Follicular atresia refers to a common degenerative process in the mammalian and non-mammalian vertebrate ovary, through which the bulk of the oocytes at different stages of development or growth are lost other than go through the ovulation process. There have been several opinions regarding the causes of follicular atresia.This implies that the cause and timing of follicular atresia is not well understood. However, the morphological, histochemical and biochemical changes of follicular atresia have been described in the recent past. Atresia is often manifested with noticeable “morphological, histochemical and biochemical changes in the various components of the follicle which can be described in relation to primordial, primary, secondary and tertiary follicles.”(Guojun Cheng) It occurs in the ovaries and makes it difficult to tell whether structural changes of oocytes and their cells are normal or degenerative. Atresia affects the primordial and primary follicles at different rates for different species and strains. The differences can be studied in “frozen gelatin sections which show little distortion.” (Guojun Cheng) Studies conducted by the electron microscope have also shown that the nuclear and ooplasmic contents condense, resulting in an increased electron density. Sub mammalian vertebrates have relatively rare cases of atresia in the primary follicles. “The morphological and histochemical features of atretic primordial and primary follicles vary greatly among the mammalian species and other vertebrates.”(Guojun Cheng) The main features by which the atretic primordial oocytes have been distinguished from normal ones is through shrinkage and crinkled appearance of the nuclear envelope. The second method of distinction is by the detection of unevenly distributed chromatin which is fragmented. In the early stages of degenerative change there is appearance of lysosomes containing dense material that varies in structure as demonstrated In vitro by the electron microscope. Mitochondrial alterations, visualization of vacuole and myelin structures are major signs of early degeneration in smaller oocytes.
The role of hormones in the development of follicular atresia can be described by the following. “Promordial follicles often remain dormant for long period of time until they are stimulated to develop; in women this can be as long as 50 years.” (Guojun Cheng) An intricate network composed of paracrine and endocrine systems is “involved in the recruitment of the dormant oocytes into the growth pool, where the follicles progress through a morphologically well characterized developmental stages of primary, secondary, tertiary, pre-ovulation and finally to ovulation.” (Guojun Cheng) Follicular atresia can be regarded as an apoptosis that is controlled by two hormones, estrogen and Follicle stimulating hormone. The two hormones are vital for “follicles to escape atresia and reach the preovulatory follicle stage. FSH elevates estrogen levels through stimulation of aromatose expression in granulose cells.” (Guojun Cheng) Growth factors are also involved in this process, “the insulinlike growth factor (IGF-1), epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and the cytokine interleukin – 1beta participate in the prevention of follicular apoptosis.” (Guojun Cheng) A study was conducted to determine the role of “Androgen receptor in the follicular atresia of estrogen receptor Beta Knockout mouse ovary.” (Guojun Cheng) The results obtained showed that in the absence of ER beta there was no regulation of Androgen receptors. This is due to the fact “that androgens enhance the recruitment of primordial follicles into the growth pool and cause atresia of the antral follicles.” (Guojun Cheng)
Works cited
Guojun Cheng. “A ROle for the Androgen Receptor in Follicular Artresia of Estrogen Receptor Beta Knockout Mouse Ovary.” biolreprod.org. 2001. Web.