-
Bone Mar 2023Bone remodeling occurs through the interactions of three major cell lineages, osteoblasts, which mediate bone formation, osteocytes, which derive from osteoblasts, sense... (Review)
Review
Bone remodeling occurs through the interactions of three major cell lineages, osteoblasts, which mediate bone formation, osteocytes, which derive from osteoblasts, sense mechanical force and direct bone turnover, and osteoclasts, which mediate bone resorption. However, multiple additional cell types within the bone marrow, including macrophages, T lymphocytes and B lymphocytes influence the process. The bone marrow microenvironment, which is supported, in part, by bone cells, forms a nurturing network for B lymphopoiesis. In turn, developing B lymphocytes influence bone cells. Bone health during homeostasis depends on the normal interactions of bone cells with other lineages in the bone marrow. In disease state these interactions become pathologic and can cause abnormal function of bone cells and inadequate repair of bone after a fracture. This review summarizes what is known about the development of B lymphocytes and the interactions of B lymphocytes with bone cells in both health and disease.
Topics: Humans; Osteocytes; Osteoclasts; Osteoblasts; Bone Resorption; Bone Remodeling; B-Lymphocytes
PubMed: 34942359
DOI: 10.1016/j.bone.2021.116296 -
The Journal of International Medical... Jul 2019Corticotomy-facilitated orthodontics is a clinical treatment modality comprising the application of conventional orthodontic forces combined with selective decortication... (Review)
Review
Corticotomy-facilitated orthodontics is a clinical treatment modality comprising the application of conventional orthodontic forces combined with selective decortication of the alveolar process of the bone, which generates a localized process of bone remodeling (turnover) that enables accelerated orthodontic tooth movement. Compared with conventional orthodontic treatment, corticotomy-facilitated orthodontics is associated with reduced treatment time and reduces the frequency of apical external root resorption; however, this modality increases morbidity and financial costs. Although the clinical outcomes of corticotomy-facilitated orthodontics appear favorable, no results of evidence-based investigations of long-term outcomes are available in the literature, and the long-term effects of corticotomy-facilitated orthodontics on the teeth and periodontium are unclear. This narrative review discusses the biological events associated with corticotomy-facilitated orthodontics. Authoritative articles found in relevant databases were critically analyzed and the findings were integrated and incorporated in the text.
Topics: Alveolar Bone Loss; Bone Regeneration; Bone Remodeling; Humans; Orthodontics; Osteotomy
PubMed: 31234667
DOI: 10.1177/0300060519856456 -
Annals of the New York Academy of... Mar 2010Glucocorticoid (GC) use results in rapid bone loss and an elevated risk of fracture. The excess bone fragility from GC treatment is multifactorial. GCs increase bone... (Review)
Review
Glucocorticoid (GC) use results in rapid bone loss and an elevated risk of fracture. The excess bone fragility from GC treatment is multifactorial. GCs increase bone remodeling through reductions in gonadal hormones, elevations in PTH from negative calcium balance, early stimulation of osteoclast maturation and activity, and delayed, sustained reduction in osteogenesis and osteoblast activity. GCs also alter the metabolism of osteocytes so that increased osteocyte lacunae size, with demineralization around the osteocyte and reduced elastic modulus, is observed in a mouse model of GC-induced bone loss. In summary, GC effects on bone fragility are multifactorial, and additional studies are now under way to clarify how GCs alter osteocyte metabolism and result in reduction in localized bone strength.
Topics: Animals; Bone Density; Bone Remodeling; Fractures, Bone; Glucocorticoids; Humans; Mice; Osteogenesis
PubMed: 20392221
DOI: 10.1111/j.1749-6632.2009.05228.x -
Progress in Orthodontics Jun 2018In this review, most of the known and postulated mechanisms of osteopontin (OPN) and its role in bone remodeling and orthodontic tooth movement are discussed based on... (Review)
Review
In this review, most of the known and postulated mechanisms of osteopontin (OPN) and its role in bone remodeling and orthodontic tooth movement are discussed based on available literature. OPN, a multifunctional protein, is considered crucial for bone remodeling, biomineralization, and periodontal remodeling during mechanical tension and stress (orthodontic tooth movement). It contributes to bone remodeling by promoting osteoclastogenesis and osteoclast activity through CD44- and αvβ3-mediated cell signaling. Further, it has a definitive role in bone remodeling by the formation of podosomes, osteoclast survival, and osteoclast motility. OPN has been shown to have a regulatory effect on hydroxyapatite crystal (HAP) growth and potently inhibits the mineralization of osteoblast cultures in a phosphate-dependent manner. Bone remodeling is vital for orthodontic tooth movement. Significant compressive and tensional forces on the periodontium induce the signaling pathways mediated by various osteogenic genes including OPN, bone sialoprotein, Osterix, and osteocalcin. The signaling pathways involved in the regulation of OPN and its effect on the periodontal tissues during orthodontic tooth movement are further discussed in this review. A limited number of studies have suggested the use of OPN as a biomarker to assess orthodontic treatment. Furthermore, the association of single nucleotide polymorphisms (SNPs) in OPN coding gene Spp1 with orthodontically induced root resorption remains largely unexplored. Accordingly, future research directions for OPN are outlined in this review.
