Bone structure and formation, the types of bone, and the cells that participate in its metabolism are all discussed in Chapter 9. Estrogens and androgens are involved in several aspects of bone physiology in all vertebrate species, including (1) skeletal sexual dimorphism; (2) peak bone mass; (3) closure of the epiphyseal growth plate; (4) mineral homeostasis during reproduction, when calcium is removed from the maternal skeleton for that of the offspring; (5) maintenance of bone mass and architecture in adults. Both androgens and estrogens contribute to bone physiology. The focus here will be on estrogens and their effects as they are understood in humans. While androgens do have a role in skeletal physiology, particularly in promoting long bone growth prior to closure of the epiphyseal plate in both males and females, in other actions the role of androgen action independent of that of estrogens has been difficult to establish due to potential conversion to estro gens in bone target cells that contain aromatase.

Table 1 summarizes the current understanding of the effects of the estrogen environment (deficient or replete) in vivo on bone during growth and in the adult skeleton. Effects vary by bone type, in keeping with the different functions of the two types of bone. Cortical bone is largely responsible for the mechanical strength of the skeleton, whereas cancellous (endocortical, trabecular, spongy) bone contributes less to strength but is more available for Ca2+ exchange and therefore maintenance of mineral homeostasis.

Table1. Effect of Estrogen Environment on Bone

In estrogen deficiency the skeleton lengthens due to delayed closure of the epiphyseal growth plate. The role of estrogen in this process in both males and females is substantiated by the skeletal lengthening seen in (extremely rare) males with defects in aromatase or ERα. In females, aromatase deficiency is detected and treated with estrogen replacement early in childhood so that the bone manifestations at and following puberty are averted. As shown in Table 1, in estrogen deficiency or resistance, the mass of cortical bone is increased due to increased width resulting from the unopposed effects of androgens; cancellous bone is decreased due to increased resorption due to estrogen deficiency. The opposite effects are seen prior to puberty in situations where an individual has been treated for estrogen deficiency with 17β-estradiol or a synthetic estrogen.

In the adult, estrogen deficiency brought about by, for example, menopause, ovariectomy, or treatment with aromatase inhibitors, leads to bone loss due to net increased resorption. This is the major underlying cause of postmenopausal osteoporosis in women. Estrogen replacement can forestall this loss of bone mineral.

As seen in Table 2, bone has very little ER of either type compared to the reproductive tissues. In more detailed studies of specific cell types, both ERα and, in lesser amounts, ERβ are found in osteoblasts of humans and in other species. Both are also present in the cells that line the cancellous bones and in growth plate chondrocytes, particularly the resting and proliferation zones. How the relative amounts of the two receptors play a role in the response of these cells to estrogens is as yet unknown. ERα is also seen in osteo clasts, in which estradiol induces apoptosis, and in osteoclast progenitor cells, speeding their differentiation into osteoclasts. Thus, estrogen could exert effects on osteoclast numbers through both osteoclastogenesis and by altering the lifespan of the mature osteoclast.

Table2. Tissue Distribution of ERα and ERβ mRNA ¹

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Polycystic Ovary Syndrome (PCOS)

Estrogen and the Cardiovascular System

Uterine Effects of Estrogen and Progesterone

Menopause

Chemistry and Metabolism of Female Steroid Hormones: Feedback Effects on the Hypothalamus and Pituitary

Control of the Ovary by the Hypothalamus and Pituitary

Synthesis of Progesterone and Estrogens

Female Steroid Hormones

The Androgen Receptor

Hypothalamic-Pituitary-Testis Axis: Feedback Control

Causes of Destructive (Low RAIU) Thyrotoxicosis

Causes of Hyperthyroidism