Which Gland Controls The Rebuilding Of Bones?

Bone remodeling is a lifelong process that adjusts the architecture of the body to meet its changing needs. It involves five distinct phases, with serotonin being one of the most important extra-skeletal biologically active compounds regulating bone remodeling. Other major hormonal regulators include calcium, parathyroid hormone (PTH), vitamin D3, and estrogen. The most important endocrine regulator of bone turnover is likely oestrogen, but other hormones regulating bone metabolism include insulin-like growth.

In vertebrates, bone modeling and remodeling are essential processes activated throughout life and regulated by distinct temporal cellular constituents. Trabecular bone remodeling is the predominant mechanism for fulfilling the homeostatic role of calcium-regulating hormones, while cortical bone is responsible for the resorption and deposition phases. Osteocytes play a significant role in the regulation of osteogenesis, releasing sclerostin (SOST), an inhibitor of bone formation.

Parathyroid hormone (PTH) exerts profound effects on skeletal homeostasis through multiple cellular and molecular mechanisms. The integration between PTH, calcitonin, and vitamin D active forms is significantly required for the formation and remodeling of the bone. Osteocytes also have the capacity to regulate bone remodeling in response to systemic hormones. The rate of remodeling is regulated by a wide variety of calcitropic hormones, such as PTH, thyroid hormone, and sex steroids.

In recent years, there has been a growing interest in understanding the role of T-cells in regulating bone remodeling during homeostasis. Overall, bone remodeling is a vital process that contributes to the development of a mature, dynamic bone structure.

What gland is responsible for bone remodeling?

Parathyroid hormone (PTH) is produced by four small glands that control calcium levels in the blood. They are sensitive to small changes in calcium concentration, and when calcium concentration decreases, PTH secretion increases. PTH acts on the kidney to conserve calcium and stimulate calcitriol production, which increases intestinal absorption of calcium. It also acts on the bone to increase movement of calcium from bone to blood.

Excessive production of PTH, usually due to a small tumor of the parathyroid glands, is called hyperparathyroidism and can lead to bone loss. PTH stimulates bone formation and resorption, and when injected intermittently, bone formation predominates and bones become stronger.

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

Calcitriol, produced from vitamin D, is the hormone produced from vitamin D by enzymes in the liver and kidney. Its most important action is to increase intestinal absorption of calcium and phosphorus, providing minerals for the skeleton. Vitamin D deficiency leads to defective mineralization diseases, such as rickets in children and osteomalacia in adults, which can result in bone pain, bowing, leg deformities, and fractures. Treatment with vitamin D can restore calcium supplies and reduce bone loss.

What endocrine gland controls the growth of bones?

The pituitary gland, a part of the brain, produces various hormones, including growth hormone (HGH), which plays a crucial role in regulating height, bone length, and muscle growth. However, some individuals misuse synthetic growth hormone, believing it will increase muscle size and strength. This can lead to an irreversible condition called acromegaly, which is the overgrowth of bones in the face, hands, and feet. It is essential to avoid synthetic growth hormone abuse to maintain overall health and well-being.

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.

Which gland controls bones?

The parathyroid glands, located in the throat, secrete parathyroid hormone, which plays a pivotal role in regulating calcium, phosphorus, and magnesium levels in bones and blood. Such issues may manifest as hyperparathyroidism or hypoparathyroidism. The treatment options available for this condition include dietary changes, the administration of supplements, and surgical removal of the affected glands, depending on the specific circumstances.

Is thyroid involved in bone remodeling?

It has been demonstrated that individuals with overt hyperthyroidism exhibit accelerated bone remodeling, diminished bone density, and an elevated risk of developing osteoporosis, which in turn increases the likelihood of sustaining fractures.

What regulates bone remodeling?

The skeleton is a metabolically active organ that undergoes continuous remodeling throughout life. Bone remodeling involves the removal of mineralized bone by osteoclasts and the formation of bone matrix through osteoblasts. The remodeling cycle consists of three phases: resorption, reversal, and formation. It adjusts bone architecture to meet changing mechanical needs, repairs microdamages in bone matrix, and maintains plasma calcium homeostasis.

Systemic and local regulation of bone remodeling is involved, with major systemic regulators including parathyroid hormone (PTH), calcitriol, growth hormone, glucocorticoids, thyroid hormones, and sex hormones. Factors such as insulin-like growth factors (IGFs), prostaglandins, tumor growth factor-beta (TGF-beta), bone morphogenetic proteins (BMP), and cytokines are also involved. Local regulation of bone remodeling involves a large number of cytokines and growth factors that affect bone cell functions.

The RANK/receptor activator of NF-kappa B ligand (RANKL)/osteoprotegerin (OPG) system tightly couples the processes of bone resorption and formation, allowing a wave of bone formation to follow each cycle of bone resorption, thus maintaining skeletal integrity.

Is bone remodeling controlled by parathyroid hormone?

PTH stimulates bone remodeling, but bone resorption is more prevalent when exposed to high levels. Low, intermittent doses of PTH lead to a net increase in bone mass. Two papers of interest, “Pharmacological mechanisms of therapeutics: parathyroid hormone” and “Calcium and phosphate homeostasis: concerted interplay of new regulators”, provide insights into the pharmacological mechanisms of therapeutics and the interplay of new regulators in bone remodeling and homeostasis.

What gland regulates bone growth?

Parathyroid hormone (PTH) is a significant endocrine regulator of calcium and phosphate levels, and chronic hyperparathyroidism can lead to bone loss due to excessive stimulation of bone resorption. However, it can also increase osteoblast numbers and bone formation. Intermittent PTH (iPTH) and parathyroid hormone related peptide (PTHrP) both signal through the same G protein-coupled receptor, and the PTHrP analog, abaloparatide, has been shown to boost bone mass and reduce fractures in patients with osteoporosis when given by once daily subcutaneous injection.

Currently, iPTH/PTHrP treatments are the only FDA-approved osteoporosis medications that stimulate new bone formation. However, the cellular and molecular mechanisms behind this process are incompletely understood. Two phenomena may limit the bone-forming efficacy of these medications: concurrent osteoclast stimulation might mitigate some gains in bone mass, and the ability of iPTH to stimulate new bone formation wanes with time and repeated dosing. Progressive blunting of the bone anabolic effect of iPTH may also limit the efficacy of prolonged treatment.

Several cellular mechanisms have been proposed to explain how iPTH treatment increases bone formation. PTH significantly decreases osteoblast apoptosis and activates bone lining cells, acts directly on early cells in the osteoblast lineage, and inhibits adipocyte differentiation of early skeletal stem cells in the osteoblast lineage. Non-cell-autonomous effects of PTH on osteoblast activity may also occur through increases in actions of growth factors.

T lymphocytes in the bone marrow microenvironment respond to iPTH by producing cytokines that stimulate osteoblast differentiation, while osteoclasts may generate factors important in increasing osteoblast numbers. Additionally, PTH reduces levels of the antiosteoblastogenic WNT inhibitor sclerostin through effects on osteocytes, providing another paracrine mechanism through which PTH might stimulate osteoblast differentiation.

Which hormone controls bone remodeling?

Hormonal regulation of bone remodeling is primarily regulated by oestrogen, with other important endocrine regulators including IGF-1, cortisol, PTH, leptin, and gut hormones also playing roles. Other sex hormones, IGF-1, cortisol, and PTH are also important. Recent research has also identified roles for leptin and gut hormones. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved.

How is bone growth and remodeling regulated?

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 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.