Mechanical stimuli-mediated modulation of bone cell function—implications for bone remodeling and angiogenesis

9610 Background: Weight-bearing exercise may slow the rate of bone loss associated with breast cancer treatment. The purpose of this study is to determine the effect of tai chi chuan (TCC) on bone health, as measured by the changes in the levels of bone resorption and bone formation. This study also aimed to investigate whether changes in bone health were correlated with growth and inflammation markers that serve as regulators of bone cell function. Methods: Female patients (N=16) who completed treatment for breast cancer within the past 30 months were randomly assigned to either the TCC group or the psycho-educational support group without exercise (ST) for 60 minutes, three times a week for a period of 12 weeks. Serum levels of bone resorption (N-telopeptides of type I collagen; NTx) and bone formation (bone specific alkaline phosphatase; BAP) were determined by ELISA at baseline and post-intervention. Using validated methods, a bone remodeling index (BRI) was calculated from levels of NTx and BAP. In addition, pre- and post-intervention levels of insulin-like growth factor binding protein 1 (IGFBP-1) and interleukin-2 (IL-2), markers associated with excessive bone resorption, were measured. Lastly, levels of interleukin-6 (IL-6), believed to enhance bone formation, were measured at both pre- and post-intervention. Results: ANCOVA analyses demonstrated that survivors in the TCC group experienced a greater increase in bone remodeling than those in the ST group (Δ BRITCC=1.6 vs Δ BRIST=0.2; p=0.04). All correlations were determined by Pearson's correlation coefficients. IGFBP-1 was negatively correlated with increasing bone remodeling levels (r=-0.43, p=0.14). IL-2 was also negatively correlated with increasing bone remodeling levels (r=-0.35, p=0.24). IL-6 was positively correlated with increasing bone remodeling levels (r=0.69, p=0.01). Conclusions: This pilot study suggests that TCC has positive effects on bone remodeling through changes in growth and inflammation factors that regulate bone cell function. A larger, more definitive trial examining the influence of TCC on bone remodeling is warranted. Funding: Sally Schindel Cone and R25 CA102618 No significant financial relationships to disclose.

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Analysis of trabecular bone structure demonstrates new mechanisms of bone cell function in primary hyperparathyroidism

Acta Endocrinologica ◽

10.1530/acta.0.117s083 ◽

1988 ◽

Vol 117 (4_Suppl) ◽

pp. S83 ◽

Cited By ~ 1

Author(s):

M. VOGEL ◽

M. HAHN ◽

G. DELLING

Keyword(s):

Primary Hyperparathyroidism ◽

Trabecular Bone ◽

Cell Function ◽

Bone Structure ◽

Bone Cell ◽

Trabecular Bone Structure

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The Development of Molecular Biology of Osteoporosis

International Journal of Molecular Sciences ◽

10.3390/ijms22158182 ◽

2021 ◽

Vol 22 (15) ◽

pp. 8182

Author(s):

Yongguang Gao ◽

Suryaji Patil ◽

Jingxian Jia

Keyword(s):

Bone Resorption ◽

Molecular Biology ◽

Bone Formation ◽

Bone Mass ◽

Bone Remodeling ◽

Bone Cells ◽

Cell Activity ◽

Bone Cell ◽

Bone Disorders ◽

Molecular Aspects

Osteoporosis is one of the major bone disorders that affects both women and men, and causes bone deterioration and bone strength. Bone remodeling maintains bone mass and mineral homeostasis through the balanced action of osteoblasts and osteoclasts, which are responsible for bone formation and bone resorption, respectively. The imbalance in bone remodeling is known to be the main cause of osteoporosis. The imbalance can be the result of the action of various molecules produced by one bone cell that acts on other bone cells and influence cell activity. The understanding of the effect of these molecules on bone can help identify new targets and therapeutics to prevent and treat bone disorders. In this article, we have focused on molecules that are produced by osteoblasts, osteocytes, and osteoclasts and their mechanism of action on these cells. We have also summarized the different pharmacological osteoporosis treatments that target different molecular aspects of these bone cells to minimize osteoporosis.

