What Is The Impact Of Mechanical Stress On Bone Remodeling?

Bone remodeling is a lifelong process that creates a mature, dynamic bone structure through a balance between bone formation by osteoblasts and resorption by osteoclasts. Physical stress (PS) stimulates bone remodeling and affects bone structure and function through complex mechanisms. Mechanical forces are indispensable for bone homeostasis, with skeletal formation, resorption, and adaptation dependent on mechanical signals and loss of cellular events.

Mechanical forces play essential roles in bone remodeling, including mechanical cyclical stretching (MCS), fluid shear stress (FSS), compression, and microgravity. Bone modeling adapts bone shape to variable mechanical demands during growth and aging through cellular events that determine bone resorption and formation. The influence of mechanical forces on bone is summarized, and the role of matrix elasticity or scaffold and signaling pathways by which these forces influence bone is also discussed.

Mechanical loading is a particularly potent stimulus for bone cells, improving bone strength and inhibiting bone loss with age. Recent studies have revealed the function of osteocytes as mechanosensors in the early stage of bone remodeling. Loaded mechanical stress is converted to a series of biochemical reactions, activating osteoclasts and osteoblasts to cause bone resorption.

Mechanical stress to bone plays a crucial role in maintaining bone homeostasis, causing the deformation of bone matrix and generating strain force. Bone responds to mechanical stress by differential growth to resist the applied stress, and mechanically induced bone remodeling is likely.

Bones can sense mechanical loads and transform their architectural shape by fluctuations of bone. Bone tissue remodeling is regulated by cells in response to physical circumstances such as mechanical stress. Experimental results confirm that bone formation is promoted by mechanical stimuli, and it is necessary to establish a theoretical model of bone remodeling.

How does mechanical stress affect remodeling?

Bone remodeling occurs due to physical circumstances like mechanical stress, with the bone matrix receiving the most efficient load. Osteocytes act as mechanosensors in the early stage of bone remodeling, converting loaded mechanical stress into biochemical reactions that activate osteoclasts and osteoblasts, causing bone resorption and formation. Recent biochemical and molecular biological studies have identified genes that are affected by mechanical stress, such as nitric oxide (NO) and cAMP, which are secreted in response to mechanical stress.

Mechanical stress-responsive genes include GLAST, NOS, and PGHS-2. The expression of IGF-I is enhanced under the control of PTH/PTHrP, and c-fos expression is increased by loading mechanical stress. AP1, a heterodimer of c-FOS/c-JUN, functions as a transcription factor of downstream genes. The promoter region of mechanical stress-response genes contains elements like AP1 sites, cyclic AMP response elements (CRE), and shear stress response elements (SSRE). The enhanced expression of osteopontin (OPN) in osteocytes of bone resorption sites was demonstrated through in situ hybridization and immunohistochemistry.

What are the effects of mechanical stress?

Several authors report device degradation due to process-induced mechanical stress, which can cause reliability issues and affect the diffusion behavior of impurities during processing. This stress can also lead to a slip during processing. The content on this site is protected by copyright and is used by ScienceDirect, its licensors, and contributors. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

What happens in bones in response to mechanical stress?

Mechanical stress on bone causes deformation of the bone matrix, generating strain force, which initiates the mechanotransduction pathway. The strain, which contains a water solution, causes fluid flow in the bone matrix. This process is facilitated by the presence of a water solution in the bone. 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 law explains the effect of mechanical stress on bone remodeling?

Wolff’s law, named after German anatomist and surgeon Julius Wolff, postulates that bone formation is contingent upon mechanical stress, as evidenced by a mathematical law. This phenomenon is frequently designated as “Wolff’s law.” Please be advised that this site employs the use of cookies and is protected by copyright held by Elsevier B. V., its licensors, and contributors. All rights are reserved for the purposes of text and data mining, artificial intelligence training, and similar technologies.

How exercise and mechanical stress affect bone tissue?

During long space missions, astronauts can lose about 1-2% of their bone mass per month due to the lack of mechanical stress on their bones due to low gravitational forces in space. This loss causes bones to lose mineral salts and collagen fibers, resulting in strength. Mechanical stress also stimulates the deposition of these minerals. Regular exercise leads to thicker bones and prevents osteoporosis.

Controlled studies show that people who exercise regularly have greater bone density than those who are more sedentary. Resistance training has a greater effect than cardiovascular activities, especially to slow down bone loss due to aging and prevent osteoporosis.

Nutrition plays a crucial role in bone health, with certain nutrients being particularly important for maintaining bone density. The lack of mechanical stress in space causes bones to lose mineral salts and collagen fibers, affecting their strength and integrity. Therefore, regular exercise is essential for maintaining bone health.

How does mechanical stress affect the skeletal system?

Mechanical forces play a pivotal role in maintaining bone homeostasis, influencing skeletal formation, resorption, and adaptation. A lack of mechanical stimulation can result in the weakening of bone structure, which may lead to the development of disuse osteoporosis and an increased risk of fracture. In their respective contributions to the field, Wolff, Frost, and Nicogossian shed light on the Utah paradigm of skeletal physiology, which encompasses bone, cartilage, and collagenous tissue organs.

