Статті в журналах: "Bone cells Metabolism"

1

INOUE, HIROMASA. "Cells phagocytizing bone. Bone metabolism and osteoclast." Kagaku To Seibutsu 23, no. 2 (1985): 99–102. http://dx.doi.org/10.1271/kagakutoseibutsu1962.23.99.

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2

Shymanskyy, I. O., O. O. Lisakovska, A. O. Mazanova, D. O. Labudzynskyi, A. V. Khomenko, and M. M. Veliky. "Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells." Ukrainian Biochemical Journal 88, no. 5 (October 31, 2016): 38–47. http://dx.doi.org/10.15407/ubj88.05.038.

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3

Locci, P., E. Becchetti, G. Venti, C. Lilli, L. Marinucci, E. Donti, G. Paludetti, and M. Maurizi. "Glycosaminoglycan metabolism in otosclerotic bone cells." Biology of the Cell 86, no. 1 (1996): 73–78. http://dx.doi.org/10.1111/j.1768-322x.1996.tb00958.x.

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4

Barry, Patrick. "Skeletal discovery: Bone cells affect metabolism." Science News 172, no. 6 (September 30, 2009): 83. http://dx.doi.org/10.1002/scin.2007.5591720602.

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5

Motyl, Katherine J., Anyonya R. Guntur, Adriana Lelis Carvalho, and Clifford J. Rosen. "Energy Metabolism of Bone." Toxicologic Pathology 45, no. 7 (October 2017): 887–93. http://dx.doi.org/10.1177/0192623317737065.

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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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6

Kumegawa, Masayoshi. "Role of Bone Cells in Bone Metabolism : Osteoclasts and Osteocytes." Journal of the Kyushu Dental Society 48, no. 5 (1994): 640–43. http://dx.doi.org/10.2504/kds.48.640.

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7

Ruzicska, Éva, and Gyula Poór. "Diabetes and bone metabolism." Orvosi Hetilap 152, no. 29 (July 2011): 1156–60. http://dx.doi.org/10.1556/oh.2011.29147.

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In the past decade several novel findings point to the critical role of the skeleton in several homeostatic processes, including energy balance. The connection begins in the bone marrow with lineage allocation of mesenchymal stem cells to adipocytes or osteoblasts. Osteoblasts and adipocytes produce factors affecting insulin homeostasis. The hormonally active adipose tissue can regulate bone metabolism. In this review authors discuss targets taking critical part in the bone-fat network: leptin, osteocalcin, PPAR γ2 and the Wnt/beta catenin pathway. Leptin regulates energy metabolism through controlling appetite. Mutation of the leptin gene resulting leptin resistance leads to high leptin levels, enormous appetite and pathologic obesity. Leptin also can influence the bone mass. The main effects of the thiazolidinedions – PPARγ agonists – are mediated through receptors located in adipocytes. However, beside their positive effects, they also suppress osteoblastogenesis and increase the risk for pathologic fractures. Osteocalcin, a known marker of bone formation, produced by osteoblasts decreases fat mass, promotes adiponectin production and insulin sensitivity, increases the number of pancreatic β-cells and increases insulin secretion. Thus, the skeletal system can regulate glucose metabolism and this substantially changed our view on this issue. Novel molecules can now be tested as targets in order to enhance bone formation and possibly prevent fractures. Orv. Hetil., 2011, 152, 1156–1160.

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8

Anderson, Paul H., Gerald J. Atkins, Andrew G. Turner, Masakazu Kogawa, David M. Findlay, and Howard A. Morris. "Vitamin D metabolism within bone cells: Effects on bone structure and strength." Molecular and Cellular Endocrinology 347, no. 1-2 (December 2011): 42–47. http://dx.doi.org/10.1016/j.mce.2011.05.024.

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9

Kim, Haemin, Brian Oh, and Kyung-Hyun Park-Min. "Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism." Cells 10, no. 1 (January 7, 2021): 89. http://dx.doi.org/10.3390/cells10010089.

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Bone is a dynamic tissue and is constantly being remodeled by bone cells. Metabolic reprogramming plays a critical role in the activation of these bone cells and skeletal metabolism, which fulfills the energy demand for bone remodeling. Among various metabolic pathways, the importance of lipid metabolism in bone cells has long been appreciated. More recent studies also establish the link between bone loss and lipid-altering conditions—such as atherosclerotic vascular disease, hyperlipidemia, and obesity—and uncover the detrimental effect of fat accumulation on skeletal homeostasis and increased risk of fracture. Targeting lipid metabolism with statin, a lipid-lowering drug, has been shown to improve bone density and quality in metabolic bone diseases. However, the molecular mechanisms of lipid-mediated regulation in osteoclasts are not completely understood. Thus, a better understanding of lipid metabolism in osteoclasts can be used to harness bone cell activity to treat pathological bone disorders. This review summarizes the recent developments of the contribution of lipid metabolism to the function and phenotype of osteoclasts.

