scispace - formally typeset
Search or ask a question

What is the process of bone remodeling? 


Best insight from top research papers

Bone remodeling is a complex physiological process crucial for maintaining bone health and structure. It involves the continuous renewal of bone tissue through a sequence of cellular events, where old bone is replaced by new bone without altering the bone's shape. This process is orchestrated by various bone cells, including osteoclasts and osteoblasts, which interact at different stages with progenitors, other cells, and bone matrix constituents. Mechanical forces play a vital role in bone remodeling, as they are essential for skeletal adaptation to changing conditions and maintaining bone homeostasis. Mathematical models have been developed to simulate bone remodeling, focusing on the mechanotransduction mechanism where mechanical stimuli are translated into biochemical signals to regulate osteoclast and osteoblast activity. Understanding bone remodeling is crucial for developing therapeutic strategies for conditions like osteoporosis.

Answers from top 4 papers

More filters
Papers (4)Insight
Open accessJournal ArticleDOI
18 Feb 2022-Bone research
70 Citations
Bone remodeling is a lifelong process involving osteoblast-mediated bone formation and osteoclast-driven resorption, adapting bones to mechanical forces. This balance maintains bone structure and mass in response to changing conditions.
Bone remodeling is regulated by a network of cells, hormones, and signaling pathways. Mechanotransduction triggers osteocytes to signal osteoclasts and osteoblasts, controlling bone resorption and formation in response to mechanical stimuli.
Bone remodeling involves evolving bulk and shear moduli independently to adapt bone tissue to environmental changes. This process is modeled based on energetic arguments, allowing for different material parameter evolutions.
Bone remodeling is a continuous, cellular operational process involving all bone cells interacting to replace old bone with new, ensuring survival and bone mechanical competence without changing bone shape.

Related Questions

What is neuronal remodeling?5 answersNeuronal remodeling refers to the process crucial for shaping the precise connectivity of the mature nervous system. It involves pruning of excessive neural connections followed by regrowth of adult-specific ones to refine neural circuits. This process is essential for normal brain development in both vertebrates and invertebrates, with Drosophila being a valuable model due to its extensive and well-characterized remodeling events during metamorphosis. Neuronal remodeling plays a significant role in neural plasticity, contributing to the dynamic changes in dendritic structures under various conditions, including both physiological and pathological states. Understanding the molecular and cellular mechanisms governing neuronal remodeling is crucial, as errors in this process are associated with neurodevelopmental disorders like schizophrenia and autism.
What are the effects of hypermagnesemia on bone remodeling?4 answersHypermagnesemia, an electrolyte disturbance characterized by elevated magnesium concentrations in the blood, can have effects on bone remodeling. Magnesium is involved in various physiological functions, including bone metabolism. Studies have shown that hypermagnesemia can lead to abnormal bone mineralization in newborns. Additionally, hypermagnesemia has been associated with adverse clinical outcomes, such as respiratory and cardiovascular negative outcomes, neuromuscular dysfunction, and coma. In terms of bone cell function, unloading and microgravity, which can induce alterations in bone cell function and skeletal structure, have been shown to affect bone metabolism. Furthermore, there is evidence to suggest that magnesium can modulate parathyroid gland function, which is critical in the pathogenesis of renal osteodystrophy, a bone disease commonly seen in dialysis patients. Overall, hypermagnesemia can have implications for bone remodeling and bone health.
In what context was the beginning of the research related to the tissue remodeling and simulation process?5 answersThe beginning of the research related to tissue remodeling and simulation process was focused on understanding the mechanism of tissue remodelling and its role in achieving mechanical stability. The concept of tensional homeostasis, where there exists a target stress for a cell and remodelling functions to move the cell stress towards that target, was an important foundation for this research. The research also aimed to study the factors that help the cell move towards mechanical stability, such as the deposition and removal rates of collagen in a fibre network. Another aspect of the research was investigating how geometrical designs of tissue mechanical constraints affect tissue remodeling processes. The integration of an in vitro mesenchymal tissue experimental model with a computational model allowed for the investigation of the relationship between mechanical design and tissue remodeling.
What is chromatin remodelling?3 answersChromatin remodeling is a process of gene expression regulation that occurs in both normal cells and pathological conditions. It involves the reconfiguration of the structure of nucleosomes, which are the basic units of chromatin. This remodeling is carried out by ATP-dependent chromatin remodeling enzymes, which act as molecular machines. These enzymes interact with chromatin through ATPase domains that contact DNA at specific locations on the nucleosome surface. They also have diverse accessory domains and subunits that play important roles in modulating their activity. Chromatin remodeling complexes, such as the SWI/SNF complex, are composed of protein subunits that can be mutated or change their expression in diseases. Non-coding RNAs (ncRNAs) also play a role in regulating chromatin remodeling. Understanding the mechanisms of chromatin remodeling and its regulation has potential clinical applications in the diagnosis, prognosis, and treatment of diseases.
What are the mechanisms of chromatin remodeling?5 answersChromatin remodeling is a complex process that involves various mechanisms. One mechanism is the percolation effects at the level of nucleosome interactions, which allows for ultrasensitive chromatin expansion. Another mechanism involves the SWI/SNF remodeling complexes, which can be affected by consistent influence on the subunits and the genes encoding them, as well as the non-coding RNAs that regulate their operation. Histone variants and their chaperones also play a crucial role in chromatin remodeling, maintaining epigenetic regulation and influencing processes such as replication, transcription, and DNA damage repair. ATP-dependent chromatin remodeling complexes utilize ATP hydrolysing-DNA translocase motors to induce structural transformations in the chromatin, including nucleosome sliding, eviction, and editing. These mechanisms of chromatin remodeling contribute to the regulation of chromatin accessibility, nucleosome assembly, and nucleosome editing, ultimately impacting cellular and developmental processes.
What is targeted bone remodeling?1 answersTargeted bone remodeling refers to a specific type of bone remodeling that is directed towards specific sites in the bone. It is different from stochastic bone remodeling, which occurs randomly throughout the bone. The extent to which targeted remodeling occurs and its relationship with non-targeted (stochastic) remodeling is still being researched. It is important to understand the control mechanisms and independence of these two forms of remodeling, as they may respond differently to therapeutic interventions.

