PubMed Health⌕ Search

PubMed · 15616887

Computer-simulated bone architecture in a simple bone-remodeling model based on a reaction-diffusion system.

Abstract

Bone is a complex system with functions including those of adaptation and repair. To understand how bone cells can create a structure adapted to the mechanical environment, we propose a simple bone remodeling model based on a reaction-diffusion system influenced by mechanical stress. Two-dimensional bone models were created and subjected to mechanical loads. The conventional finite element method (FEM) was used to calculate stress distribution. A stress-reactive reaction-diffusion model was constructed and used to simulate bone remodeling under mechanical loads. When an external mechanical stress was applied, stimulated bone formation and subsequent activation of bone resorption produced an efficient adaptation of the internal shape of the model bone to a given stress, and demonstrated major structures of trabecular bone seen in the human femoral neck. The degree of adaptation could be controlled by modulating the diffusion constants of hypothetical local factors. We also tried to demonstrate the deformation of bone structure during osteoporosis by the modulation of a parameter affecting the balance between formation and resorption. This simple model gives us an insight into how bone cells can create an architecture adapted to environmental stress, and will serve as a useful tool to understand both physiological and pathological states of bone based on structural information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ken-ichi Tezuka, Yoshitaka Wada, Akiyuki Takahashi, Masanori Kikuchi. 2005. Computer-simulated bone architecture in a simple bone-remodeling model based on a reaction-diffusion system.. https://doi.org/10.1007/s00774-004-0533-z

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Posterior subluxation and dislocation of the shoulder in obstetric brachial plexus palsy.

We describe the results of surgical treatment in a prospective study of 183 consecutive cases of subluxation (101) and dislocation (82) of the shoulder secondary to obstetric brachial plexus palsy between 1995 and 2000. Neurological recovery was rated 'good' or 'useful' in all children, whose lesions fell into groups 1, 2 or 3 of the Narakas classification. The mean age at operation was 47 months (3 to 204). The mean follow-up was 40 months (24 to 124). The mean gain in function was 3.6 levels (9.4 to 13) using the Mallet score and 2 (2.1 to 4.1) on the Gilbert score. The mean active global range of shoulder movement was increased by 73 degrees ; the mean range of active lateral rotation by 58 degrees and that of supination of the forearm by 51 degrees . Active medial rotation was decreased by a mean of 10 degrees . There were 20 failures. The functional outcome is related to the severity of the neurological lesion, the duration of the dislocation and onset of deformity.

Bone Remodeling↗

Human microvascular endothelial cell activation by IL-1 and TNF-alpha stimulates the adhesion and transendothelial migration of circulating human CD14+ monocytes that develop with RANKL into functional osteoclasts.

UNLABELLED: Circulating pre-OCs may be recruited to locally inflamed sites through specific interactions with activated microvasculature. We found that HMVECs stimulated the adhesion and TEM of circulating pre-OCs, in an ICAM-1- and CD44-dependent manner, leading to greater RANKL-induced OC formation and bone pit resorption. INTRODUCTION: Inflammation is critical for healing processes but causes severe tissue destruction when chronic. Local osteoclast (OC) formation and bone resorption may increase at inflammatory sites through multiple mechanisms, including direct stimulation by inflamed microvasculature of circulating OC precursor (pre-OC) migration through a blood vessel barrier into bone or joint tissue. How this might occur is not yet well understood. MATERIALS AND METHODS: Cytokine-activated human microvascular endothelial cell (HMVEC) monolayers, with or without IL-1 and TNF-alpha preactivation (24 h), were incubated in adhesion (1-3 h) or porous transwell transendothelial migration (TEM; 3 h) assays with human peripheral blood mononuclear cells (hPBMCs) or CD14+ monocyte or CD14- lymphocyte subsets. The number of cells that adhered or transmigrated, and their ability to thereafter develop with macrophage-colony stimulating factor (M-CSF) + RANKL into bone pit-resorbing OCs, were analyzed. Immunostaining and neutralizing antibodies to key cell adhesion molecules were used to determine their potential involvement in stimulated CD14+ monocyte TEM. RESULTS: M-CSF + RANKL caused OC and bone pit formation only from hPBMCs and CD14+ cells but not CD14- cells. Adhesion of hPBMCs or CD14+ cells but not CD14- cells was stimulated by cytokine preactivation of HMVECs and led to the full capture of all circulating pre-OCs capable of developing into OCs. Cytokine-preactivated HMVECs also promoted the postadhesion TEM of hPBMCs and CD14+ populations, resulting in markedly greater OC formation and bone pit resorption by transmigrated cells. Immunodetectable vascular cell adhesion molecule (VCAM-1), intercellular adhesion molecule (ICAM-1), and CD44 levels increased on cytokine-treated HMVEC surfaces, and neutralizing antibodies to ICAM-1 or CD44, but not VCAM-1 or platelet endothelial cell adhesion molecule (PECAM-1), inhibited stimulated CD14+ cell TEM through activated HMVECs. CONCLUSIONS: This is the first demonstration that cytokine-activated HMVECs efficiently capture and promote the TEM of circulating pre-OCs capable of differentiating into bone-resorbing OCs. Thus, direct pre-OC recruitment by activated microvasculature at inflammatory sites may significantly contribute to normal OC bone remodeling during fracture healing or exacerbate pathological bone loss in various chronic inflammatory disorders.

Bone Remodeling↗