Bone remodeling

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Bone tissue is removed by osteoclasts, and then new bone tissue is formed by osteoblasts. Both processes utilize cytokine (TGF-b, IGF) signalling. Bonemetabolism.svg
Bone tissue is removed by osteoclasts, and then new bone tissue is formed by osteoblasts. Both processes utilize cytokine (TGF-β, IGF) signalling.

In osteology, bone remodeling or bone metabolism is a lifelong process where mature bone tissue is removed from the skeleton (a process called bone resorption ) and new bone tissue is formed (a process called ossification or new bone formation). Recent research has identified a specialised subset of blood vessels, termed Type R endothelial cells, in the bone microenvironment. [1] These blood vessels play a crucial role in adult bone remodelling by mediating interactions between bone-resorbing osteoclasts and bone-forming osteoblasts. Type R blood vessels are characterised by their association with post-arterial capillaries and exhibit unique remodelling properties crucial for bone homeostasis. [2] These processes also control the reshaping or replacement of bone following injuries like fractures but also micro-damage, which occurs during normal activity. Remodeling responds also to functional demands of the mechanical loading.

Contents

In the first year of life, almost 100% of the skeleton is replaced. In adults, remodeling proceeds at about 10% per year. [3]

An imbalance in the regulation of bone remodeling's two sub-processes, bone resorption and bone formation, results in many metabolic bone diseases, such as osteoporosis. [4]

Physiology

Bone homeostasis involves multiple but coordinated cellular and molecular events. [5] Two main types of cells are responsible for bone metabolism: osteoblasts (which secrete new bone), and osteoclasts (which break bone down). The structure of bones as well as adequate supply of calcium requires close cooperation between these two cell types and other cell populations present at the bone remodeling sites (e.g. immune cells). [6] Bone metabolism relies on complex signaling pathways and control mechanisms to achieve proper rates of growth and differentiation. These controls include the action of several hormones, including parathyroid hormone (PTH), vitamin D, growth hormone, steroids, and calcitonin, as well as several bone marrow-derived membrane and soluble cytokines and growth factors (e.g. M-CSF, RANKL, VEGF and IL-6 family). [7] It is in this way that the body is able to maintain proper levels of calcium required for physiological processes. Thus bone remodeling is not just occasional "repair of bone damage" but rather an active, continual process that is always happening in a healthy body.

Subsequent to appropriate signaling, osteoclasts move to resorb the surface of the bone, followed by deposition of bone by osteoblasts. Together, the cells that are responsible for bone remodeling are known as the basic multicellular unit (BMU), and the temporal duration (i.e. lifespan) of the BMU is referred to as the bone remodeling period. [8]

See also

Related Research Articles

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<span class="mw-page-title-main">Bone healing</span> Healing from bone injury

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<span class="mw-page-title-main">Parathyroid hormone</span> Mammalian protein found in humans

Parathyroid hormone (PTH), also called parathormone or parathyrin, is a peptide hormone secreted by the parathyroid glands that regulates the serum calcium concentration through its effects on bone, kidney, and intestine.

<span class="mw-page-title-main">Osteoblast</span> Cells secreting extracellular matrix

Osteoblasts are cells with a single nucleus that synthesize bone. However, in the process of bone formation, osteoblasts function in groups of connected cells. Individual cells cannot make bone. A group of organized osteoblasts together with the bone made by a unit of cells is usually called the osteon.

<span class="mw-page-title-main">Osteopetrosis</span> Rare disease of the bones

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<span class="mw-page-title-main">Parathyroid hormone-related protein</span> Mammalian protein

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<span class="mw-page-title-main">Osteoclast</span> Cell that breaks down bone tissue

An osteoclast is a type of bone cell that breaks down bone tissue. This function is critical in the maintenance, repair, and remodeling of bones of the vertebral skeleton. The osteoclast disassembles and digests the composite of hydrated protein and mineral at a molecular level by secreting acid and a collagenase, a process known as bone resorption. This process also helps regulate the level of blood calcium.

<span class="mw-page-title-main">Osteoprotegerin</span> Mammalian protein found in Homo sapiens

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<span class="mw-page-title-main">Ossification</span> Development process in bones

Ossification in bone remodeling is the process of laying down new bone material by cells named osteoblasts. It is synonymous with bone tissue formation. There are two processes resulting in the formation of normal, healthy bone tissue: Intramembranous ossification is the direct laying down of bone into the primitive connective tissue (mesenchyme), while endochondral ossification involves cartilage as a precursor.

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<span class="mw-page-title-main">Bone resorption</span> Breakdown of bone tissue to be absorbed into the blood

Bone resorption is resorption of bone tissue, that is, the process by which osteoclasts break down the tissue in bones and release the minerals, resulting in a transfer of calcium from bone tissue to the blood.

<span class="mw-page-title-main">RANKL</span> Mammalian protein found in Homo sapiens

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<span class="mw-page-title-main">Tooth resorption</span> Breakdown of the tooth root to be absorbed by the blood

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In bone physiology, the bone remodeling period describes the temporal duration of the basic multicellular unit (BMU) that is responsible for bone turnover. Historically, this was referred to as the sigma (σ) or sigma period, but the terminology is now outdated.

Nikos Athanasou is an Australian short story writer and novelist and musculoskeletal pathologist and scientist. He was born in Perth and grew up in Sydney where he studied medicine. He moved to England and is currently Professor of Musculoskeletal Pathology at Oxford University and a Fellow of Wadham College.

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