Topics: Animals; Bone Remodeling; Humans; Osteopontin; Tooth Movement Techniques
PubMed: 29938297
DOI: 10.1186/s40510-018-0216-2 -
Frontiers in Public Health 2022Ferroptosis was induced the programmed cell death with iron overload Fenton reaction. Currently, ferroptosis has not been studied thoroughly. Existing studies have... (Review)
Review
Ferroptosis was induced the programmed cell death with iron overload Fenton reaction. Currently, ferroptosis has not been studied thoroughly. Existing studies have confirmed that ferroptosis involves the metabolisms of the Fe, lipids, amino acid, each mechanism is mutually independent but interrelated, and they are formed a complex regulatory network. Other evidence supports that ferroptosis is participated osteoporotic bone remodeling, predominantly affecting the interaction between bone formation and bone resorption, explicitly bone resorption exceeded bone formation. Based on previous studies, this review will summarize the regulatory network mechanism of ferroptosis on bone remodeling and reveal the role of ferroptosis in osteoporosis (OP).
Topics: Bone Remodeling; Bone Resorption; Ferroptosis; Humans; Osteoporosis
PubMed: 35844870
DOI: 10.3389/fpubh.2022.910675 -
Henry Ford Hospital Medical Journal 1988
Topics: Aging; Biomarkers; Bone Regeneration; Bone Resorption; Bone and Bones; Female; Humans; Male; Minerals
PubMed: 3250946
DOI: No ID Found -
Current Osteoporosis Reports Dec 2023Orthodontic tooth movement is characterized by periodontal tissue responses to mechanical loading, leading to clinically relevant functional adaptation of jaw bone.... (Review)
Review
PURPOSE OF REVIEW
Orthodontic tooth movement is characterized by periodontal tissue responses to mechanical loading, leading to clinically relevant functional adaptation of jaw bone. Since osteocytes are significant in mechanotransduction and orchestrate osteoclast and osteoblast activity, they likely play a central role in orthodontic tooth movement. In this review, we attempt to shed light on the impact and role of osteocyte mechanotransduction during orthodontic tooth movement.
RECENT FINDINGS
Mechanically loaded osteocytes produce signaling molecules, e.g., bone morphogenetic proteins, Wnts, prostaglandins, osteopontin, nitric oxide, sclerostin, and RANKL, which modulate the recruitment, differentiation, and activity of osteoblasts and osteoclasts. The major signaling pathways activated by mechanical loading in osteocytes are the wingless-related integration site (Wnt)/β-catenin and RANKL pathways, which are key regulators of bone metabolism. Moreover, osteocytes are capable of orchestrating bone adaptation during orthodontic tooth movement. A better understanding of the role of osteocyte mechanotransduction is crucial to advance orthodontic treatment. The optimal force level on the periodontal tissues for orthodontic tooth movement producing an adequate biological response, is debated. This review emphasizes that both mechanoresponses and inflammation are essential for achieving tooth movement clinically. To fully comprehend the role of osteocyte mechanotransduction in orthodontic tooth movement, more knowledge is needed of the biological pathways involved. This will contribute to optimization of orthodontic treatment and enhance patient outcomes.
