The human sebaceous gland undergoes both extrinsic and intrinsic ageing. Th
e latter is associated with morphological changes and alteration in the seb
aceous gland activity. The high androgen-dependent sebum secretion in neona
tes falls during childhood, starts to rise again during puberty and reaches
its maximum in young adults. While the number of sebaceous glands remains
the same during life, sebum levels tend to decrease after menopause in fema
les, whereas no major changes appear until the eighth decade of life in men
. Reduced androgen levels in aged individuals lead to a slow cellular turno
ver in the sebaceous glands resulting in hyperplasia of the facial sebaceou
s glands in advanced age. Ultraviolet radiation and immune suppression (cyc
losporin A with corticosteroids) represent cofactors for the development of
sebaceous gland hyperplasia. Current molecular findings indicate that over
expression of the ageing-associated gene Smad7 and parathormone-related pro
tein correlate with sebaceous gland hyperplasia, whereas c-myc overexpressi
on is associated with enhanced sebum production. On the other hand, down-re
gulation of the mismatch repair genes hMLH-1 and hMSH-2 may promote the dev
elopment of sebaceous gland carcinoma. In addition to spontaneous single tu
mours, sebaceous gland carcinomas have been reported in immune-suppressed t
ransplant. recipients (azathiorpine, cisplatin, cyclosporin A) and in assoc
iation with the Muir-Torre syndrome. Microsatellite instability with a loss
of the mismatch repair gene hMSH-2 has been detected in immune suppressed
patients and under photo-induced DNA damage. Topical and systemic oestrogen
s offer treatment options for skin xerosis in menopausal females. A combina
tion of isotretinoin and interferon-a may prevent tumour development in pat
ients with Muir-Torre syndrome.