How Does Bone Remodeling Get Regulated By Physical Stress?

Physical stress (PS) is a complex process that stimulates bone remodeling and affects bone structure and function. It plays a role in bone remodeling by transmitting signals to nearby osteocytes about bone stress, such as tendons pulling on the jaw bone during surgery like mandibular distraction osteogenesis. Bone remodeling replaces old and damaged bones with new ones through a sequence of cellular events occurring on the same surface without any change in bone.

Bone remodeling is essential for adult bone homeostasis, consisting of two phases: bone formation and resorption. The balance between these phases is crucial for sustaining the body. The purpose of bone remodeling is to regulate calcium homeostasis, repair micro-damage to bones from everyday stress, and shape the skeleton during growth.

Remodeling also makes bones thicker at points where muscles place the most stress on them. Additionally, remodeling helps regulate mineral homeostasis by releasing minerals from bones into the environment.

Mechanical forces are indispensable for bone homeostasis, as skeletal formation, resorption, and adaptation are dependent on mechanical signals. Loaded mechanical stress is converted into a series of biochemical reactions, activating osteoclasts and osteoblasts to cause bone resorption and bone density decrease.

The skeleton’s primary mechanical function is to provide rigid levers for muscles to act against as they hold the body upright in defiance of gravity. In exercise, osteocytes can sense variation in mechanical stress and respond and send signals to surrounding cells, regulating bone development.

Psychological stress may be partly responsible for epigenetic regulation of skeletal development and mediate the relationship between socioeconomic factors and bone remodeling.

How do bones typically respond to stress?

Wolff’s Law is a 19th-century theory that suggests that natural healthy bones will naturally adapt to stress. It suggests that when exposed to heavier loads, bones will naturally reconstruct themselves to accommodate that weight. This response is a key aspect of bone theory, which explains how bones respond to stress and how they become stronger to resist strain. In the inverse case, Wolff’s Law explains the effect of decreased weight on bones, as they become less dense and weaker. In severe cases, a drastic reduction in weight can lead to bone replacement.

How bone growth is stimulated by physical stress?

Appositional growth is a process where bones increase in thickness or diameter throughout life due to stress from increased muscle activity or weight. Osteoblasts in the periosteum form compact bone around the external bone surface, while osteoclasts in the endosteum break down bone on the internal bone surface, around the medullary cavity. These processes increase bone diameter while preventing excessive weight and bulkiness.

What are the 3 main things that affect bone 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.

What type of change does physical stress encourage in bones?

Physical stress (PS) stimulates bone remodeling and affects bone structure and function through complex mechanotransduction mechanisms. Recent research suggests that mental stress (MS) also influences bone biology, leading to osteoporosis and increased bone fracture risk. These effects are likely exerted by modulating hypothalamic–pituitary–adrenal axis activity, resulting in altered release of growth hormones, glucocorticoids, and cytokines. A molecular cross talk between mental and PS is thought to exist, with either synergistic or preventative effects on bone disease progression depending on the characteristics of the applied stressor.

Bones are essential components of the musculoskeletal system, protecting vital organs, supporting the body, assisting in movement, producing blood cells, and storing nutrients and minerals. Disturbances in these mechanisms often result in reduced bone mass and an increased risk for fractures. Aging, especially in postmenopausal women, impacts bone health, leading to the accumulation of osteoporosis risk factors, including a gradual inability to cope with physical and mental stressors, which can result in biochemical alterations and consequences on bone adaptation.

What two factors control bone remodeling?

Calcium and phosphate homeostasis hormones significantly impact bone remodeling rates and extent. PTH increases the number of bone sites undergoing remodeling, while only tiny units of bone undergo it at any one time. 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.

What are the factors regulating bone remodeling?

The remodeling process of osteoclasts is influenced by various factors, including parathyroid hormone (PTH) and thyroxine, while it is decreased by estrogen, testosterone, vitamin D, calcium, high phosphorus levels, and other substances. The exact details of the remodeling process remain unclear, but it is believed that these factors contribute to the resorption of bone. The use of cookies is also a part of this process.

How do bones adapt to stress?

Wolff’s Law postulates that when stress is applied to the bones, they undergo remodeling to adapt, resulting in the bones in a tennis player’s dominant arm being up to 20 times thicker than those in their non-dominant arm.

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.

How does physical activity affect bone remodeling?

Exercise plays a crucial role in regulating bone remodeling and preventing osteoporosis. Cell surface receptors, such as focal adhesions, integrins, purinergic receptors, connexin, polycystins, Piezos, Wnt signaling, and sclerostin, play a crucial role in this process. Exercise-induced regulation of bone environment also occurs through cytokines, including inflammatory factors and myokines like irisin. These factors collectively affect bone remodeling. Exercise promotes bone mass and maintains healthy bone, while lack of exercise results in osteoporosis and fracture.

The focal adhesion complex is the most important component of the integrin-based adhesion complex, which transduces mechanical stress from the extracellular matrix (ECM) into the cytoplasm. Integrin proteins, including α and β subunits, are essential for transducing mechanical stress from the ECM into the cytoplasm. The integrin family consists of 24 members, with different tissues expressing different types of integrin. Integrins are expressed in various bone cells, such as osteoblasts, osteocytes, and osteoclasts.

What effect does physical stress have on the bone?

High stress levels can lead to bone loss, osteoporosis, and increased fracture risk. The hormone cortisol, produced by cholesterol from adrenal glands, triggers this reaction by triggering the body’s “fight-or-flight” response in highly stressful situations. Chronic stress invites inflammation into the body, leading to increased cortisol levels, which can wreak havoc on bone health.

Cortisol increases bone resorption, causing bone density to decrease as the body creates osteoclasts in greater amounts. It also blocks calcium from entering bones, making the body less efficient at absorbing calcium. This results in decreased bone density over time. Elevated cortisol levels also stunt bone formation, leading to weaker bones.

To minimize stress side-effects, there are three ways to “de-stress” each day. First, encourage healthy eating. Stress causes oxidative stress, which oxidizes cells, leading to worn-down cells. To combat oxidation, incorporate antioxidants into your diet, such as flavonoids, lutein, and lycopene. These antioxidants are crucial for a normal immune response and maintaining health.

Incorporating a variety of antioxidants into your diet can help maintain a healthy immune system and prevent the buildup of harmful free radicals. By incorporating these antioxidants into your diet, you can help maintain healthy bones and reduce the risk of osteoporosis and increased fracture risk.

How does the body control bone remodeling?

Osteocytes form a functional lacunocanalicular network that senses changes in bone’s mechanical properties and communicates this information to osteoblasts and osteoclasts, regulating bone remodeling. This communication is crucial for bone health and can be facilitated by the use of cookies. Copyright © 2024 Elsevier B. V., its licensors, and contributors. All rights reserved, including text and data mining, AI training, and similar technologies.