Topics: Humans; Osteocytes; Mechanotransduction, Cellular; Tooth Movement Techniques; Osteoclasts; Osteoblasts; Bone Remodeling
PubMed: 37792246
DOI: 10.1007/s11914-023-00826-2 -
Journal of Dental Research Aug 2018In lamellar bone, a network of highly oriented interconnected osteocytes is organized in concentric layers. Through their cellular processes contained within canaliculi,... (Review)
Review
In lamellar bone, a network of highly oriented interconnected osteocytes is organized in concentric layers. Through their cellular processes contained within canaliculi, osteocytes are highly mechanosensitive and locally modulate bone remodeling. We review the recent developments demonstrating the significance of the osteocyte lacuno-canalicular network in bone maintenance around implant biomaterials. Drilling during implant site preparation triggers osteocyte apoptosis, the magnitude of which correlates with drilling speed and heat generation, resulting in extensive remodeling and delayed healing. In peri-implant bone, osteocytes physically communicate with implant surfaces via canaliculi and are responsive to mechanical loading, leading to changes in osteocyte numbers and morphology. Certain implant design features allow peri-implant osteocytes to retain a less aged phenotype, despite highly advanced extracellular matrix maturation. Physicochemical properties of anodically oxidized surfaces stimulate bone formation and remodeling by regulating the expression of RANKL (receptor activator of nuclear factor-κB ligand), RANK, and OPG (osteoprotegerin) from implant-adherent cells. Modulation of certain osteocyte-related molecular signaling mechanisms (e.g., sclerostin blockade) may enhance the biomechanical anchorage of implants. Evaluation of the peri-implant osteocyte lacuno-canalicular network should therefore be a necessary component in future investigations of osseointegration to more completely characterize the biological response to materials for load-bearing applications in dentistry and orthopedics.
Topics: Animals; Biocompatible Materials; Bone Remodeling; Bone-Implant Interface; Dental Implants; Humans; Osseointegration; Osteocytes; Osteogenesis; Surface Properties
PubMed: 29863948
DOI: 10.1177/0022034518778033 -
International Journal of Molecular... Oct 2020Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone...
Osteoporosis is a common skeletal disorder, occurring as a result of an imbalance between bone resorption and bone formation, with bone breakdown exceeding bone building. Bone resorption inhibitors, e.g., bisphosphonates, have been designed to treat osteoporosis. Teriparatide, an anabolic agent, stimulates bone formation and corrects the characteristic changes in the trabecular microarchitecture. However, these drugs are associated with significant side effects. It is therefore crucial that we continue to research the pathogenesis of osteoporosis and seek novel modes of therapy. This editorial summarizes and discusses the themes of the ten articles published in our Special Issue "Osteoporosis: From Molecular Mechanisms to Therapies 2.0", a continuation of our 2019 Special Issue "Osteoporosis: From Molecular Mechanisms to Therapies" (https://www.mdpi.com/journal/ijms/special_issues/osteoporosis_ijms). These Special Issues detail important global scientific findings that contribute to our current understanding of osteoporosis.
Topics: Animals; Bone Density Conservation Agents; Bone Remodeling; Bone Resorption; Humans; Osteoporosis
PubMed: 33126410
DOI: 10.3390/ijms21218005 -
Frontiers in Endocrinology 2022Bone is a highly dynamic tissue that undergoes continuous remodeling by bone resorbing osteoclasts and bone forming osteoblasts, a process regulated in large part by... (Review)
Review
Bone is a highly dynamic tissue that undergoes continuous remodeling by bone resorbing osteoclasts and bone forming osteoblasts, a process regulated in large part by osteocytes. Dysregulation of these coupled catabolic and anabolic processes as in the case of menopause, type 2 diabetes mellitus, anorexia nervosa, and chronic kidney disease is known to increase fracture risk. Recent advances in the field of bone cell metabolism and bioenergetics have revealed that maintenance of the skeleton places a high energy demand on these cells involved in bone remodeling. These new insights highlight the reason that bone tissue is the beneficiary of a substantial proportion of cardiac output and post-prandial chylomicron remnants and requires a rich supply of nutrients. Studies designed for the specific purpose of investigating the impact of dietary modifications on bone homeostasis or that alter diet composition and food intake to produce the model can be found throughout the literature; however, confounding dietary factors are often overlooked in some of the preclinical models. This review will examine some of the common pre-clinical models used to study skeletal biology and its pathologies and the subsequent impact of various dietary factors on these model systems. Furthermore, the review will include how inadvertent effects of some of these dietary components can influence bone cell function and study outcomes.
Topics: Bone Remodeling; Bone and Bones; Diabetes Mellitus, Type 2; Humans; Osteoclasts; Osteocytes
PubMed: 35909523
DOI: 10.3389/fendo.2022.932343