What Regulates The Hormone Stress Diet And Bone Remodeling?

Bone remodeling is a lifelong process that balances bone formation by osteoblasts and resorption by osteocytes. Endocrine influences play a crucial role in bone turnover, with oestrogen being the most important endocrine regulator. Other hormones regulating bone metabolism include insulin-like growth factor-1, parathyroid hormone, gut and adipocyte hormones, and FGF23 and osteocalcin. Thyroid hormones can also stimulate bone resorption and formation, maintaining normal bone remodeling.

Calcitonin (CT), parathyroid hormone (PTH), vitamin D3, and estrogen are major hormonal regulators of osteoclastic bone resorption. The regulation of bone formation and resorption is underpinned by the interaction of estrogens, testosterone, parathyroid hormone, vitamin D, and other hormones. Lifestyle-based interventions, such as nutrition and stress management, help to maintain bone homeostasis.

FGF21, a hormone secreted by the liver, regulates energy metabolism and is essential for bone remodeling. The pituitary gland secretes growth hormone (GH), which controls bone growth in several ways, triggering chondrocyte proliferation. Bone remodeling is influenced by both physical stimuli and biochemical factors, with mechanical stress affecting the former and hormones affecting the latter.

Estrogens reduce bone loss by inhibiting the generation of new osteoclasts, reducing the activation frequency of the bone multicellular unit (BMU), and promoting apoptosis of mature osteoblasts. Hormones long thought to solely modulate energy and mineral homeostasis may influence adipocytic function, as osteoblasts are a target of insulin.

How does estrogen regulate bone remodeling?

Estrogen is a hormone that inhibits bone remodeling and resorption, primarily through direct effects on osteoclasts. It also plays a role in osteoblast/osteocyte and T-cell regulation of osteoclasts. Estrogen deficiency is associated with a gap between bone resorption and formation, likely due to the loss of estrogen’s effects on decreasing osteoblast apoptosis, oxidative stress, and osteoblastic NF-κB activity.

This study was supported by research grants NIH AG004875, AR027065, and the Kogod Center on Aging, Mayo Foundation. The manuscript is an unedited PDF file accepted for publication, which will undergo copyediting, typesetting, and review before being published in its final citable form.

What factors regulate bone remodeling?

The remodeling phases of bone involve hormones and factors regulating the activation phase, osteoclast recruitment and resorption phase, and glucocorticoid receptor alpha. The activation phase includes factors such as PTH, IGF-1, IL-1, IL-6, PGE2, Calcitriol, TNF-α−, estrogen, and retinoic acid. The osteoclast recruitment and resorption phase involves factors like RANKL, M-CSF, αvβ3 integrins, IL-1β, IL-1α, TNF-α, retinoic acid, S1P−, OPG, GM-CSF, estrogen, Calcitonin, IL-4, IL-18, and TGF-β.

The repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation. Estrogen receptor-alpha signaling in osteoblast progenitors stimulates cortical bone accrual.

What are the factors affecting bone growth and remodeling?

Bone remodeling is influenced by various hormones, cytokines, and growth factors with endocrine, paracrine, and autocrine actions. These include parathyroid hormone, calcitonin, thyroid hormones, growth hormone, and sexual steroids. Other hormones, cytokines, and growth factors also play a crucial role. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including those for text and data mining, AI training, and similar technologies.

What hormones regulate bone growth and remodeling?

Calcium-regulating hormones are crucial for producing healthy bones. Parathyroid hormone (PTH) maintains calcium levels and stimulates bone resorption and formation. Calcium-derived hormone calcitriol stimulates the intestines to absorb calcium and phosphorus, directly affecting bone. PTH also inhibits bone breakdown and may protect against excessively high calcium levels in the blood. PTH is produced by four small glands adjacent to the thyroid gland, which control calcium levels in the blood.