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 are examples of mechanical stress?

In continuum mechanics, stress is a physical quantity that describes forces during deformation, such as tensile stress and compressive stress. The greater the force and the smaller the cross-sectional area of the body, the greater the stress. Stress is measured in newtons per square meter (N/m2) or pascal (Pa). It expresses the internal forces that neighboring particles of a continuous material exert on each other, while strain measures the relative deformation of the material.

Strain inside a material may arise from various mechanisms, such as stress applied by external forces or surface forces. Any strain (deformation) of a solid material generates an internal elastic stress, similar to the reaction force of a spring, that tends to restore the material to its original non-deformed state. In liquids and gases, only deformations that change the volume generate persistent elastic stress.

If the deformation changes gradually with time, even in fluids, there will usually be some viscous stress, opposing that change. Elastic and viscous stresses are usually combined under the name mechanical stress.

What is mechanical stress on bones?

Mechanical stress stimulation induces stress on bone cells, which are activated by binding specific ligands, triggering a signal cascade that enhances the expression of downstream target genes, playing a role in bone metabolism. This process is regulated by multiple signal pathways, including the Wnt/β-catenin pathway. Exposure of transmembrane co-receptors Lrp5, Lrp6, and Frizzled to Wnt activates the Lrp/FZD receptor complex on the cell surface, inhibiting the degradation activity of β-Catenin through phosphorylation of downstream protein kinases.

β-catenin in the cytoplasm enters the nucleus and combines with the T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factor family to initiate transcription of downstream target genes, promoting osteogenic genes and bone formation.

Mouses with Lrp5 deletion mutations show low bone mass, while human patients with Lrp5 missense mutations have severe osteoporosis due to weakening anabolic response to mechanical stress. Lrp5 and Lrp6 are crucial in bone cell mechanical transduction, and heterozygous deletion of β-catenin in a single osteocyte in mice eliminates the bone synthesis response to mechanical load and the ability to form new bone. Numerous studies have demonstrated the involvement of the Wnt pathway in mechanical stress, but SOST negatively regulates the Wnt/β-catenin pathway.

How does mechanical stress force contribute to remodeling during childhood?

Bone remodeling is a crucial process that promotes the longitudinal growth of bones and adapts the skeleton to mechanical stress. Exercise leads to bone adaptation by cellular mechano transduction, with mechanosensors like stretch-activated ion channels and integrins modifying their conformation. As the skeleton undergoes substantial architectural and metabolic modifications, it may predispose to osteoporosis and increased fracture risk.

Bone health impairment occurs during the developmental age, when over a third of bone mass is accumulated, reaching a peak around the second decade of life. This critical period of bone growth with bone loading and physical activity represents a “window of opportunity” to develop a healthy skeleton. Environmental factors, such as diet and exercise, impact 20-40 of peak bone mass in adulthood.

Physical activity is recognized as a means of health promotion and disease prevention throughout life, although there are few specific recommendations in infancy and childhood. An adequate development of skeletal muscles during these two periods may have long-term consequences on body composition and inclination to engage in physical activity throughout life. Early physical training can play an important role in “fiber reprogramming”.

Bone mineral content (BMC) and bone mineral density (BMD) increase in response to repetitive and variable loading activities through increased force and strain. Moderate or intense physical activity and several sports inducing greater than normal bone load are critical for achieving bone strength. Implementing exercise interventions during childhood and adolescence could maximize peak bone mass and slow down the onset of osteoporosis.

In summary, bone health involves bone modeling, bone remodeling, and peak bone mass. Exercise can help maintain bone strength and reduce the risk of osteoporosis.

What does mechanical stress applied to bone increase?

Mechanical stimulation can activate calcium channels on the cell membrane, promoting the transport of extracellular calcium into the cell and increasing intracellular calcium concentration. Piezo1 and Piezo2 are important mechanosensitive channels that enable osteoblasts to sense and respond to changes in mechanical load, which are required for gene expression changes caused by fluid shear stress (FSS).

Piezo1 expression in osteoblasts may also be promoted by mechanical tensile force, and its deficiency in osteoblasts promotes bone resorption and contributes to osteoporosis in mice, but does not affect bone mass.

Removing Piezo1 from osteoblasts and bone cells does not completely eliminate the response of bones to mechanical stimuli. Piezo2 is more involved in the development of the nervous system and the perception of touch and pain than Piezo 1, and other channels, such as the transient receptor potential (TRP) vanilloid (TRPV) and certain members of the epithelial Na+ channel (ENaC) protein family, can guide cation influx under a hypertonic environment or membrane tension, converting mechanical force signals into electrical and chemical signals.

The cytoskeleton, a network structure in cells composed of protein fiber, microtubules, actin fibers, and intermediate filaments, plays an important role in maintaining cell morphology, bearing external forces, and maintaining internal cellular structure. The integrin glycoprotein family located on the cell membrane senses mechanical signals through interactions between the extracellular matrix (ECM) and intracellular signals.

Microtubule actin cross-linking factor 1 (MACF1) is a regulator of cytoskeletal dynamics necessary for maintaining bone tissue integrity, while actin in the cytoskeleton is mainly involved in mechanical stress.