What should I know about Acne?

Acne vulgaris is the most common skin disease, affecting 80% of the population between the ages of 12 and 25. (1) It usually has a limited life span of its own; however, some cases may persist for years and the more severe cases may potentially lead to scarring and disfigurement. The lesions of acne are generally classified as inflammatory or noninflammatory, and occur most frequently on the face, neck, chest, and back.

The causes of acne are very complex and involve many different systems and chemicals within the body. Hormones, enzymes, and the immune system all interact together resulting in different reactions in each individual. Understanding this complex system has kept dermatologists busy for decades.

One of the factors responsible in the development of acne is called sebum, which is produced by the sebaceous glands. Sebaceous glands are located throughout the body except for the palms of the hands, soles of the feet, and the lower lip. Each person has approximately 5,000 sebaceous follicles. These glands are the largest and most numerous on the face, back, chest, and upper outer arms. Sebaceous glands are large at birth, and then reduce in size until adolescence. They once again enlarge during pre-puberty with changes in hormone levels influencing sebaceous gland secretion. This increase in production of sebum is the reason that acne is so prevalent in adolescents and teenagers.

When there is excess sebum, bumps called comedones, appear because there is a blockage of follicles by this excess sebum. Inside these comedomes, there are bacteria and yeast that work on the sebum causing it to release free fatty acids. When this happens, there is inflammation and sometimes a rupture of the bump or comedome. Sebum levels are increased when testosterone is converted into dihydrotestosterone in the skin. When this happens the dihydrotestosterone acts directly on the sebaceous gland to increase its size and metabolic rate. Estrogens, on the other hand, work differently and actually decrease sebaceous gland secretion. Early acne lesions result from blockage of the follicle canals. These canals become blocked when sebum mixes with keratin, which is also affected by hormonal changes. This new mixture increases the number of cornified cells that stick to the walls of the canal and a plug is formed just above the opening of the sebaceous gland duct. All of this change that occurs within the follicle is important, but not fully understood. It is not known whether this activity is a cause of or a result of irritation and other factors. (2)

The earliest lesions that are most often seen in adolescence are mildly inflamed or non-inflamed comedones on the forehead. Comedones may be open (blackhead), or closed (whitehead). The contents of closed comedones are usually not easily expressed, and are often the first sign of the inflammatory lesions of acne vulgaris. It is unsure where open comedones get their black color. It is not from accumulation of dirt, and may not even be the accumulation of melanin, which was the source most recently thought to be the cause. Open comedones generally do not result in inflammatory acne lesions, are easily expressible, and contain oxidized, darkened, oily debris.

The severest forms of acne are most frequently seen in males, but acne is generally more persistent in females. Also, females tend to have flare-ups prior to menstrual periods. This may continue until menopause. Low grade, persistent acne is often found in professional women. One author thinks that chronic stress leads to enhanced secretion of adrenal androgens, resulting in the production of comedones. (3)

Acne is considered an inherited disease, although it is impossible to know which members of a family may suffer from the disease, and which members will not. Acne is not caused by greasy foods, and is not caused by dirt. Avoiding all greasy foods may help curb obesity, but will likely not affect acne. While keeping the skin clean is always recommended, excessive washing of the skin to remove dirt may actually interfere with some treatment programs. For this reason, when visiting a healthcare professional regarding acne, it is important to request information on how to care for the skin at home.

Sometimes acne is caused by elements that are not internal. One such type of acne is termed occupational acne, and involves exposure to certain industrial solvents or other chemicals. Another type of acne is called acne mechanica and is caused by irritation of the skin by the use of chin-straps or forehead guards often found inside of sports helmets.

Acne may sometimes become very severe. This category of acne, known as nodulocystic acne, includes localized cystic acne, in which a few cysts appear on the face, chest, or back, and diffuse cystic acne, which involves a wider area of cystic lesions. Pyoderma faciale is the term that is used for inflamed cysts that appear on the face in females. Acne conglobata describes a highly inflammatory form of nodulocystic acne. Acne fulminans is a rare ulcerative form of acne with an unknown cause. 40% of patients with acne fulminans experience painful bone lesions, muscle pain, and sometimes weight loss.


National Institute of Arthritis and Musculoskeletal and Skin Diseases. 2001.

  • Nearly 17 million Americans have acne
  • Acne is the most common skin disease in the US
  • Between the ages of 12 and 24, almost 85% develop acne

Signs and Symptoms

The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.

