Clinical Overview of Acne Vulgaris

Rich Callahan MSPA, PA-C

ICM I – Summer 2009

A disease of the pilosebaceous unit

• Anatomy of this structure is key to full understanding of the disease.

• Each PS unit built around a long, narrow tube (a.k.a. – “pore”) vertically oriented in the skin, which houses a single hair follicle.

• Epithelial lining at entrance of pore is stratum corneum, prone to overkeratinization (“clogging”) if the right etiological factors are present.

• Sebaceous gland activity is the biggest player in instigating the disease.

Sebaceous Glands

• Distributed most densely on face, chest, back, upper arms.

• Positioned around the infundibulum (main tube) of the pore, each having a single duct communicating with it.

• Secrete sebum (oil) into the duct. Sebum is rich in triglycerides.

• Highly sensitive to hormonal stimulation by androgens.

• Circulating testosterone reaches the skin, where it is changed into dihydrotestosterone (DHT.)

• DHT acts on the sebaceous glands causing increase in size and oil production.

Hormonal aspect will become much more relevant later when we talk about treatment of acne

• We know that hormonal influences during puberty cause increased sebum production/keratinization in both men and women. Majority of these cases resolve post-puberty.

• Some research suggests that increased cortisol production secondary to prolonged stress can lead to androgen over- production and acne.

• Middle aged women with recurrent pre-menstrual acne are often showing a sensitivity to the brief surge of testosterone produced by the ovaries prior to initiation of menses.

Other structures in the pilosebaceous unit

• Apocrine sweat glands – have a duct communicating with infundibulum of PS unit which secretes apocrine sweat (clear sweat mixed with cytoplasmic components of the gland which add odor, phermones, etc.)

• Eccrine sweat glands – positioned alongside the PS unit in the skin, but has its own vertically-oriented duct communicating directly with the skin surface. As you might expect, they secrete eccrine (clear) sweat.

• Arrector pili muscle – tiny muscle connecting infundibulum with skin surface. Cause of “goose bumps”

Pathogenesis of Acne Starts with formation of microcomedos

• In predisposed individuals, starts with increased sebum production from sebaceous glands and overgrowth of keratin-producing cells lining the pore walls. Excess keratinization leads to the formation of a sticky plug which blocks the superficial aspect of the pore.

• This is a microcomedo – the precursor lesion to acne.

• At this stage the sebaceous glands are still producing sebum, which is now unable to drain out to the skin surface, causing the formation of a comedo.

A comedo is the basic lesion of acne vulgaris. It has two subtypes:

• Open comedone – a “blackhead.” Forms when the pore wall is able to dilate in response to the increased pressure created by the trapped sebum, creating a non-inflamed lesion.

• Closed comedone – a “whitehead.” A semi-firm, white, dome-shaped papule, which is also non-inflamed. Forms when trapped sebum pushes up against the non-dilated opening of the pore.

• All the acne you see starts with one or both of these lesions.

Pathogenesis of Acne – What Happens Next?Inflammation and bacterial overgrowth

• Propionibacterium Acnes: Anaerobic bacteria which is normal flora within PS unit. Has ability to digest sebum.

• Large plug of sebum stimulates p. acnes to produce lipase, which breaks down (hydrolyzes) the triglycerides in the sebum to free fatty acids.

• Free fatty acids highly irritating to PS unit and surrounding tissues, causing inflammation and further comedo formation.

• Neutrophils are attracted to inflamed site, attach to follicular wall, and release hydrolases which further weaken it. Wall eventually ruptures, spilling out highly irritating FFA’s into surrounding tissue.

Now we are ready to talk about what happens after comedogenesis

• Pustule formation – Inflamed comedo starts to fill with purulent material which pools at the surface.

• Papule formation – Inflamed comedo enlarges into a red papule without pooling of purulent material at top.

• Nodule formation – Follicular walls of papules/pustules rupture and spill inflamed contents into surrounding tissue. Lesion increases in size and becomes a nodule (>5mm diameter.) At this point level of skin involvement creates risk for later scarring. Nodules can become hemhorragic, secondarily infected, or form communications between multiple draining lesions (sinus tracks.)

How Severity of Acne is graded:

• Overall severity of acne classified as Grades 1-4, with higher grades having a higher overall lesion count, more inflammation, larger lesions, etc.

• Further characterized as comedonal, pustular, papularpustular, nodular and nodulocystic.

• (Important to remember that by definition, comedonal acne is the only subtype which is non-inflamed.)

• For Example: A mild case would be Grade I comedonal. You see scattered open comedones on forehead and face.

• A severe case could be Grade 3 nodulocystic acne characterized by presence of many inflamed, tender nodules and cysts.

Clinical Presentation

• Acne presents as solitary or grouped comedones, papules, pustules, nodules and cysts. Mild to severe inflammation will accompany all with the exception of comedones.

• Generally distributed on forehead, face, neck, chest and back. Rarely appears on scalp. Corresponds with areas of highest sebaceous gland density.

• Patients are usually, although not always anxious and self-conscious about their condition, which can lend the disease a strong emotional component.

• Many patients previously diagnosed and frustrated with treatment.

Diagnosis

• Almost always a straightforward, visual diagnosis.• Vast majority of cases are pre-pubescent and pubescent

males and females. Significant number of cases middle-aged women; rare in post-pubescent males.

• I have seen a few cases of acne suddenly appearing in patients with no prior history and who don’t fit into the above categories

• When you see this look for occupational acne: Workplace exposure to light oils (machine oil, cosmetics) which occludes pores leading to comedogenesis and acne. This is the only type of acne I have needed to biopsy for diagnosis.

Speaking of Oil, let’s not forget about Pomade Acne

• Unique form of acne secondary to chronic use of oily hair mousses, gels, tonics by susceptible individuals.

• Always distributed on upper forehead/hairline/anterior scalp with a fairly clear border. Lower face unaffected.

• Patient will usually present with offending substance in their hair which helps the diagnosis

• Usually an easy problem to fix: They stop using the product, the acne clears in 2-6 weeks!

Treatment of Acne – Guided by the Severity of Disease

• Topical retinoids are first-line: adapelene (differin,) tretinoin (Retin-A) and tazarotene (Tazorac)

• Benzoyl peroxide creams, gels and washes.

• Topical antibiotics (clindamycin, erythromycin, dapsone)

• Azeleic acid (Azelex, Finacea): Unique plant-derived compound that has anti-bacterial and anti-comedogenic properties (and Pregnancy Category B)

• Salycylic and Glycolic Acid gels and washes (Two of the active ingredients of ProActiv, as endorsed by Shawn “Puffy” Combs!)

Treatment of Acne – Guided by the Severity of Disease

• Oral antibiotics – minocycline, tetracycline, doxycycline. Also to a lesser degree trimethoprim-sulfamethoxasole (Bactrim) and beta-lactams/derivatives like PCN, amoxicillin and cephalexin.

• Isotretinoin (Accutane) – The big gun of acne medications. Drastically attenuates activity of sebaceous glands and rate of keratinization in epidermis. Many potential side effects. Teratogenic. Photosensitizing. Can be a permanent cure for approximately 85% of patients on 6 month course.

• Now subject to a massive federal regulatory apparatus called I-Pledge.