The dogma that cutaneous wound healing is impaired as a function of ag
e is largely unsubstantiated. This can be attributed to poor experimen
tal design of human studies, the lack of subject characterisation with
the exclusion of disease processes, and the study of inappropriate an
imal models. Structural and functional changes in skin with age have b
een reported, such as a decrease in dermal thickness, decline in colla
gen content, a subtle alteration in the glycosaminoglycan profile, and
a loss of elasticity, but these reports are subject to the above crit
icisms in addition to the often-neglected requirement for site specifi
city. Wound repair can be thought of as a culmination of three major o
verlapping phases: inflammation, proliferation and remodelling. The in
flammatory process has not been studied systematically with respect to
age, and despite a reported decline in cellular function and number,
there is a confounding increase in the production of specific cytokine
s involved in the process of repair. The proliferative phase is associ
ated with a loss of cellular responsiveness to specific cytokines with
a decline in motility and proliferation; however caution in interpret
ing these findings is important as, for example, the definition of 'ag
eing' is used rather loosely with the result that neonatal versus youn
g adult cells are compared instead of young versus old adults. During
remodelling, fibronectin and collagen production may increase with age
, as may wound contraction; the deposition of elastin has not been ass
essed and the resulting mechanical properties of the scar are controve
rsial, not least because human in vivo studies have been ignored. The
absence of a critical review on the effects of advancing age on would
healing has conspired to permit the perpetuation of the belief that we
ll defined tenets exist. This review aims to redress this imbalance an
d to highlight the need for well designed research into an increasingl
y important field.