Acne may be considered inflammatory or noninflammatory. Early acne usually presents as noninflammatory or mildly inflammatory closed comedones (whiteheads), or open comedones (blackheads). Once an inflammatory response has occurred, lesions may occur as erythematous papules, superficial pustules, or in cases of more severe acne, deep pustules, or suppurative nodules. These may be accompanied by pain and sometimes hemorrhage.

Noninflammatory (obstructive)

  • Open comedones (blackheads)
  • Closed comedones (whiteheads)


  • Papules
  • Pustules
  • Erythema
  • Pain
  • Hemorrhage
  • Nodules or cysts

Treatment Options


There are many processes involved in acne and therefore there are often multiple treatment programs designed to control this condition. Usually the therapy involves some type of topical treatment. Systemic therapy is generally reserved for patients who are at risk for scarring, or who do not respond to topical therapy. Aggressive therapy may be necessary for the patient with inflammatory acne. In addition to the suggested treatment, the healthcare professional may recommend removing any substances that might aggravate the condition such as certain cosmetics, oils, and creams. The healthcare professional may also recommend a change in certain medications such as birth control pills or any types of steroids, iodides, and bromides.

One of the more common prescriptions used for acne is retinoic acid (Tretinoin, Retin-A). It is available in cream, gel, and liquid. Dryness and irritation are the greatest potential side effects, and occur more frequently with the gels and hydroalcoholic solutions. Many people tolerate the cream, which has less irritating effects. The liquid is most frequently used on individuals with severe involvement on the back and chest, who tolerate the cream and gel, but are not getting the level of improvement they were looking for.

Benzoyl peroxide is a topical agent frequently used in combination with retinoic acid. It is available over-the-counter in the form of soaps, lotions, creams, and gels. The strength ranges from 2.5-10 percent and is applied every other day initially, then twice daily thereafter. If used in combination with retinoic acid, it is generally used once daily approximately 8 to 12 hours after the retinoic acid. Benzoyl peroxide is decomposed on the skin by cysteine, liberating free oxygen radicals that oxidize bacterial proteins. (4) Benzoyl peroxide increases the sloughing rate of surface cells and loosens the follicular plug structure. (5)

Topical antibiotics may also be used to treat mildly inflammatory acne. This is a preventive form of therapy that does little to help pre-existing acne. The antibiotics used are clindamycin, erythromycin, and tetracycline. Systemic antibiotics, or antibiotics that are taken internally, are frequently used to treat inflammatory acne and are the best means of preventing new inflammatory lesions. Since they have no effect upon existing lesions, it may take 6-8 weeks of therapy before clinical results are noticed. The antibiotics most frequently used are tetracycline, erythromycin, and clindamycin. Ampicllin, trimethoprim/sulfamethoxizole, and cephalosporins may also be used. The most cost effective treatments are generic erythromycin or tetracycline.

Intralesional corticosteroids may be used on patients with nodulocystic lesions. Triamcinolone acetonide 2-2.5mg/ml in saline is directly injected into specific lesions. This treatment has been shown to hasten involution of lesions and reduce scarring. Some dermatologists may also use cryotherapy, that is, freezing tissues with liquid nitrogen. Caution must be exercised to avoid excessive freezing and tissue destruction. Isotretinoin therapy is reserved for patients with severe acne that has not responded to other therapies.

Oral contraceptives may be used in women with moderate acne, since androgen levels correlate with sebum production. The action exhibited is a decrease in unbound, biologically active androgens such as free testosterone. In 1997, the FDA approved Ortho Tri-Cyclen for use as anti-acne therapy.

Finally, in patients with acne scars, dermabrasion, collagen injection, and other corrective procedures may be considered. (6)

Nutritional Suplementation

Niacinamide 4% Topical Gel
In an 8-week double-blind trial, 38 patients with moderate inflammatory acne vulgaris were treated with 4% niacinamide topical gel while an equal number were treated with 1% clindamycin topical gel. Patients treated with 4% niacinamide gel made slightly greater improvements compared to the patients treated with 1% clindamycin gel. (7) Because it is safe, effective, and without the antibiotic-associated risk developing resistant strains of bacteria, 4% niacinamide topical gel should be considered as an important alternative treatment for acne vulgaris.