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10

Kim, Haemin, Brian Oh, and Kyung-Hyun Park-Min. "Regulation of Osteoclast Differentiation and Activity by Lipid Metabolism." Cells 10, no. 1 (January 7, 2021): 89. http://dx.doi.org/10.3390/cells10010089.

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Анотація:

Bone is a dynamic tissue and is constantly being remodeled by bone cells. Metabolic reprogramming plays a critical role in the activation of these bone cells and skeletal metabolism, which fulfills the energy demand for bone remodeling. Among various metabolic pathways, the importance of lipid metabolism in bone cells has long been appreciated. More recent studies also establish the link between bone loss and lipid-altering conditions—such as atherosclerotic vascular disease, hyperlipidemia, and obesity—and uncover the detrimental effect of fat accumulation on skeletal homeostasis and increased risk of fracture. Targeting lipid metabolism with statin, a lipid-lowering drug, has been shown to improve bone density and quality in metabolic bone diseases. However, the molecular mechanisms of lipid-mediated regulation in osteoclasts are not completely understood. Thus, a better understanding of lipid metabolism in osteoclasts can be used to harness bone cell activity to treat pathological bone disorders. This review summarizes the recent developments of the contribution of lipid metabolism to the function and phenotype of osteoclasts.

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11

Wang, Qingxuan, Mengmeng Duan, Jingfeng Liao, Jing Xie, and Chenchen Zhou. "Are Osteoclasts Mechanosensitive Cells?" Journal of Biomedical Nanotechnology 17, no. 10 (October 1, 2021): 1917–38. http://dx.doi.org/10.1166/jbn.2021.3171.

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Skeleton metabolism is a process in which osteoclasts constantly remove old bone and osteoblasts form new osteoid and induce mineralization; disruption of this balance may cause diseases. Osteoclasts play a key role in bone metabolism, as osteoclastogenesis marks the beginning of each bone remodeling cycle. As the only cell capable of bone resorption, osteoclasts are derived from the monocyte/macrophage hematopoietic precursors that terminally adhere to mineralized extracellular matrix, and they subsequently break down the extracellular compartment. Bone is generally considered the load-burdening tissue, bone homeostasis is critically affected by mechanical conductions, and the bone cells are mechanosensitive. The functions of various bone cells under mechanical forces such as chondrocytes and osteoblasts have been reported; however, the unique bone-resorbing osteoclasts are less studied. The oversuppression of osteoclasts in mechanical studies may be because of its complicated differentiation progress and flexible structure, which increases difficulty in targeting mechanical structures. This paper will focus on recent findings regarding osteoclasts and attempt to uncover proposed candidate mechanosensing structures in osteoclasts including podosome-associated complexes, gap junctions and transient receptor potential family (ion channels). We will additionally describe possible mechanotransduction signaling pathways including GTPase ras homologue family member A (RhoA), Yes-associated protein/transcriptional co-activator with PDZ-binding motif (TAZ), Ca2+ signaling and non-canonical Wnt signaling. According to numerous studies, evaluating the possible influence of various physical environments on osteoclastogenesis is conducive to the study of bone homeostasis.

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12

Aubin, Jane E. "Bone blood stem cells." Bone 43 (October 2008): S15—S16. http://dx.doi.org/10.1016/j.bone.2008.07.018.

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13

Zeng, Zhipeng, Xuchang Zhou, Yan Wang, Hong Cao, Jianmin Guo, Ping Wang, Yajing Yang, and Yan Wang. "Mitophagy—A New Target of Bone Disease." Biomolecules 12, no. 10 (October 4, 2022): 1420. http://dx.doi.org/10.3390/biom12101420.

