Trisomy 21 placentas: Histopathological and immunohistochemical findings using proliferating cell nuclear antigen

Faisal Qureshi*, Suzanne M. Jacques, Mark P. Johnson, Roderick F. Hume, Ralph L. Kramer, Yuval Yaron, Mark I. Evans

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Objective: The cause of growth retardation in trisomy 21 and other autosomal trisomies is not known, but may be the result of defective cell proliferation, slowing of the cell cycle, or placental structural abnormalities. Abnormalities of the fetal cell cycle may be reflected in placental growth and can be detected using proliferating cell nuclear antigen (PCNA). Methods: Twelve second-trimester and six third-trimester trisomy 21 placentas were examined histopathologically and stained immunohistochemically using antibodies to PCNA. Normal age-matched placentas were used as controls. Results: The second-trimester trisomy 21 placentas all exhibited many large irregular hypovascular villi. The third-trimester trisomy 21 placentas showed two patterns: (i) many large, irregular hypovascular villi, and (ii) relatively normal-appearing villi with only a few abnormal villi and focal hypervascularity. PCNA staining was significantly greater in second-trimester placentas when compared to third-trimester placentas for both trisomy 21 and controls. There was no significant difference in PCNA staining in trisomy 21 placentas when compared to the normal age-matched controls. Conclusions: PCNA staining indicates no significant differences in proliferation between normal and trisomy 21 placentas. Trisomy 21 placentas show villus abnormalities, including hypovascularity.

Original languageEnglish
Pages (from-to)210-215
Number of pages6
JournalFetal Diagnosis and Therapy
Issue number4
StatePublished - 1 Jan 1997
Externally publishedYes


  • Growth retardation
  • Histopathology
  • Placenta
  • Proliferating cell nuclear antigen
  • Trisomy 21


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