In an open trial, men and women with moderate to severe acne were treated with a combination of 200 mcg of selenium and 10 mg of vitamin E twice daily for a period of 6 to 12 weeks. Good improvements were achieved, especially in patients with pustular acne who had initially been found to have low levels of glutathione peroxidase activity. (8)


The mechanism of zinc’s action in acne is not fully understood. However, it has been reported that both men and women with acne have lower serum zinc levels compared to healthy controls and individuals with severe acne have lower serum zinc levels than individuals with milder cases of acne. (9) , (10) In one study, patients with inflammatory acne who were treated with 200 mg/day of zinc gluconate, corresponding to 30 mg of elemental zinc, experienced a significantly greater reduction in inflammation compared to placebo controls. (11) In other double-blind studies evaluating acne vulgaris, patients treated with 400 to 600 mg of zinc sulfate daily experience greater clinical improvement compared to placebo controls. (12) , (13) , (14)

Vitamin E

One study reported that orally ingested vitamin A is not absorbed in the presence of vitamin E deficiency. Consequently, they noted that some cases of acne vulgaris that did not respond to vitamin A therapy responded well with a combination of vitamin A and vitamin E. Vitamin E may inhibit bacteria-induced lipid peroxidation in the sebum, resulting in a reduction of the inflammation that is often present in acne lesions. (15)

Herbal Suplementation

Tea Tree Oil

A study compared the use of topical tea tree oil (5% gel) with benzoyl peroxide (5% gel) in the treatment of mild to moderate acne. The results of this study reported that both 5% tea-tree oil and 5% benzoyl peroxide had a significant effect in ameliorating the patients’ acne by reducing the number of inflamed and non-inflamed lesions (open and closed comedones), although the onset of action in the case of tea-tree oil was slower. Encouragingly, patients treated with tea-tree oil experienced fewer side effects. (16)


An interesting study comparing tetracycline and guggul showed surprising promise in using guggul to treat nodulocyctic acne. In this study, twenty patients were randomly assigned to a group taking either Tetracycline at 500mg twice each day for 90 days, or a group taking gugulipid twice each day for 90 days. There was a slightly better outcome with the guggul group as well as slightly fewer relapses reported. In addition, participants with oily skin seemed to respond better to the gugulipid treatment. (17)


  1. Leyden JJ. Therapy for acne vulgaris. N Engl J Med. 1997;336:1156-1162.
  2. Han NH, et al. Acne and Psorasis. In: DiPiro JT, et al, eds. Pharmacotherapy, A Pathophysiologic Approach, 4th ed. Stamford CT: Appleton & Lange; 1999:1490-1496.
  3. View Abstract: Kligman AM. Postadolescent acne in women. Cutis. 1991;48:75-77.
  4. Arndt KA, ed. Acne. In: Manual of Dermatologic Therapeutics, 5th ed. Boston: Little & Brown; 1995:3-15.
  5. Melski JW, et al. Topical therapy for acne. N Engl J Med. 1980;302:503-506.
  6. View Abstract: Fulton JE Jr, et al. Resurfacing the acne-scarred face. Dermatol Surg. May1999;25(5):353-9.
  7. View Abstract: Shalita AR, et al. Topical Nicotinamide Compared with Clindamycin Gel in the Treatment of Inflammatory Acne Vulgaris. Int J Dermatol. Jun1995:34(6);434-37.
  8. View Abstract: Michaelsson G, et al. Erythrocyte glutathione peroxidase activity in acne vulgaris and the effect of selenium and vitamin E treatment. Acta Derm Venereol. 1984;64(1):9-14.
  9. View Abstract: Amer M, et al. Serum zinc in acne vulgaris. Int J Dermatol. Oct1982;21(8):481-4.
  10. View Abstract: Michaelsson G, et al. Patients with dermatitis herpetiformis, acne, psoriasis and Darier’s disease have low epidermal zinc concentrations. Acta Derm Venereol. 1990;70(4):304-8.
  11. View Abstract: Dreno B, et al. Low doses of zinc gluconate for inflammatory acne. Acta Derm Venereol. 1989;69(6):541-3.
  12. View Abstract: Verma KC. Oral zinc sulphate therapy in acne vulgaris: a double-blind trial. Acta Derm Venereol. Jan1980;60(4):337-40.
  13. View Abstract: Lidén S. Clinical evaluation in acne. Acta Derm Venereol Suppl (Stockh). Jan1980;89:47-52.
  14. View Abstract: Meynadier J. Efficacy and safety study of two zinc gluconate regimens in the treatment of inflammatory acne. Eur J Dermatol. Jun2000;10(4):269-73.
  15. View Abstract: Ayres S Jr, et al. Acne vulgaris: therapy directed at pathophysiologic defects. Cutis. Jul1981;28(1):41-2.
  16. View Abstract: Bassett IB, et al. A comparative study of tea-tree oil versus benzoylperoxide in the treatment of acne. Med J Aust. Oct1990;153(8):455-8.
  17. View Abstract: Thappa DM, et al. Nodulocystic acne: oral gugulipid versus tetracycline. J Dermatol. Oct1994;21(10):729-31.
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