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Bone diseases are usually caused by abnormal metabolism and death of cells in bones, including osteoblasts, osteoclasts, osteocytes, chondrocytes, and bone marrow mesenchymal stem cells. Mitochondrial dysfunction, as an important cause of abnormal cell metabolism, is widely involved in the occurrence and progression of multiple bone diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma. As selective mitochondrial autophagy for damaged or dysfunctional mitochondria, mitophagy is closely related to mitochondrial quality control and homeostasis. Accumulating evidence suggests that mitophagy plays an important regulatory role in bone disease, indicating that regulating the level of mitophagy may be a new strategy for bone-related diseases. Therefore, by reviewing the relevant literature in recent years, this paper reviews the potential mechanism of mitophagy in bone-related diseases, including osteoarthritis, intervertebral disc degeneration, osteoporosis, and osteosarcoma, to provide a theoretical basis for the related research of mitophagy in bone diseases.

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14

Mankani, Mahesh H., and Pamela Gehron Robey. "Transplantation of Bone-Forming Cells." Endocrinologist 8, no. 6 (November 1998): 459–68. http://dx.doi.org/10.1097/00019616-199811000-00009.

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15

Qaw, Fuad S., Hugh L. J. Makin, and Glenville Jones. "Metabolism of 25-hydroxydihydrotachysterol3 in bone cells in vitro." Steroids 57, no. 5 (May 1992): 236–43. http://dx.doi.org/10.1016/0039-128x(92)90108-l.

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16

Westacott, Carole I., Ginette R. Webb, Mark G. Warnock, Jane V. Sims, and Christopher J. Elson. "Alteration of cartilage metabolism by cells from osteoarthritic bone." Arthritis & Rheumatism 40, no. 7 (July 1997): 1282–91. http://dx.doi.org/10.1002/1529-0131(199707)40:7<1282::aid-art13>3.0.co;2-e.

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17

Compston, JE. "Bone marrow and bone: a functional unit." Journal of Endocrinology 173, no. 3 (June 1, 2002): 387–94. http://dx.doi.org/10.1677/joe.0.1730387.

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Bone and bone marrow, although often regarded as separate systems, function as a single unit. Cells in the bone marrow are the precursors of bone remodelling cells and exert an important regulatory role both on their own development and the remodelling process, acting as mediators for the effects of systemic and local factors. Other cells, such as immune cells and megakaryocytes, also contribute to the regulation of bone cell development and activity. Many diseases that affect the bone marrow have profound effects on bone, involving interactions between abnormal and normal marrow cells and those of bone. Although recent advances in bone physiology have produced new insights into the relationship between bone marrow and bone cells, much remains to be learnt about the mechanisms by which marrow and bone act in synergy to regulate bone remodelling, both in health and disease.

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18

Zhou, Xuchang, Hong Cao, Jianming Guo, Yu Yuan, and Guoxin Ni. "Effects of BMSC-Derived EVs on Bone Metabolism." Pharmaceutics 14, no. 5 (May 8, 2022): 1012. http://dx.doi.org/10.3390/pharmaceutics14051012.

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Extracellular vesicles (EVs) are small membrane vesicles that can be secreted by most cells. EVs can be released into the extracellular environment through exocytosis, transporting endogenous cargo (proteins, lipids, RNAs, etc.) to target cells and thereby triggering the release of these biomolecules and participating in various physiological and pathological processes. Among them, EVs derived from bone marrow mesenchymal stem cells (BMSC-EVs) have similar therapeutic effects to BMSCs, including repairing damaged tissues, inhibiting macrophage polarization and promoting angiogenesis. In addition, BMSC-EVs, as efficient and feasible natural nanocarriers for drug delivery, have the advantages of low immunogenicity, no ethical controversy, good stability and easy storage, thus providing a promising therapeutic strategy for many diseases. In particular, BMSC-EVs show great potential in the treatment of bone metabolic diseases. This article reviews the mechanism of BMSC-EVs in bone formation and bone resorption, which provides new insights for future research on therapeutic strategies for bone metabolic diseases.

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19

Phulpin, Bérengère, Gilles Dolivet, Pierre-Yves Marie, Sylvain Poussier, Sandrine Huger, Pierre Bravetti, Pierre Graff, Jean-Louis Merlin, and Nguyen Tran. "Feasibility of Treating Irradiated Bone with Intramedullary Delivered Autologous Mesenchymal Stem Cells." Journal of Biomedicine and Biotechnology 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/560257.

