Computer Simulation of Human Mandibular Bone Structure by iBone, a Novel Reaction-Diffusion Bone Remodeling Model

Author(s):  
Ken-Ichi Tezuka ◽  
Akiyuki Takahashi ◽  
Tomoko Takeda ◽  
Yoshitaka Wada ◽  
Masanori Kikuchi
2006 ◽  
Vol 306-308 ◽  
pp. 1277-1282
Author(s):  
Ken-Ichi Tezuka ◽  
Akiyuki Takahashi ◽  
Tomoko Takeda ◽  
Yoshitaka Wada ◽  
Masanori Kikuchi

Bone is a complex system with adaptation and repair functions. To understand how bone cells can create a structure adapted to the mechanical environment, we proposed a simple bone remodeling model, iBone, based on a reaction-diffusion system [1]. A 3-dimensional mandibular bone model consisting of approximately 1.4 million elements was constructed from sequential computer tomography (CT) images of a 14-year old female. Both teeth and bone were modeled with isoparametric voxel elements with Young's Modulus = 20 GPa and Poisson's ratio = 0.3. Both heads of the mandible were fixed allowing rotation and horizontal movement. Teeth were fixed vertically allowing horizontal movements. Incisor, right/left group, and right/left molar biting conditions were simulated. The locations and directions of muscles, and their forces were predicted from the CT images. Remodeling simulation was performed by 10 sets of finite element method analysis and reaction-diffusion remodeling simulation to obtain internal structure adapted to each loading condition. As a result, the major part of the corpus of the simulated mandibular bone showed similar internal structures under different biting conditions. Moreover, these simulated structures were satisfactorily similar to that of the real mandible. Computer simulation of three-dimensional bone structures based on CT images will be very useful for understanding the patho-physiological state of bone under various mechanical conditions, and may assist orthopedic doctors to predict the risk and efficacy of surgical therapies.


2013 ◽  
Vol 423-426 ◽  
pp. 1813-1818
Author(s):  
Kaysar Rahman ◽  
Nurmamat Helil ◽  
Rahmatjan Imin ◽  
Mamtimin Geni

Bone is a dynamic living tissue that undergoes continuous adaptation of its mass and structure in response to mechanical and biological environment demands. In this paper, we firstly propose a mathematical model based on cross-type reaction diffusion equations of bone adaptation during a remodeling cycle due to mechanical stimulus. The model captures qualitatively very well the bone adaptation and cell interactions during the bone remodeling. Secondly assuming the bone structure to be a self-optimizing biological material which maximizes its own structural stiffness, bone remodeling model coupled with finite element method by using the add and remove element a new topology optimization of continuum structure is presented. Two Numerical examples demonstrate that the proposed approach greatly improves numerical efficiency, compared with the others well known methods for structural topology optimization in open literatures.


2017 ◽  
Vol 45 (7) ◽  
pp. 887-893 ◽  
Author(s):  
Katherine J. Motyl ◽  
Anyonya R. Guntur ◽  
Adriana Lelis Carvalho ◽  
Clifford J. Rosen

Biological processes utilize energy and therefore must be prioritized based on fuel availability. Bone is no exception to this, and the benefit of remodeling when necessary outweighs the energy costs. Bone remodeling is important for maintaining blood calcium homeostasis, repairing micro cracks and fractures, and modifying bone structure so that it is better suited to withstand loading demands. Osteoclasts, osteoblasts, and osteocytes are the primary cells responsible for bone remodeling, although bone marrow adipocytes and other cells may also play an indirect role. There is a renewed interest in bone cell energetics because of the potential for these processes to be targeted for osteoporosis therapies. In contrast, due to the intimate link between bone and energy homeostasis, pharmaceuticals that treat metabolic disease or have metabolic side effects often have deleterious bone consequences. In this brief review, we will introduce osteoporosis, discuss how bone cells utilize energy to function, evidence for bone regulating whole body energy homeostasis, and some of the unanswered questions and opportunities for further research in the field.


2020 ◽  
Vol 7 ◽  
Author(s):  
Jingke Du ◽  
Jiancheng Yang ◽  
Zihao He ◽  
Junqi Cui ◽  
Yiqi Yang ◽  
...  

PurposeBone remodeling is affected by mechanical stimulation. Osteocytes are the primary mechanical load-sensing cells in the bone, and can regulate osteoblast and osteoclast activity, thus playing a key role in bone remodeling. Further, bone mass during exercise is also regulated by Leukemia inhibitory factor (LIF). This study aimed to investigate the role of LIF in the mechanical response of the bone, in vivo and in vitro, and to elucidate the mechanism by which osteocytes secrete LIF to regulate osteoblasts and osteoclasts.MethodsA tail-suspension (TS) mouse model was used in this study to mimic muscular disuse. ELISA and immunohistochemistry were performed to detect bone and serum LIF levels. Micro-computed tomography (CT) of the mouse femurs was performed to measure three-dimensional bone structure parameters. Fluid shear stress (FSS) and microgravity simulation experiments were performed to study mechanical stress-induced LIF secretion and its resultant effects. Bone marrow macrophages (BMMs) and bone mesenchymal stem cells (BMSCs) were cultured to induce in vitro osteoclastogenesis and osteogenesis, respectively.ResultsMicro-CT results showed that TS mice exhibited deteriorated bone microstructure and lower serum LIF expression. LIF secretion by osteocytes was promoted by FSS and was repressed in a microgravity environment. Further experiments showed that LIF could elevate the tartrate-resistant acid phosphatase activity in BMM-derived osteoclasts through the STAT3 signaling pathway. LIF also enhanced alkaline phosphatase staining and osteogenesis-related gene expression during the osteogenic differentiation of BMSCs.ConclusionMechanical loading affected LIF expression levels in osteocytes, thereby altering the balance between osteoclastogenesis and osteogenesis.


1993 ◽  
Vol 11 (4) ◽  
pp. 500-513 ◽  
Author(s):  
H. Weinans ◽  
R. Huiskes ◽  
B. Van Rietbergen ◽  
D. R. Sumner ◽  
T. M. Turner ◽  
...  

2010 ◽  
Vol 43 (2) ◽  
pp. 287-293 ◽  
Author(s):  
Daniel Lin ◽  
Qing Li ◽  
Wei Li ◽  
Naughton Duckmanton ◽  
Michael Swain

2003 ◽  
Vol 2003.7 (0) ◽  
pp. 151-152
Author(s):  
Kenichi TEZUKA ◽  
Akiyuki TAKAHASHI ◽  
Yoshitaka WADA ◽  
Takahiro YOSHIDA ◽  
Masanori KIKUCHI

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