Bone remodeling simulation for prediction of micro trabecular morphology corresponding to macro bone density

2017 ◽  
Vol 2017 (0) ◽  
pp. J0210204
Author(s):  
Yuki UCHIGASHIMA ◽  
Daisuke TAWARA ◽  
Tetsuya TSUJIKAMI
Keyword(s):  
Bone Density ◽  
Bone Remodeling ◽  
Bone Remodeling Simulation

scholarly journals On the effect of antiresorptive drugs on the bone remodeling of the mandible after dental implantation: a mathematical model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mehran Ashrafi ◽  
Farzan Ghalichi ◽  
Behnam Mirzakouchaki ◽  
Manuel Doblare
Keyword(s):  
Mathematical Model ◽  
Bone Density ◽  
Bone Remodeling ◽  
Dental Implants ◽  
Implant Design ◽  
Patient Specific ◽  
Dental Implantation ◽  
Antiresorptive Agents ◽  
Antiresorptive Drugs

AbstractBone remodeling identifies the process of permanent bone change with new bone formation and old bone resorption. Understanding this process is essential in many applications, such as optimizing the treatment of diseases like osteoporosis, maintaining bone density in long-term periods of disuse, or assessing the long-term evolution of the bone surrounding prostheses after implantation. A particular case of study is the bone remodeling process after dental implantation. Despite the overall success of this type of implants, the increasing life expectancy in developed countries has boosted the demand for dental implants in patients with osteoporosis. Although several studies demonstrate a high success rate of dental implants in osteoporotic patients, it is also known that the healing time and the failure rate increase, necessitating the adoption of pharmacological measures to improve bone quality in those patients. However, the general efficacy of these antiresorptive drugs for osteoporotic patients is still controversial, requiring more experimental and clinical studies. In this work, we investigate the effect of different doses of several drugs, used nowadays in osteoporotic patients, on the evolution of bone density after dental implantation. With this aim, we use a pharmacokinetic–pharmacodynamic (PK/PD) mathematical model that includes the effect of antiresorptive drugs on the RANK/RANK-L/OPG pathway, as well as the mechano-chemical coupling with external mechanical loads. This mechano-PK/PD model is then used to analyze the evolution of bone in normal and osteoporotic mandibles after dental implantation with different drug dosages. We show that using antiresorptive agents such as bisphosphonates or denosumab increases bone density and the associated mechanical properties, but at the same time, it also increases bone brittleness. We conclude that, despite the many limitations of these very complex models, the one presented here is capable of predicting qualitatively the evolution of some of the main biological and chemical variables associated with the process of bone remodeling in patients receiving drugs for osteoporosis, so it could be used to optimize dental implant design and coating for osteoporotic patients, as well as the drug dosage protocol for patient-specific treatments.

Bone density and markers of bone remodeling in type 1 male diabetic patients

2006 ◽  
Vol 32 (5) ◽  
pp. 453-458 ◽  
Author(s):  
O Alexopoulou ◽  
J Jamart ◽  
JP Devogelaer ◽  
S Brichard ◽  
P de Nayer ◽  
...  
Keyword(s):  
Bone Density ◽  
Bone Remodeling ◽  
Diabetic Patients

Bone density, body composition, and markers of bone remodeling in type 1 diabetic patients

2011 ◽  
Vol 71 (5) ◽  
pp. 387-393 ◽  
Author(s):  
Soha M. Abd El Dayem ◽  
Amal M. El-Shehaby ◽  
Asmat Abd El Gafar ◽  
Ashraf Fawzy ◽  
Hassan Salama
Keyword(s):  
Body Composition ◽  
Bone Density ◽  
Bone Remodeling ◽  
Diabetic Patients ◽  
Type 1 Diabetic Patients

scholarly journals Hyperthyroidism and Hypothyroidism in Male Mice and Their Effects on Bone Mass, Bone Turnover, and the Wnt Inhibitors Sclerostin and Dickkopf-1

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3517-3527 ◽  
Author(s):  
Elena Tsourdi ◽  
Eddy Rijntjes ◽  
Josef Köhrle ◽  
Lorenz C. Hofbauer ◽  
Martina Rauner
Keyword(s):  
Thyroid Hormone ◽  
Bone Density ◽  
Bone Mass ◽  
Bone Turnover ◽  
Thyroid Hormones ◽  
Wnt Signaling ◽  
Cortical Bone ◽  
Bone Remodeling ◽  
Wnt Inhibitors ◽  
Dickkopf 1

