What is the pathophysiology of seborrheic keratosis?

Updated: Oct 14, 2020
  • Author: Arthur K Balin, MD, PhD, FACP; Chief Editor: William D James, MD  more...
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Seborrheic keratoses are thought to result from a clonal expansion of a mutated epidermal keratinocyte. [1] Seborrheic keratoses exhibit histologic evidence of proliferation. Increased cell replication has been demonstrated in seborrheic keratoses with bromodeoxyuridine incorporation studies and immunohistochemistry for proliferation-associated antigens.

Reticulated seborrheic keratoses are usually found on sun-exposed skin, and the reticulated type of seborrheic keratoses may develop from solar lentigines.

Epidermal growth factors and their receptors have been studied in the development of seborrheic keratoses. [2, 3, 4] No difference was observed in the expression of immunoreactive growth hormone receptors in keratinocytes from normal epidermis and keratinocytes from seborrheic keratoses. The expression of BCL2, an apoptosis-suppressing oncogene, is low in seborrheic keratosis in contrast to the high values in basal cell and squamous cell carcinoma. [5] No increase is observed in the sonic hedgehog signal transducers patched (ptc) and smoothened (smo) messenger RNA (mRNA) in seborrheic keratosis over normal skin. [6]

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