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Pathogenesis of benign prostatic hyperplasia.

R J Bosch1

  • 1Department of Urology, Erasmus University Hospital, Rotterdam, The Netherlands.

European Urology
|January 1, 1991
PubMed
Summary
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Benign prostatic hyperplasia (BPH) pathogenesis is unclear, with three main theories: dihydrotestosterone, embryonic reawakening, and stem cell involvement. These mechanisms likely interact to cause BPH development.

Area of Science:

  • Urology
  • Cell Biology
  • Endocrinology

Background:

  • The exact causes of benign prostatic hyperplasia (BPH) are not fully understood.
  • Existing theories propose different mechanisms driving BPH development.

Purpose of the Study:

  • To review and synthesize the major theories on BPH pathogenesis.
  • To highlight the potential interplay between different causative mechanisms.

Main Methods:

  • Literature review of established theories on BPH pathogenesis.
  • Analysis of the dihydrotestosterone hypothesis, embryonic reawakening theory, and stem cell theory.

Main Results:

  • The dihydrotestosterone hypothesis links BPH to hormonal changes, supported by castration studies.

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  • The embryonic reawakening theory suggests prostatic stroma's developmental potential is reactivated.
  • The stem cell theory proposes BPH arises from increased stem cell numbers or abnormal clonal expansion.

    • Conclusions:

    • Multiple theories, including hormonal, developmental, and cellular mechanisms, contribute to BPH pathogenesis.
    • These pathways may not be mutually exclusive and likely act in concert.
    • Further research is needed to fully elucidate the complex etiology of BPH.