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It has been shown clinically that postmenopausal women are more sus-ceptible to wound complications. The decline of postmenopausal estro-gens leads to dysregulation of extracellular matrix turnover (ECM) and increased inflammation in wounds.1This process is prevented or reversed by topical and systemic 17β-estradiol (E2) replacement therapy.2 Skin is a direct estrogen target tissue and expresses both ERα and ERβ.3 In humans, both topical and systemic estrogens have been shown to improve wound healing through a number of mechanisms: inflammatory response modulation, cytokine stimulation, matrix deposition, re-epithelialization rate enhance-ment, angiogenesis stimulation, and proteolysis regulation.2,4 In addition