Acne is a very common skin disease afflicting the majority of adolescents, typically starting in early puberty. Very mild acne occurs so frequently that it has sometimes been characterized as "physiological". Seven percent of adolescents will continue to have acne well into their 30s, while 8% of patients with late type acne (acne tarda) develop the condition in their late 20s or 30s.

Acne is a multifactorial disease of the pilosebaceous units, the main pathogenic factors being:

• hyperseborrhea
• abnormal keratinization of the intrafollicular epithelium
• abnormal growth and activity of the Propionibacterium acnes
• follicular/perifollicular inflammation processes

The disease is characterized by

• a polymorphic clinical presentation with coexistence of:
  • non-inflammatory lesions (closed and open comedones)
  • inflammatory lesions (papules, pustules, nodules)
• a large variety in acne severity
  • mild
  • moderate
  • more severe courses

The most common form of acne is acne vulgaris, typically occurring on the face, back and chest. Several physiological and environmental factors such as ultraviolet light and stress may modify acne. The physical signs of acne are seborrhea, non-inflamed and inflamed lesions and scarring.

Three types of non-inflammatory lesions can be distinguished:

• microcomedones (clinically not visible)
• whiteheads
• blackheads.

Inflammatory lesions may either be

• superficial papules or pustules
• deep pustules
• nodules.

Most patients will display a variety of clinical lesions, although some extremes do exist (with inflammatory lesions only or with extensive comedonal acne).

Pathophysiology

The development of acne centers on the interaction of the following major pathogenic factors:

Hyperseborrhea

Most acne patients suffer from hyperseborrhea, an increased sebum production. The sebaceous gland and the pilosebaceous duct are mainly controlled by androgens. In rare cases of acne (androgenic acne) patients have increased androgen blood levels (hyperandrogenism) causing symptoms like severe hypersborrhea, male pattern alopecia, hirsutism, deepening of the voice, etc. (see www.diane35.com).

The majority of female patients though, does not show increased levels of circulating androgens nor an endocrine disorder.

Ductal hypercornification

An increased production of ductal keratinocytes and/or an inadequate desquamation of ductal corneocytes produces comedones.

Bacterial colonization and inflammation

The combination of sebum and desquamated cells provides an environment that promotes the proliferation of three different organisms:

• Staphylococcus epidermidis
• Malassezia furfur
• Propionibacterium acnes,

the latter being the most common microorganism in inflammatory acne lesions.

P. acnes is capable of hydrolyzing the triglycerides found in sebum into glycerol and free fatty acids (FFA). The FFA act as an irritant, thus eliciting pro-inflammatory reactions and potentially promoting the rupture of the follicular wall. The subsequent release of keratin-enriched corneocytes and sebum into the dermis leads to further inflammation.