When calcium concentration decreases, PTH secretion increases. PTH conserves calcium and stimulates calcitriol production, increasing intestinal absorption of calcium. It also increases calcium movement from bone to blood. Hyperparathyroidism, caused by a small tumor of the parathyroid glands, can lead to bone loss. PTH stimulates bone formation and resorption, and when injected intermittently, bones become stronger. A new treatment for osteoporosis is based on PTH.

A second hormone related to PTH, parathyroid hormone-related protein (PTHrP), regulates cartilage and bone development in fetuses but can be over-produced by individuals with certain types of cancer. PTHrP causes excessive bone breakdown and abnormally high blood calcium levels, known as hypercalcemia of malignancy.

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.

What controls bone remodeling in Chegg?

Bone remodeling is influenced by both physical stimuli and biochemical factors. Mechanical stress can be defined as a physical stimulus, whereas hormones can be defined as a biochemical factor.

What dietary factors influence bone remodeling?

The risk of osteoporosis is influenced by various factors, including a diet low in calcium, physical activity, tobacco and alcohol use, sex, size, age, race and family history, hormone levels, eating disorders, and certain medications.

A low calcium diet can lead to diminished bone density, early bone loss, and an increased risk of fractures. Physically inactive individuals have a higher risk of osteoporosis than more-active individuals. Women have less bone tissue than men, and those with a body mass index of 19 or less or a small body frame are at higher risk. Age and race also play a role in the risk, with white or Asian descent individuals at greater risk.

Hormone levels can also contribute to bone loss, with women experiencing increased bone loss at menopause due to dropping estrogen levels. Eating disorders and other conditions, such as severe restriction of food intake and underweight, can also weaken bones.

Medications like corticosteroid medications, aromatase inhibitors, selective serotonin reuptake inhibitors, methotrexate, anti-seizure medications, and proton pump inhibitors can also increase the risk of osteoporosis. To prevent or slow bone loss, it is essential to include plenty of calcium in your diet, which is recommended for adults aged 19 to 50 and men aged 51 to 70.

What directly controls bone remodeling?

Recent studies have shown that the activity of osteocytes during bone remodeling is tightly controlled by hormones secreted by other endocrine glands, such as parathyroid hormone (PTH) and gonadal estrogen. Osteocytes communicate with osteoblasts in a paracrine manner, and their ability to modulate osteoblast function is associated with the synthesis of SOST, an inhibitor of bone formation. This interaction slows down the rate of bone formation. Osteocytes can also affect osteoblasts by secreting prostaglandin E2, nitric oxide (NO), and ATP, which stimulate their activity.

During bone remodeling, osteoblasts are activated via RANKL and M-CSF, while osteoblasts are inhibited via OPG, NO, and TGFβ. Osteocytes-derived PGE2, NO, and ATP stimulate osteoblasts, while sclerostin or DKK1 decrease osteoblast activity. Osteoblasts interact with osteoclasts through RANKL, and bone-lining cells support the process of bone turnover. The role of SOST in the regulation of bone growth and remodeling is discussed in the following section.

What controls bone remodeling hormones and diet?

Remodelling is influenced by mechanical loading and is influenced by local and systemic factors. Hormones like oestrogens, cortisol, androgens, growth hormone/IGF-1, PTH, intestinal and adipocyte hormones regulate bone metabolism. ScienceDirect uses cookies and all rights are reserved for text and data mining, AI training, and similar technologies. Open access content is licensed under Creative Commons terms.

How is bone remodeling controlled?

The rate of bone remodeling is influenced by the amount of RANKL and OPG secreted near the bone’s surface. This information is sourced from ScienceDirect, a website that uses cookies and is copyrighted by Elsevier B. V., its licensors, and contributors. The website also provides information on AI training and similar technologies, with Creative Commons licensing terms for open access content.

How does stress affect bone remodeling?

Recent studies have shown that osteocytes act as mechanosensors during the early stages of bone remodeling. Loaded mechanical stress is converted into biochemical reactions, activating osteoclasts and osteoblasts to cause bone resorption and formation. This process is crucial for bone resorption and formation. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including those for text and data mining, AI training, and similar technologies.