The increased prevalence in the elderly of chronic wound-healing conditions, such as venous and diabetic ulceration, is firmly established. This same population additionally suffers from impaired healing of acute wounds, which are characterized by delayed closure, increased local inflammation, and excessive proteolytic activity. In females, this decline in the effectiveness of skin repair mechanisms follows the menopause, and a series of clinical studies has identified estrogens as being endogenous enhancers of healing processes. The administration of 17beta-estradiol, either systemically or topically, has been shown to reverse the fundamental repair defects observed in postmenopausal women. By contrast, androgenic species retard repair and interfere with the accumulation of the structural proteins that reconstitute the damaged dermis. Since estrogen-based hormone replacement therapy produces wide-ranging effects, not all of which are considered to be desirable, more recent studies have sought to identify downstream mediators of estrogenic effects in order to formulate better targeted strategies for improving skin repair in the elderly.