The etiology of acne is complex and multifactorial. There are four key components that contribute to the development of acne. These include hypercornification of follicular epithelium at the infra-infundibulum with the development of a keratin plug, blocking the outflow of sebum to the skin surface; hyperplasia of the sebaceous glands and hypersecretion of sebum with the onset of puberty, or increased activity due to the stimulation of androgen hormone; lipase-synthesizing bacteria (Propionibacterium acnes) colonizing the upper and mid-portion of the hair follicle, converting lipids within sebum to proinflammatory fatty acids; and finally, immune response and induction of inflammation in the follicle associated with the release of cytotoxic and chemotactic factors (Fig. 17.1) [22-25].
Follicular hypercornification or hyperkeratinization is an abnormal proliferation of follicular epithelium. This epithelium sheds and mixes with other materials, such as sebum and bacteria, and collects within the follicular canal, forming a microcomedone. When these materials plug the drainage of the pilosebaceous unit for awhile, debris will accumulate in this canal and enlarge, forming a macrocomedone. This process is believed to be the most important in the pathogenesis of acne. There have been many effective modalities to treat this condition, that is, using keratolytic agents such as salicylic acid, glycolic acid, and retinoic acid to control this condition. However, it takes several weeks to get a good result, and some of them can cause irritation to the skin.
Hyperfuncional sebaceous glands are the second-most important feature in the pathophysiology of acne. Hyperfunctional sebaceous glands lead to increased sebum production in response to stimulation of the androgen hormone. High levels of this hormone, especially during puberty, can produce a greater amount of sebum. A mixture of debris and a greater amount of sebum can plug the follicle and create the appropriate environment for P acnes. Treatment of hyperfunctional sebaceous glands includes isotretinoin and anti-androgens. These are effective medications; however, systemic side effects and teratogenicity have to be considered.
Table 17.1 Reasons Why Phototherapy Developed
P. acnes is a gram positive, anaerobic bacteria which is usually a part of the normal flora of the skin. P. acnes can change triglycerides, which are the main component of sebum, to free fatty acids. These free fatty acids can trigger inflammation. Treatment of P. acnes includes both topical and oral antibiotics; however, resistance to these medications is a problem for treatment.
Perifollicular inflammation can occur due to a response to the overgrowth of P. acnes, free fatty acid which leaks from the follicle, and the follicular rupture that allows the contents (cell debris, bacteria, and sebum) into the adjacent dermis [26]. Although corticosteroids can control inflammation, systemic forms can depress immunity, and topical forms can cause steroid-induced acne. If we can normalize hypercornification or rid the area of P. acnes, we can control the acne.
Acne that is left untreated may cause excoriation, secondary bacterial infections (e. g. gram positive or gram negative bacteria), pigmentary alterations, prolonged erythema,
scars (atrophic and hypertrophic/keloids), and psychological problems. Currently, there are many physical modalities for acne treatment. The blue-light system is widely used and accepted as the simple, safe, and painless method for the improvement of acne. Its benefits, indications, and technique will be discussed in this chapter.