How Does Estrogen Impact The Remodeling Of Bones?

Estrogen plays a crucial role in bone growth, development, and maintenance throughout a person’s life, including longitudinal bone growth, bone healing, and adaptation to mechanical forces. Its direct effects on osteocytes, osteoclasts, and osteoblasts lead to inhibition of bone remodeling, decreased bone resorption, and maintenance of bone formation. Estrogen binds with estrogen receptors to promote the expression of osteoprotegerin (OPG) and suppress the action of nuclear factor-κβ ligand (RANKL). Estrogen (E2) promotes bone formation by opposing osteoclastogenesis and enhancing osteoblast activity.

Estrogen receptor α (ERα)-mediated direct effects of estrogens on osteoclasts, and direct or indirect effects on B lymphocytes, attenuate the resorption of trabecular bone. Estrogen is essential for bone growth and development and for the maintenance of bone health in adulthood. The cellular responses of osteoblasts and osteoclasts to estrogen are essential for bone homeostasis throughout a person’s life.

Estrogen is critical for skeletal homeostasis and regulates bone remodeling, in part by modulating the expression of receptor activator of NF-κB ligand (RANKL). At the cellular level in bone, estrogen inhibits differentiation of osteoclasts, decreasing their number and reducing the amount of active remodeling units. During the maintenance phase, estrogens and androgens have a slowing effect on osteoclast and osteoblast differentiation and therefore bone remodeling.

Estrogen deficiency leads to increased bone remodeling, bone loss, and osteoporosis because bone resorption surpasses bone formation. Estrogen plays a protective role in bone health, as when estrogen levels decrease, such as after menopause, the risk of osteoporosis and bone loss increases. Estrogen also regulates RANKL and OPG, promoting the expression of OPG and reducing bone resorption.

Does estrogen promote the production of new bone?

Studies in animals have shown that estrogen may stimulate osteoblast function, with evidence of bone formation in vivo in various species like rodents and dogs. This is supported by studies in vivo, and the use of cookies is a part of the research process. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including those for text and data mining, AI training, and similar technologies.

How does estrogen and testosterone affect bone growth?

Sex hormones play a crucial role in maintaining a strong skeleton in men. Estrogen regulates cortical bone turnover, while testosterone maintains trabecular turnover. In normal men, sex hormone-binding protein is an independent risk factor for fractures. Cookies are used by this site, and all rights are reserved for text and data mining, AI training, and similar technologies. Creative Commons licensing terms apply for open access content.

What is the relationship between estrogen and calcium?

Oestrogen, 1, 25-dihydroxyvitamin D, and parathyroid hormone play a crucial role in bone metabolism. Cytokines are key mediators of oestrogen, which inhibits bone resorption by acting on osteoblasts and osteoclasts. In normal women, oestrogen withdrawal increases bone resorption and causes a rise in serum calcium. 1, 25-dihydroxyvitamin D is the major direct regulator of active transcellular calcium absorption via vitamin D receptors in intestinal mucosal cells.

Oestrogen can increase calcium absorption directly and indirectly by stimulating 1-α hydroxylaseactivity in the kidney. Withdrawal of oestrogens would theoretically reduce calcium absorption, but hypercalcaemia in these cases cannot be explained by this mechanism. The effects of oestrogen on bone and calcium metabolism are monitored by the calcium sensing receptor on parathyroid cells, which respond by altering parathyroid hormone secretion.

Parathyroid hormone is a major modulator of osteoclast activity, and in the absence of parathyroid hormone, the balance between the action of 1, 25-dihydroxyvitamin D and oestrogen may become more crucial. Clinical awareness of this phenomenon allows for appropriate monitoring of patients and adjustment of their vitamin D dose at menopause or while starting or stopping hormone replacement therapy.

How does growth hormone affect bone remodeling?

Growth hormone (GH) is a peptide hormone secreted from the pituitary gland, regulated by the hypothalamus. It plays a significant role in bone metabolism and growth, affecting bone mass. Bone mass increases steadily through childhood, peaking in the mid-20s, and then slows down in late life. During childhood, bone mass accumulation is a combination of bone growth and bone remodeling. GH stimulates osteoblast proliferation and activity, promoting bone formation and resorption.

The absence of GH results in a reduced rate of bone remodeling and a gradual loss of bone mineral density. Bone growth occurs at the epiphyseal growth plates, primarily regulated by chondrocytes. GH has direct effects on chondrocytes, primarily through IGF-I, which stimulates cell proliferation and matrix production. GH deficiency severely limits bone growth and accumulation of bone mass. GH deficiency is not uncommon in oncology and has long-term effects on bone health. The effects of growth hormone on cortical and cancellous bone are also discussed.

How does estrogen affect bone Remodelling?

Estrogen plays a crucial role in bone growth, maturation, and bone turnover regulation. It is necessary for proper closure of epiphyseal growth plates in both males and females during bone growth. In young skeletons, estrogen deficiency leads to increased osteoclast formation and enhanced bone resorption. In menopause, estrogen deficiency induces bone loss in cancellous and cortical bones, leading to general bone loss and destruction of local architecture.

