Cryptorchidism is a male congenital disorder with an unspecified, multifactorial etiology. This review evaluated the strength of select factors in the development of cryptorchidism to better understand its etiology. The strength of relationship between factors and their respective functions during testicular descent was evaluated. Factors evaluated in the causal pathway include the signaling mechanisms Desert Hedgehog (DHH), Insulin-like Hormone 3 (INSL3) and Platelet-Derived Growth Factor (PDGF), as well as sex hormone regulation (androgen: estrogen ratio, aromatase expression). Articles supporting a factor in testicular descent were evaluated and scored. These scores were summed to create the “Step Score” for each step in the causal pathway. An arrow system was developed which ranked the strength of each pathway step as either “weak”, “moderate” or “strong”. Thus, step scores and the strength of factors in the pathological pathway were determined: DHH (15-moderate), PDGF (10-weak), INSL3 (24-strong) and Androgen: Estrogen ratio, Aromatase (23-strong). The pathological pathway produced by this review represents a literature based perspective of the research regarding cryptorchidism etiology. Literature indicates that prenatal exposure to endocrine disrupting chemicals in animals and humans may lead to abnormal genital development. Recently, prenatal maternal cigarette smoke was demonstrated to be a risk factor for cryptorchidism. This controversial finding was explored in the context of endocrine disrupting chemicals. However, literature has provided very little evidence in support of this hypothesis and more research is needed to better evaluate prenatal maternal smoking as a risk factor for undescended testis.
Rovito, Michael J.
Bachelor of Science (B.S.)
College of Health and Public Affairs
Department of Health Professions
Orlando (Main) Campus
Morrissey, Andrew R., "Causal Factors of Cryptorchidism and Endocrine Disurpting Chemicals Such as Prenatal Maternal Cigarette Smoke: A Narrative Review" (2016). Honors in the Major Theses. 8.