See what other people are reading

Does serotonin change during breastfeeding?
5 answers
Serotonin levels do change during breastfeeding. Research indicates that lactating mice show alterations in central and peripheral serotonin systems, with lower immunoreactive 5-HT in the dorsal raphe nucleus and higher serum 5-HT concentrations compared to non-lactating controls. Additionally, feeding serotonin precursors during the transition from pregnancy to lactation increases 5-HT production in pregnant rats, leading to elevated serum and mammary gland 5-HT levels. These changes in serotonin levels during lactation have implications for mood regulation and affective behaviors, as evidenced by lactating mice exhibiting different responses to selective serotonin reuptake inhibitor (SSRI) treatment compared to non-lactating and nulliparous females. Therefore, serotonin does undergo variations during breastfeeding, impacting both physiological and behavioral aspects.
What are the current treatment options and prognosis for individuals with WHIM syndrome?
5 answers
Current treatment options for individuals with WHIM syndrome include investigational drugs like mavorixafor, a CXCR4 antagonist, which has shown promising results in increasing white blood cell counts, reducing infection rates, and decreasing cutaneous warts. Plerixafor, another CXCR4 antagonist, has also demonstrated potential in treating WHIM syndrome by addressing neutropenia and other cytopenias. Patients with WHIM syndrome often receive symptomatic treatments like granulocyte colony-stimulating factor (G-CSF) to manage neutropenia. The prognosis for individuals with WHIM syndrome can vary, with some experiencing recurrent sinopulmonary infections, susceptibility to HPV infections, and increased risk of malignancy due to warts. However, ongoing research and clinical trials, such as the phase 3 trial of mavorixafor, offer hope for improved outcomes and targeted therapy for WHIM syndrome patients.
Is inflammation there before changes to the bone or cartilage in osteoarthritis?
4 answers
In osteoarthritis (OA), inflammation plays a crucial role before changes occur in the bone or cartilage. Traumatic knee injuries trigger an immediate increase in inflammatory cytokines, indicating the presence of inflammation accompanying joint tissue damage. Studies highlight that inflammatory cytokines are released in response to mechanical injury, leading to chondrocyte death and matrix degradation in the affected tissues. Additionally, systemic inflammation induced by factors like lipopolysaccharide administration can exacerbate OA outcomes, causing more severe phenotypes in terms of cartilage and subchondral bone loss. These findings emphasize the significant role of inflammation in the initiation and progression of osteoarthritis, suggesting that targeting inflammation could be a potential therapeutic strategy to mitigate OA development.
Can FOXO1 binds to NLRP3 promoter?
5 answers
Yes, FOXO1 can bind to the NLRP3 promoter. Studies have shown that FOXO1 deficiency correlates with halting age-related alveolar bone resorption, with a mechanistic link to enhanced NLRP3 inflammasome signaling under oxidative stress. Additionally, in the context of intracerebral hemorrhage (ICH), silencing FOXO3 attenuated neuronal ferroptosis by down-regulating NOX4 transcription levels, which is regulated by FOXO3 binding to the NOX4 promoter. Furthermore, FOXO1 has been found to inhibit STAT3-mediated leptin signaling by directly interacting with STAT3, preventing its binding to the POMC promoter complex. These findings collectively suggest that FOXO transcription factors, including FOXO1 and FOXO3, play crucial roles in regulating gene expression by binding to specific promoters, such as NLRP3, NOX4, and POMC.
Can foxo1 binds to NLRP3 promoter region?
5 answers
Yes, FoxO1 can bind to specific promoter regions, but the target varies depending on the context. In the provided research, FoxO1 was found to interact with the NLRP3 inflammasome signaling in osteoblasts under oxidative stress. Additionally, FoxO3 was identified to bind to the NOX4 promoter region in the context of neuronal ferroptosis after intracerebral hemorrhage. Furthermore, FoxO1 was shown to inhibit STAT3-mediated leptin signaling by directly interacting with STAT3, affecting the POMC promoter complex. These studies highlight the diverse roles of FoxO proteins in binding to different promoter regions to regulate various cellular processes, emphasizing the versatility and importance of these transcription factors in mediating gene expression and cellular responses.
What is the pathogenesis of Marfan syndrome?
4 answers
The pathogenesis of Marfan syndrome (MFS) involves genetic mutations, particularly in the FBN1 gene, leading to defective connective tissue synthesis and abnormalities in the TGF-β signaling pathway. These mutations result in the defective formation of microfibrils, increased levels of active TGF-β, and instability in elastic structures, contributing to cardiovascular, ocular, and skeletal manifestations. Mechanosensitive signaling pathways involving proteins like XOR, FAK, p38 MAPK, and Egr-1 are aberrantly activated in MFS, leading to ROS generation and aortic aneurysm formation. Additionally, epigenetic factors such as DNA methylation and histone acetylation play regulatory roles in MFS, further influencing disease development. Overall, the complex interplay of genetic, molecular, and mechanosensitive factors underlies the pathogenesis of Marfan syndrome.
