Normal pubertal development and the menstrual cycle as a vital sign *
Joseph S. Sanfilippo, Eduardo Lara-Torre, Veronica Gomez-Lobo in Sanfilippo's Textbook of Pediatric and Adolescent GynecologySecond Edition, 2019
Objective measures to evaluate pubertal physical changes allow the clinician to better monitor the normal rate of development. The standard universal system in use today was initially described by Tanner in 1969 and is currently known as the Sexual Maturity Scale (SMS).3 Activation of the HPG axis leads to production of sex steroids, estrogen and androgens from the ovaries. The effect of estrogen includes breast development, estrogenization of the vagina and growth of female internal reproductive organs, body fat deposition, and linear growth. Androgens secreted by the adrenal gland contribute to body odor and the growth of pubic and axillary hair. Previous studies focused significantly on differences by ethnic background, but now these ages need to be considered carefully, because the pure lines of racial origin are not as clear as in the past.
Pregnancy and infertility
Martin Andrew Crook in Clinical Biochemistry & Metabolic Medicine, 2013
Prolactin, oestrogens, progesterone and (human) placental lactogen stimulate breast development in preparation for lactation. High plasma oestrogen concentrations inhibit milk secretion; lactation can start only when plasma concentrations fall after delivery of the placenta. Initially lactation depends on prolactin. Suckling stimulates secretion of the hormone, but, even during lactation, plasma prolactin concentrations fall progressively post partum and reach non-pregnant levels after 2 or 3 months. Apart from the effects on the breast, the high plasma concentration of prolactin interferes with gonadotrophin and ovarian function and produces a period of relative infertility.
Reproductive System and Mammary Gland
Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard in Toxicologic Pathology, 2018
The development and structure of the mammary gland are highly dependent upon the interactions of a number of steroid and protein hormones and growth factors. Much of our knowledge of the endocrine regulation of mammary gland development has been derived from rodent models in which hormones were administered alone or in combination to animals from which various endocrine organs have been removed. More recently, the use of mouse models in which hormone or hormone receptor genes are disrupted has contributed greatly to refining our understanding of the molecular basis of mammary growth (Cardiff et al. 2007; Rudmann et al. 2012).
Cross talk of vascular endothelial growth factor and neurotrophins in mammary gland development
Published in Growth Factors, 2020
Kamini Dangat, Amrita Khaire, Sadhana Joshi
The current review describes the role of neurotrophins and angiogenic factors in mammary gland development. Angiogenesis in the mammary gland alveolar cells plays an important role in milk production. Both VEGF and neurotrophins are known to play a significant role in influencing placental angiogenesis. It is likely that there is a cross talk between these growth factors and together they regulate angiogenesis in the mammary gland. It is therefore necessary to undertake animal studies to understand the possible molecular mechanisms through which neurotrophins and angiogenic factors influence mammary gland development. It is also essential to understand their role in pregnancy complications like preeclampsia, GDM and adverse birth outcomes like preterm birth and IUGR. These studies will be of significance in understanding factors which regulate mammary gland development to optimise milk production. It is well known that during the first six months of life, breast milk is the only nutritional source for the healthy growth of infants and can play a key role in improving the neurodevelopmental outcome in infants.
Breast cancer and environmental contamination: A real connection?
Published in Cogent Medicine, 2018
Fernando Delgado-López, S. Pilar Zamora-León
On the other side, several studies suggest that BPA increase the risk of breast cancer, especially if the exposure is early in life. There are animal studies indicating that fetal environmental exposure, and also during lactation, can affect mammary gland development, even at low doses, and those changes were associated with development of breast cancer during adulthood (Acevedo, Davis, Schaeberle, Sonnenschein, & Soto, 2013; Betancourt, Eltourn, Desmond, Russo, & Lamartiniere, 2010; Mandrup, Boberg, Isling, Christiansen, & Hass, 2016; Paulose, Speroni, Sonnenschein, & Soto, 2015; Weber & Keri, 2011). In addition, rats exposed to BPA in womb presented abnormalities in adult mammary tissue and alterations in the milk protein content by the time they were feedings their pups (Kass, Altamirano, Bosquiazzo, Luque, & Muñoz-de-Toro, 2012). It has also been shown that mice prenatal exposure to BPA alters gene transcription of epithelial cellular genes and genes that are associated with the stroma of the mouse fetal mammary gland. Considering that BPA is an EDC, after birth, BFA exposure alters the sensitivity to estradiol-dependent mammary gland development and progesterone-dependent mammary cell proliferation. Additionally, BPA affects both ER-dependent and ER-independent pathways (Ibrahim, Elbakry, & Bayomy, 2016; Paulose et al., 2015; Zhang et al. 2015).
Long-term effects of treatment of central precocious puberty with gonadotropin-releasing hormone analogs every three months
Published in Gynecological Endocrinology, 2020
Anastasia Vatopoulou, Evelien Roos, Angelos Daniilidis, Konstantinos Dinas
Patients’ characteristics after the end of treatment are shown in Table 2. Mean follow-up was 3.1 years. Height gain ranged between 4 and 6 cm. Actual height at the end of treatment did not differ significantly from the predicted height. The difference between chronological age and bone age at the end of treatment was smaller than at baseline (p<.05). Bone mineral density (BMD) was not affected. Body mass index (BMI) increased in all subjects but none was obese at the end of follow-up. All patients resumed normal menstruation on an average of 16 months after the end of treatment. Mean age of menarche was 12 years (range, 8–13 years). Suppression of breast development was observed in all patients. No treatment-related side effects were observed.
Related Knowledge Centers
- Atrophy
- Biological Process
- Breast
- Growth Factor
- Mammary Gland
- Puberty
- Menopause
- Pregnancy
- Prenatal Development
- Hormone