The differential diagnosis of acne includes gram-negative fol-liculitis, perioral dermatitis, sebaceous hyperplasia, syringoma, tuberous sclerosis (adenoma sebaceum), trichoepithelioma, Demodex folliculitis, bacterial folliculitis, and papular sarcoido-sis. The diseases that most closely resemble acne, but are said to be distinguishable from it, include:
Acne can occur in tandem with other eruptions and can result in scarring that lasts beyond its resolution. It can overlap with acne rosacea or seborrheic dermatitis. It can also be concurrent with gram-negative folliculitis; the latter may be manifested following months of therapy with antibiotics (typically tetracyclines). Acne can leave behind hypertropic scars, pitted (“icepick”) scars, sinus tracts, keloids, and atrophic scars.
In men of color, pseudofolliculitis is a common sequela of acne in the beard area. In old age, people who had acne in earlier life and experienced actinic damage can manifest Favre-Racouchot syndrome. The relationship of the syndrome to acne is unclear.
Biofilm and Enzymatic Tools of P. acnes
To understand the mechanisms, utility, and basis of the cornerstones of topical therapy—retinoids and benzoyl drug—it is important to comprehend the organism P. acnes.
P. acnes resides within the pilosebaceous unit in a biofilm. An important factor in the persistence and effect of P. acnes is its ability to form such a biofilm, including the production of an exopolymer that is similar in appearance to the polysaccha-ride intercellular adhesin of S. epidermidis. This glycocalyx polymer forms a protective exoskeleton and may be an important immunogenic agent that feeds the inflammation that sometimes is associated with acne. This biofilm functions as a physical barrier that prevents the elevation of concentrations of antimicrobial agents proximate to the bacteria sufficient to hinder the bacteria. The role of biofilm probably explains the parameters of successful treatment of acne, including:
P. acnes possesses other means of engendering acne. The organism can produce active enzymes and inflammatory mediators that can contribute to acne’s progression, including smooth-muscle contracting substances, lipases, proteases, hyaluronate lyase, and phosphatase. Lipases can convert triglycerides in sebum to free fatty acids; this increases the clumping of P. acnes in the follicles, thereby facilitating an increase in the number of bacteria.