What are the specific signaling pathways activated by Notch in zebrafish cardiac regeneration?
5 answers
Notch signaling in zebrafish cardiac regeneration activates specific pathways such as BMP and Klf2-Wnt9a. The activation of BMP signaling acts downstream of Notch signaling, influencing ventricle regeneration and cardiomyocyte proliferation. Additionally, Notch activation in the endocardium is crucial for myocardial regeneration, mediated by hemodynamic changes that lead to Klf2 gene expression and subsequent Notch pathway activation. Furthermore, in the zebrafish embryo, high fluid shear stress induces Notch and Klf2 signaling in endocardial cells, contributing to atrioventricular valvulogenesis. The interaction between Brg1, Kdm7aa, and Notch in cardiac endothelial cells, including the endocardium, modulates H3K4me3 levels in Notch promoters, regulating myocardial proliferation and regeneration in zebrafish.
Is there a connection between glucocorticoids and the initiation of autophagy or lysosomal degradation of proteins?
5 answers
Glucocorticoids (GCs) have been found to induce autophagy in various cell types, including osteoclasts, endotheliocytes, and pancreatic ductal adenocarcinoma (PDAC) cells. Specifically, studies have shown that GCs like Dexamethasone (DEX) can trigger autophagy by promoting the formation of autolysosomes, enhancing LC3-II levels, and decreasing SQSTM1/p62 expression. Furthermore, GC-induced autophagy has been linked to the activation of the PI3K/Akt/mTOR signaling pathway in osteoclasts, which mediates the increased autophagy levels under GC treatment. Additionally, the IRE1α/XBP-1s axis, a downstream pathway of endoplasmic reticulum (ER) stress, has been associated with GC-induced autophagy in endotheliocytes, where autophagy plays a protective role against GC-induced apoptosis and inhibition of proliferation. These findings collectively suggest a clear connection between glucocorticoids and the initiation of autophagy or lysosomal degradation of proteins in various cell types.
Are all osteocytes the same?
5 answers
Osteocytes are not all the same, as they exhibit variations in size, orientation, and responses to mechanical stimuli. Studies have shown that osteocytes display heterogeneity in their activation patterns following mechanical loading, with sub-populations of osteocytes responding differently. Additionally, osteocyte volume varies within bones, among different bones in an individual, and across species, with larger osteocyte lacunae observed in faster-depositing bone and in species with larger genomes. Osteocytes play diverse roles, acting as mechanosensors, communicating with other bone cells, and even functioning as endocrine cells to regulate various physiological processes beyond bone maintenance. These findings highlight the complexity and diversity of osteocytes, indicating that they are not uniform in structure or function.
Can ozone break down bones?
5 answers
Ozone exposure has been linked to adverse effects on bone health. Studies have shown that ozone exposure is associated with increased fracture risk due to oxidative stress-induced bone mineral density loss. Additionally, long-term exposure to ambient ozone has been found to be associated with decreased concentrations of bone turnover markers in children, potentially affecting bone metabolism. However, in a study involving ozone treatment in bone defects, it was observed that ozone did not alter the morphological structures of bones but actually increased bone resistance during mechanical testing, indicating a positive impact on bone strength. While ozone therapy has shown effectiveness in tissue repair and the prevention of bone necrosis, it was found that ozone treatment cannot inactivate HIV in bone for transplantation purposes.
What are the effects of osteopathy on diabetes type 2 patients?
5 answers
Osteopathy plays a significant role in managing diabetes type 2 patients by addressing complications like diabetic osteopathy, bone fragility, and autonomic dysfunctions. Patients with diabetes type 2 often exhibit altered bone remodeling, leading to increased fracture risks. Osteopathy can help in balancing the autonomic nervous system, which is crucial for diabetic patients with autonomic dysfunctions. Additionally, the pathophysiological mechanisms underlying osteoporotic changes in diabetes type 2 involve factors like hyperglycemia, oxidative stress, and the effects of antidiabetic drugs on bone metabolism, all of which can be addressed through osteopathic interventions. Therefore, osteopathic treatments can aid in improving bone health, reducing fracture risks, and managing autonomic dysfunctions in patients with diabetes type 2.