China
Africa
Explore chapters and articles related to this topic
Skeletal Mechanobiology
Published in Jiro Nagatomi, Eno Essien Ebong, Mechanobiology Handbook, 2018
Alesha B. Castillo, Christopher R. Jacobs
Osteocytes, terminally differentiated bone cells located throughout the mineralized matrix, are formed from osteoblasts that become embedded during bone formation. Osteocytes are stellate cells that communicate with one another at the bone surface via gap junctions to regulate bone metabolism. Osteoblasts and osteocytes exhibit different expression profiles,27,28 and markers specific for osteocytes include E11/gp38, a glycoprotein important in the formation of dendritic processes,29 and sclerostin, a glycoprotein that is a potent inhibitor of osteoblast function.30 Additional osteocyte-derived factors that have been shown to regulate skeletal metabolism are the dentin matrix protein 1 (DMP-1),31 the fibroblast growth factor 23 (FGF23),32 Phex,33 and the heparin-binding growth-associated molecule (HB-GAM).34
Craniofacial Regeneration—Bone
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Laura Guadalupe Hernandez, Lucia Pérez Sánchez, Rafael Hernández González, Janeth Serrano-Bello
Remodeling has basically four stages, the activation phase; in which initiation with the osteocyte cell death is caused by bone microdamage, traumatic bone fractures, the decreased sclerostin levels active in BMU, in this phase the osteoclasts precursor cells are recruited to the altered bone surface, alert signals are produced for recruit immune cells and the mediator’s inflammatory process such as Vascular Endothelial Growth Factor (VEGF), angiopoietins, HMGB-1 and cytokines such as IGF-1, growth factors such as Transforming Growth Factor-β (TGF-β) induce osteoblast differentiation, basic Fibroblast Growth Factor (bFGF) and PDGF activate osteoblast and inhibition osteoclast action, Platelet-Derived Growth Factor-BB (PDGF-BB), and Inulin-like Growth Factor-I (IGF-I) contribute to the induction of callus formation, released from bone matrix, and then activating osteoblast differentiation. Next is the resorption phase, when the mature osteoclast degrade the mineralized matrix, the main signals in this step are Macrophage Colony Stimulating Factor M-CSF and ligand Receptor Activator of Nuclear Factor kappa-B RANKL they promote the differentiation of osteoclasts precursors; following the reversal phase, activated osteoblasts advance in the wake of bone-destroying cutting cones to replenish the cavity left behind by the latter, the osteoblasts are recruited and the osteoclasts undergo apoptosis; later during the formation phase, where the osteoblasts lay down new organic bone matrix that subsequently mineralizes, some of the active osteoblasts become trapped in the matrix that they secrete and subsequently differentiate into mature osteocytes. All these phases together contribute to the formation of a complete remodeled bone which is both structurally and functionally similar (Langdahl et al. 2016; Arias et al. 2018).
Serum sclerostin and cytokine responses to prolonged sculling exercise in highly-trained male rowers
Published in Journal of Sports Sciences, 2021
Jaak Jürimäe, Priit Purge, Vallo Tillmann
Osteocytes, with their mechanoreceptors able to sense mechanical strain, may be involved in bone responses to acute exercise (Pickering et al., 2017). Osteocytes have emerged as a regulator of bone mass through their ability to influence bone remodelling (Pickering et al., 2017). Osteocytes secrete sclerostin, which is an inhibitor of bone formation in osteoblasts by blocking the osteogenic Wnt signalling pathway (Redlich & Smolen, 2012). Typically, athletes have higher circulating sclerostin levels compared to non-athletes (Jürimäe et al., 2016a; Lombardi et al., 2012), while acute increases in sclerostin levels after different modes of high-impact exercises have been reported in untrained participants with different age and sex (Falk et al., 2016; Gombos et al., 2016; Pickering et al., 2017). Recently, similar increases in sclerostin concentrations were observed following short-term high-intensity interval running and cycling exercises in non-athletic participants (Kouvelioti et al., 2018, 2019a). The response of sclerostin to high-intensity interval exercise was independent of exercise impact and was not related to changes in bone turnover markers (Kouvelioti et al., 2018, 2019a). In contrast, sclerostin concentration was not increased after acute resistance exercise in young females (Sharma-Ghimire et al., 2019). Accordingly, the response of sclerostin to acute exercise may depend on the possible interaction of mode, intensity and duration of the exercise and also on the sex, age and physical fitness of the participants.