In cortical bone, estrogen withdrawal leads to increased endocortical resorption and intracortical porosity, resulting in decreased bone mass, disturbed architecture, and reduced bone strength. Estrogen inhibits osteoclast differentiation, decreasing their number and active remodeling units. Estrogen regulates the expression of IL-6 in bone marrow cells through an unknown mechanism. It is unclear if estrogen’s effects on osteoblasts are direct or due to a coupling phenomenon between bone formation and resorption.

How does estrogen change bone structure?

Skeletal sexual dimorphism occurs at the end of puberty, with male and female bone geometry being similar before puberty. The GH/IGF-1 axis stimulates longitudinal growth at the level of epiphyseal plates. At puberty, sex hormones, estrogens and androgens, play a key role in skeletal growth. Both estrogens and androgens contribute to bone size expansion and mineralization in both sexes, with estrogens acting predominant in females and androgens in males.

Males have a more pronounced periosteal apposition, leading to a bigger cortical diameter and greater endocortical diameter. At the end of growth, males have longer and wider bones than females, but volumetric bone mineral density remains unchanged. Trabecular bone volume, regulated by both estrogens and androgens, is greater in males due to greater trabecular thickness. This raises questions about bone health in transgender adolescents.

What role do hormones play in bone remodeling?

Osteoclasts play a crucial role in bone remodeling and resorption, while osteoblasts lay down new bone. Two hormones that affect osteoclasts are parathyroid hormone (PTH) and calcitonin. PTH stimulates osteoclast proliferation, releasing calcium into the bloodstream and promoting calcium reabsorption by kidney tubules, which can affect calcium homeostasis. PTH indirectly affects the small intestine by stimulating vitamin D synthesis, which promotes calcium absorption.

Calcitonin, secreted by the thyroid gland, inhibits osteoclast activity and stimulates calcium uptake by bones, reducing calcium ion concentration in the blood. PTH and calcitonin are generally not secreted simultaneously, as they have opposing functions in maintaining calcium homeostasis.

What role does estrogen play in bone remodeling rank rankl opg?

Osteoclasts are formed through various factors, including NF-κB signaling, which is activated when binding with RANKL and suppressed when binding with osteoprotegerin (OPG). Estrogen regulates RANKL and OPG, promoting the expression of OPG and reducing bone resorption. It also inhibits osteoclast differentiation and advocates osteoclast apoptosis by increasing TGFβ production. In the absence of estrogen, osteocytes are unable to provoke adequate responses to mechanical strain, indicating that estrogen deficiency is associated with the impairment of mechanosensors in osteocytes.

Despite this, osteocytes produce RANKL, which activates osteoclast formation. Osteocytes also inhibit Wnt signaling by forming sclerostin, which reduces bone formation. In contrast, estrogen retrains sclerostin production, protecting bone stability.

Estrogen deficiency leads to an increase in IL-7, promoting T cell activation, which induces pro-inflammatory molecules like IL-1, IL-6, and TNFα, resulting in osteoclast formation. Additionally, estrogen deficiency amplifies T cell activation and osteoclastogenesis by increasing reactive oxygen species (ROS), leading to the production of TNF. RANKL levels are also upregulated in mesenchymal stem cells (MSCs), T cells, and B cells, causing osteoporosis.

What role does estrogen play in bone remodeling Rankl?

Osteoclasts are formed through various factors, including NF-κB signaling, which is activated when binding with RANKL and suppressed when binding with osteoprotegerin (OPG). Estrogen regulates RANKL and OPG, promoting the expression of OPG and reducing bone resorption. It also inhibits osteoclast differentiation and advocates osteoclast apoptosis by increasing TGFβ production. In the absence of estrogen, osteocytes are unable to provoke adequate responses to mechanical strain, indicating that estrogen deficiency is associated with the impairment of mechanosensors in osteocytes.

Despite this, osteocytes produce RANKL, which activates osteoclast formation. Osteocytes also inhibit Wnt signaling by forming sclerostin, which reduces bone formation. In contrast, estrogen retrains sclerostin production, protecting bone stability.

Estrogen deficiency leads to an increase in IL-7, promoting T cell activation, which induces pro-inflammatory molecules like IL-1, IL-6, and TNFα, resulting in osteoclast formation. Additionally, estrogen deficiency amplifies T cell activation and osteoclastogenesis by increasing reactive oxygen species (ROS), leading to the production of TNF. RANKL levels are also upregulated in mesenchymal stem cells (MSCs), T cells, and B cells, causing osteoporosis.

What role does estrogen play in bone remodeling Quizlet?

The hormone estrogen plays a role in bone formation and resorption. In women experiencing menopause, estrogen can deactivate osteoclast activity, which may contribute to bone mass loss.

Does growth hormone change bone structure?

High doses of synthetic growth hormone, produced by the brain’s pituitary gland, can only thicken bones rather than lengthen them. Any increase in muscle size due to synthetic growth hormone is due to an increase in connective tissue, which does not contribute to muscle strength. Some people abuse synthetic growth hormone in the belief it will help them increase muscle size and strength, leading to an irreversible condition called acromegaly, which is the overgrowth of bones in the face, hands, and feet.