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Cadmium toxicity: A role in bone cell function and teeth development

The Science of The Total Environment ◽

10.1016/j.scitotenv.2020.144646 ◽

2021 ◽

Vol 769 ◽

pp. 144646

Author(s):

Yonggang Ma ◽

Di Ran ◽

Xueni Shi ◽

Hongyan Zhao ◽

Zongping Liu

Keyword(s):

Cell Function ◽

Cadmium Toxicity ◽

Bone Cell ◽

Teeth Development

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Cells of the Immune System Orchestrate Changes in Bone Cell Function

Calcified Tissue International ◽

10.1007/s00223-013-9764-0 ◽

2013 ◽

Vol 94 (1) ◽

pp. 98-111 ◽

Cited By ~ 17

Author(s):

Sarah E. Wythe ◽

Vicky Nicolaidou ◽

Nicole J. Horwood

Keyword(s):

Immune System ◽

Cell Function ◽

Bone Cell

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Energy Metabolism of Bone

Toxicologic Pathology ◽

10.1177/0192623317737065 ◽

2017 ◽

Vol 45 (7) ◽

pp. 887-893 ◽

Cited By ~ 10

Author(s):

Katherine J. Motyl ◽

Anyonya R. Guntur ◽

Adriana Lelis Carvalho ◽

Clifford J. Rosen

Keyword(s):

Bone Remodeling ◽

Energy Homeostasis ◽

Bone Structure ◽

Bone Cells ◽

Bone Cell ◽

Whole Body ◽

Blood Calcium ◽

Micro Cracks ◽

Intimate Link ◽

Body Energy

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.

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Role of calcium in bone maturation arrest after thyroparathyroidectomy in the rat

AJP Renal Physiology ◽

10.1152/ajprenal.1977.232.1.f33 ◽

1977 ◽

Vol 232 (1) ◽

pp. F33-F41

Author(s):

J. M. Burnell ◽

E. Teubner ◽

D. Korn ◽

A. Miller

Keyword(s):

Cell Function ◽

Bone Cell ◽

X Ray Diffraction ◽

Mineral Density ◽

Bone Maturation ◽

Bone Changes ◽

Chemical Studies ◽

Normal Increase ◽

Bone Abnormalities

Thyroparathyroidectomy in the rat results in decreased plasma calcium and magnesium and increased phosphorus. The associated bone changes are decreased calcium, hydroxyproline, carbonate, and wholebone density. Bone magnesium, sodium, mineral density, and percent crystallinity are increased. The delayed matrix formation and mineralization previously identified by histologic techniques are herein characterized by direct measurement as arrest of the normal increase of hydroxyproline/matrix and percent mineral. The bone mineral present is of high density and x-ray-diffraction crystallinity, suggesting a decrease in the mineralization front high in the amorphous phase and/or small nondiffracting crystalloids. The chemical studies reveal that in the absence of available Ca, Mg and Na are substituted, and CO3 is decreased. The restoration of these plasma and bone abnormalities to normal by a diet high in CaCO3 adds further emphasis to the essential role of Ca in bone cell function.

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Clopidogrel (plavix), a P2Y12 receptor antagonist, inhibits bone cell function in vitro and decreases trabecular bone in vivo

Bone ◽

10.1016/j.bone.2012.02.121 ◽

2012 ◽

Vol 50 ◽

pp. S45

Author(s):

S. Syberg ◽

A. Brandao-Burch ◽

J.J. Patel ◽

M.O. Hajjawi ◽

T.R. Arnett ◽

...

Keyword(s):

Receptor Antagonist ◽

Trabecular Bone ◽

Cell Function ◽

Bone Cell ◽

P2y12 Receptor ◽

P2y12 Receptor Antagonist

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High Fidelity Computational Model of Bone Remodeling Cellular Mechanisms

ASME 2010 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2010-19464 ◽

2010 ◽

Author(s):

Charles L. Penninger ◽

Andrés Tovar ◽

Glen L. Niebur ◽

John E. Renaud

Keyword(s):

Bone Remodeling ◽

Computational Models ◽

Bone Adaptation ◽

Daily Activities ◽

High Fidelity ◽

Mechanical Stimuli ◽

Cellular Activity ◽

Cellular Mechanisms ◽

Mechanical Loads ◽

Metabolic Activities

One of the most intriguing aspects of bone is its ability to grow, repair damage, adapt to mechanical loads, and maintain mineral homeostasis [1]. It is generally accepted that bone adaptation occurs in response to the mechanical demands of our daily activities; moreover, strain and microdamage have been implicated as potential stimuli that regulate bone remodeling [2]. Computational models have been used to simulate remodeling in an attempt to better understand the metabolic activities which possess the key information of how this process is carried out [3]. At present, the connection between the cellular activity of remodeling and the applied mechanical stimuli is not fully understood. Only a few mathematical models have been formulated to characterize the remolding process in terms of the cellular mechanisms that occur [4,5].

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