Differential time responses in inflammatory and oxidative stress markers after a marathon: An observational study
Published in Journal of Sports Sciences, 2020
Emil List Larsen, Henrik Enghusen Poulsen, Cristina Michaelsen, Laura Kofoed Kjær, Mark Lyngbæk, Emilie Skytte Andersen, Christina Petersen-Bønding, Clara Lemoine, Matthew Gillum, Niklas Rye Jørgensen, Thorkil Ploug, Tina Vilsbøll, Filip Krag Knop, Kristian Karstoft
In this study, we observed transient effects on bone metabolism acutely after the marathon that did not persist 4 days after the marathon. We observed increased concentrations of sclerostin, which inhibits bone formation. Usually, sclerostin is downregulated upon mechanical loading to bone (Galea et al., 2017). However, the magnitude and duration of loading and the metabolic challenges during strenuous exercise such as a marathon may instead increase sclerostin production in bone resulting in an inhibition of bone formation. In line with this, we found that both markers of bone formation (P1NP) and bone resorption (CTX) were decreased. These changes indicate that bone turnover is inhibited following a marathon, which seems appropriate in a stressful situation. However, diurnal variations in plasma concentrations of CTX are known to occur (Qvist et al., 2002). Also, food intake is known to affect CTX concentrations (Qvist et al., 2002). The concentrations of CTX that promote bone resorption may be explained by differences in the timing of samples and fasting state. Therefore, CTX concentration from immediately after the marathon might not be directly comparable to concentrations from the other three timepoints. Adjusting to hydration state using plasma albumin, no changes in osteocalcin were evident compared to baseline. However, unadjusted plasma concentrations of osteocalcin revealed increased plasma concentrations. This underlines the importance of accounting for changes in plasma volume following exercise. None of the bone metabolism markers were associated with the inflammatory cytokines.
Effects of running a marathon on sclerostin and parathyroid hormone concentration in males aged over 50
Published in Journal of Sports Sciences, 2023
Aleksandra Zagrodna, Anna Książek, Małgorzata Słowińska-Lisowska, Jan Chmura, Piotr Ponikowski, Giovanni Lombardi
Sclerostin is expressed and released by mature osteocytes and acts on osteoblast progenitors to inhibit their differentiation. The expression of this protein is primarily dependent upon mechanical stimulation of a bony segment (Amrein et al., 2012; Khosla et al., 2008). Osteocytes, indeed, are detectors of mechanical tensions in bones and microtraumas, mechanosensitive cells with processes that branch out within the canalicular system to reach other osteocytes and bone lining cells (osteoblasts) on the bone surface. The cellular processes are equipped with sensor proteins (cadherins, integrins, ion channels, G protein-coupled receptors) that sense both extracellular matrix and cell membrane deformations as well as modifications of the intracanalicular fluid shear stresses, determined by loadings, and activate intracellular cascades that bring, among the other responses, to either induction (under unloading conditions) or suppression (under loading conditions) of sclerostin (Ardawi et al., 2012; Gaudio et al., 2010; Gerosa & Lombardi, 2021). Sclerostin acts as an inhibitor of Wnt (Armamento-Villareal et al., 2012; Kramer et al., 2010). The Wnt/β-catenin pathway is critical in osteoblast differentiation and bone tissue formation (Yavropoulou & Yovos, 2007). Inhibition of sclerostin and the consequent activation of the Wnt/β-catenin signalling pathway are tantamount to the anabolic effect and thus to the prevalence of osteogenic mechanisms (Bonnet & Ferrari, 2010; Sims & Chia, 2012). Animal studies have consistently shown that mechanical loading suppresses transcription of the SOST gene and sclerostin production, and this is associated with an increase in bone mass (Bonnet & Ferrari, 2010; Moustafa et al., 2012). In humans, sclerostin response to exercise is not yet clear and may be related to the type, duration, and intensity of exercise, as the osteogenic response is known to desensitise quickly during prolonged stimulation, while it can be maintained by the application of intermittent loadings (Lombardi et al., 2012; Robling et al., 2000). Importantly, the differential acute response of sclerostin to long-lasting physical effort has not been examined and could provide insight into the specificity of bone response to different modes of exercise.