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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 11 5321-5327
Copyright © 2004 by The Endocrine Society

Stockpiling of Transitional and Classic Primary Follicles in Ovaries of Women with Polycystic Ovary Syndrome

Gustavo A. R. Maciel, Edmund Chada Baracat, Jo Ann Benda, Sanford M. Markham, Krista Hensinger, R. Jeffrey Chang and Gregory F. Erickson

Department of Reproductive Medicine (G.A.R.M., K.H., R.J.C., G.F.E.), University of California, San Diego, La Jolla, California 92093; Universidade Federal de São Paulo (E.C.B.), São Paulo, Brazil 01311-940; University of Iowa Carver College of Medicine (J.A.B., S.M.M.), Iowa City, Iowa 52242

Address all correspondence and requests for reprints to: Gregory F. Erickson, Ph.D., Department of Reproductive Medicine, University of California San Diego, La Jolla, CA 92093-0674. E-mail: gerickson{at}ucsd.edu.

Recently, we proposed an oocyte-growth differentiation factor-9 hypothesis that predicts alterations in the initial stages of folliculogenesis in polycystic ovary syndrome (PCOS) ovaries. Here, we test this hypothesis by scoring the composition of follicles in normal and PCOS ovaries. Follicles were classified as primordial, transitional primary, classic primary, secondary, and Graafian. A total of 2274 follicles were scored. The total number of growing follicles was significantly greater in PCOS ovaries than normal, but the number of nongrowing primordial follicles did not differ. Consequently, the increase in growing follicles in PCOS cannot be explained by increased primordial follicle recruitment. Differential counts showed that the number of growing follicles at each stage of development was significantly greater: PCOS had 2.7-fold more primary, 1.8-fold more secondary, and 2-fold more Graafian follicles than normal. The greatest effect was on the classic primary follicles where the number was almost 5-fold greater in PCOS ovaries. The absence of apoptosis in normal and PCOS preantral follicles argues that the increase in growing follicles in PCOS cannot be explained by changes in atresia. We conclude, therefore, that primary follicle growth is abnormally slow in PCOS and the dynamics are reflected in a stockpiling of classic primary follicles.




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