Benzoyl peroxide has been available for the treatment of acne for at least twenty years. It is available in different formulations  in  various countries, either alone  or  in combination,  in particular with  sulphur,  hydroxyquinolone or miconazole (and, in the USA, erythromycin). It is available in concentrations of 2.5, 5,10 and 20 per cent as a cream and a gel and, more recently in the UK, as a wash.

 

  Benzoyl  peroxide was  probably  the  first proven effective topical treatment  for acne vulgaris. Unfortunately, there are limited dose-response studies indicating an increased effectiveness  of even the 10 per cent over the 2.5  per cent concentration. It  is  assumed, therefore, with little proof, that there may be a dose-response effect. However, the prescribing  of  a higher concentration of benzoyl peroxide is  of psychological benefit in a patient whose acne treatment is proceeding quite well and in whom the doctor does not wish - as yet - to give oral therapy. In this way the physician can 'play games' with  the  patient  and  indicate  that an increased strength  of benzoyl peroxide might work better. To prove convincingly whether either sulphur, miconazole, erythromycin or hydroxyquinolone helps in addition to the benzoyl peroxide would require many large-scale studies. The combination with erythromycin seems promising, however.

  There  are four main aetiological factors responsible for the development of acne lesions: increased sebum excretion, comedogenesis, microbial colonization of the pilosebaceous duct and the production of inflammation. The  effect of benzoyl peroxide on sebum excretion is questionable. It has been shown that it reduces sebum synthesis.

However, the  techniques used  involved thymidine uptake and the result is probably due to an artefact - possibly caused  by an interaction of the benzoyl peroxide with the thymidine - rather than  a real  effect. This  conclusion is supported by another study which showed no effect of benzoyl  peroxide on sebum production.11 In contrast, Cunliffe et al showed that benzoyl peroxide may increase the sebum excretion rate by up to 16 per cent.12  These authors emphasized that  it is unlikely that the drug has a direct  effect on sebum production  but, by reducing comedogenesis, may affect the  outflow  of sebum and so produce an apparent increase.

 

   Studies on the effect of benzoyl peroxide  on comedogenesis (using the follicular cast model, which gives a reasonable measure of the number of microcomedones) show that benzoyl peroxide has only a slight effect of  about  10 per cent.13 This figure  is similar to that  of placebo. However,  at a clinical level benzoyl peroxide has been shown by many authors significantly to reduce  the  number  of visible closed and open comedones.

   This effect of benzoyl peroxide is possibly secondary to its dramatic effect on cutaneous bacteria, reducing by 2 log cycles the number of skin surface Propionibacterium acnes and Staphylococcus epidermidis.16 One study on ductal bacteria confirms that  benzoyl peroxide reduces colonization in the duct. Although it is no longer accepted that free  fatty acids are important in  the development of acne, the measurement of skin surface free  fatty acids  is a good marker of bacterial function. The  free fatty acids arise by hydrolysis  of sebaceous triglycerides by P. acnes and Staph, epidermidis.16 Benzoyl peroxide in doses of 2.5, 5 and 10 per cent has been shown to produce 40-50 per cent suppression of skin surface free  fattv acids.

 

  The suggestion that benzoyl  peroxide  may  have a direct anti-inflammatory  effect is supported by  studies in man which have shown a reduction in the number and size of active inflamed lesions early in treatment.