Thyroid hormones are key regulators of bone homeostasis, and Wnt signaling has been implicated in thyroid hormone-associated bone loss. Here we tested whether hyperthyroidism and hypothyroidism interfere with dickkopf-1 (DKK1) and sclerostin, two inhibitors of Wnt signaling. Twelve-week-old male C57BL/6 mice were rendered either hyperthyroid or hypothyroid. Hyperthyroid mice displayed decreased trabecular (−54%, P < .001) and cortical bone density (−5%, P < .05) and reduced cortical thickness (−15%, P < .001), whereas hypothyroid mice showed a higher trabecular bone density (+26%, P < .001) with unchanged cortical bone parameters. Histomorphometry and biochemical markers of bone remodeling indicated high bone turnover in hyperthyroid mice and low bone turnover in hypothyroid mice. In vivo, serum DKK1 concentrations were decreased in hyperthyroid mice (−24%, P < .001) and increased in hypothyroid mice (+18%, P < .01). The increase of the number of DKK1-positive cells in hypothyroid mice was confirmed at the tissue level. Interestingly, sclerostin was increased in both disease models, although to a higher extent in hyperthyroid mice (+50%, P < .001, and +24%, P < .05). Serum sclerostin concentrations adjusted for bone mass were increased by 3.3-fold in hyperthyroid (P < .001) but not in hypothyroid mice. Consistently, sclerostin mRNA expression and the number of sclerostin-positive cells were increased in hyperthyroid but not in hypothyroid mice. Our data show that thyroid hormone-induced changes in bone remodeling are associated with a divergent regulation of DKK1 and sclerostin. Thus, the modulation of Wnt signaling by thyroid hormones may contribute to thyroid hormone-associated bone disease and altered expression of Wnt inhibitors may emerge as potential therapeutic targets.

scholarly journals Computation of static-equivalent load sets for bone remodeling simulation

PAMM ◽  
2007 ◽  
Vol 7 (1) ◽  
pp. 4020007-4020008 ◽  
Author(s):  
André Lutz ◽  
Udo Nackenhorst
Keyword(s):  
Bone Remodeling ◽  
Bone Remodeling Simulation ◽  
Equivalent Load

scholarly journals Loss of p53 in mesenchymal stem cells promotes alteration of bone remodeling through negative regulation of osteoprotegerin

2020 ◽  
Vol 28 (1) ◽  
pp. 156-169
Author(s):  
Tania Velletri ◽  
Yin Huang ◽  
Yu Wang ◽  
Qing Li ◽  
Mingyuan Hu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Bone Density ◽  
Osteogenic Differentiation ◽  
Bone Remodeling ◽  
Bone Homeostasis ◽  
Loss Of Function ◽  
P53 Expression ◽  
Receptor Activator

Abstractp53 plays a pivotal role in controlling the differentiation of mesenchymal stem cells (MSCs) by regulating genes involved in cell cycle and early steps of differentiation process. In the context of osteogenic differentiation of MSCs and bone homeostasis, the osteoprotegerin/receptor activator of NF-κB ligand/receptor activator of NF-κB (OPG/RANKL/RANK) axis is a critical signaling pathway. The absence or loss of function of p53 has been implicated in aberrant osteogenic differentiation of MSCs that results in higher bone formation versus erosion, leading to an unbalanced bone remodeling. Here, we show by microCT that mice with p53 deletion systemically or specifically in mesenchymal cells possess significantly higher bone density than their respective littermate controls. There is a negative correlation between p53 and OPG both in vivo by analysis of serum from p53+/+, p53+/−, and p53−/− mice and in vitro by p53 knockdown and ChIP assay in MSCs. Notably, high expression of Opg or its combination with low level of p53 are prominent features in clinical cancer lesion of osteosarcoma and prostate cancer respectively, which correlate with poor survival. Intra-bone marrow injection of prostate cancer cells, together with androgen can suppress p53 expression and enhance local Opg expression, leading to an enhancement of bone density. Our results support the notion that MSCs, as osteoblast progenitor cells and one major component of bone microenvironment, represent a cellular source of OPG, whose amount is regulated by the p53 status. It also highlights a key role for the p53-OPG axis in regulating the cancer associated bone remodeling.

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