Dermnet Videos
Acniform eruptions Videos
- Acne Cause and Pathophysiology
- Acne Lesions and Classification
- Acne Pimples – Papules and Pustules
- Acne Psychology and Approach to Patient
- Acne Treatment – How Acne Medicine Works
- Acne Treatment Antiandrogens and Birth Control Pills
- Acne Treatment with Accutane Isotretinoin Part 1
- Acne Treatment with Accutane Isotretinoin Part 2
- Acne Treatment with Oral Antibiotics Doxycycline
- Acne Treatment with Topical Retinoids Retin-A
- Blackhead and Whitehead Comedone Acne
- Cystic Acne Cases and Acne Scars
- Cystic Acne Information
Video Topics
Acne Treatment – How Acne Medicine Works
Mode Of Action Of Therapeutic Agents
Formation of the microcomedo or comedogenesis is thought to be the primary process in the pathogenesis of acne. Excess desquamation of follicular keratinocytes, abnormalities in sebum production and migration of immune cells that release proinflammatory cytokines are responsible for creation of the microcomedo. This lesion may evolve into noninflammatory open and closed comedones.
P. acne bacteria proliferation in this sebum-keratinocyte mixture generates free fatty acids which are comedogenic. They also induce the formation of cytokines that induce inflammatory cells to invade and produce papules, pustules and cysts.
Acne treatments are designed to reverse abnormal desquamation of epithelial cells, stop the proliferation of P. acnes and reduce the excess production of sebum.
Reduction of Epithelial Desquamation
Topical agents that affect the desquamation of follicular epithelial cells and have activity against comedogenesis are tretinoin, tazarotene, adapalene, azelaic acid and salicylic acid.
Topical tretinoin reduces the numbers of microcomedones and comedones by slowing the desquamation processes. Oral isotretinoin causes a decrease in the size of comedones and a reduction their formation.
Topical and systemic antibiotics cause a small reduction in the number of comedones. Salicylic acid has a week effect on comedogenesis.
Prevention of Proliferation of P. acnes
P. acnes proliferates in the lipid environment of the sebaceous follicles. The bacteria is sensitive to many antibiotics. The problem is to find agents that can effectively penetrate the lipid environment. Antibiotics kill the bacteria and inhibit the production of proinflammatory mediators by P. acnes that are not killed. Topical agents with antibiotic activity include benzoyl peroxide, clindamycin, erythromycin and azelaic acid.
Effective oral antibiotics include tetracycline, erythromycin, doxycycline, minocycline, clindamycin, and trimethoprim and sulfamethoxazole.
Reduction of Sebum Production
Topical therapies do not influence the production of sebum. Sebaceous glands are androgen-dependent therefore estrogens and antiandrogens are effective.
Low dose estrogen contraceptives are moderately effective.
Higher dose contraceptives with 50 or more of ethinyl estradiol or other estrogens were used in the past and were more effective but had more side effects. Spironolactone 25 to 200 mg per day reduces sebum production and can be very effective. Only women are treated with this antiandrogen. Isotretinoin profoundly reduces sebum production and results in prolonged remissions. A four-to-five-month course of therapy at an average dose of 1.0 mg per kilogram of body weight is required to obtain this effect.
The use of combinations of agents to attack every pathogenic factor is the most effective strategy for managing acne.