inflammatory lesions

Cutebacterium acnes (previously Propionibacterium acnes) Bacteria colonizes sebum
P. acnes secretes a Lipase that hydrolyzes sebum
1. Converts Triglycerides into free Fatty Acids
2. Free Fatty Acids irritate local cells