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Background. We aimed to explore (i) the short-term retention of intramedullary implanted mesenchymal stem cells BMSCs and (ii) their impact on the bone blood flow and metabolism in a rat model of hindlimb irradiation.Methods. Three months after 30 Gy irradiation, fourteen animals were referred into 2 groups: a sham-operated group (n=6) and a treated group (n=8) in which111In-labelled BMSCs (2×106cells) were injected in irradiated tibias. Bone blood flow and metabolism were assessed by serialT99mc-HDP scintigraphy and 1-wk cell retention by recordings ofT99mc/111In activities.Results. The amount of intramedullary implanted BMSCs was of 70% at 2 H, 40% at 48 H, and 38% at 168 H. Bone blood flow and bone metabolism were significantly increased during the first week after cell transplantation, but these effects were found to reduce at 2-mo followup.Conclusion. Short-term cell retention produced concomitant enhancement in irradiated bone blood flow and metabolism.

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20

Zhou, Tao, Yuqing Yang, Qianming Chen, and Liang Xie. "Glutamine Metabolism Is Essential for Stemness of Bone Marrow Mesenchymal Stem Cells and Bone Homeostasis." Stem Cells International 2019 (September 12, 2019): 1–13. http://dx.doi.org/10.1155/2019/8928934.

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Skeleton has emerged as an endocrine organ which is both capable of regulating energy metabolism and being a target for it. Glutamine is the most bountiful and flexible amino acid in the body which provides adenosine 5′-triphosphate (ATP) demands for cells. Emerging evidences support that glutamine which acts as the second metabolic regulator after glucose exerts crucial roles in bone homeostasis at cellular level, including the lineage allocation and proliferation of bone mesenchymal stem cells (BMSCs), the matrix mineralization of osteoblasts, and the biosynthesis in chondrocytes. The integrated mechanism consisting of WNT, mammalian target of rapamycin (mTOR), and reactive oxygen species (ROS) signaling pathway in a glutamine-dependent pattern is responsible to regulate the complex intrinsic biological process, despite more extensive molecules are deserved to be elucidated in glutamine metabolism further. Indeed, dysfunctional glutamine metabolism enhances the development of degenerative bone diseases, such as osteoporosis and osteoarthritis, and glutamine or glutamine progenitor supplementation can partially restore bone defects which may promote treatment of bone diseases, although the mechanisms are not quite clear. In this review, we will summarize and update the latest research findings and clinical trials on the crucial regulatory roles of glutamine metabolism in BMSCs and BMSC-derived bone cells, also followed with the osteoclasts which are important in bone resorption.

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21

Lyu, Zhong-Shi, Wei-Li Yao, Qi Wen, Hong-Yan Zhao, Fei-Fei Tang, Yu Wang, Lan-Ping Xu, et al. "Glycolysis Restoration Attenuates Damaged Bone Marrow Endothelial Cells." Blood 134, Supplement_1 (November 13, 2019): 2491. http://dx.doi.org/10.1182/blood-2019-122794.

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Background: Bone marrow(BM) endothelial cells(ECs), a key component of BM microenvironment, is essential for the physiology and regeneration of hematopoietic stem cells (HSCs). The damage of ECs is recognized by us and other researchers as a mainstay in the pathophysiology of a serious of life-threatening complications after chemoradiotherapy and myeloablative hematopoietic cell transplantation(HSCT), including poor graft function (PGF) (2013BBMT, 2015BMT, 2016Blood, 2019Blood Advances). Despite numerous researches focused on the BM ECs contributing to HSC regeneration following myelotoxicity, the mechanisms underlying the injured BM ECs itself remain to be elucidated. Under physiological conditions, energy metabolism plays an instrumental role in maintaining EC function, and markedly perturbed of EC metabolism is linked to many pathologies, like cancer and diabetes. However, little is known about the metabolism state and its role in impaired BM ECs. Aims: The current study was performed to investigate the metabolism status in BM ECs after chemotherapy-induced injury. Moreover, we evaluated the metabolic state and its role in BM ECs of PGF patients post-allotransplant. Finally, we evaluated the therapeutical potential of anti-metabolic drugs to the dysfunctional BM ECs derived from PGF patients. Methods: Two EC injury models in vitro were established with the cultivated human BM ECs treated by 5-Fluorouracil (5-FU) and hydrogen peroxide. The findings from the above models were further validated by a prospective case-control study enrolled 15 patients with PGF, 30 matched patients with good graft function (GGF) and 15 healthy donors (HD). To determine the metabolic status of BM ECs, the expression of metabolism regulating genes was analyzed by qRT-PCR (mRNA level) and flow cytometry (protein level). Glucose metabolism levels were measured by glucose consumption and lactate production assays. To evaluate the functions of BM ECs, apoptosis, migration and tube formation assays were performed. To investigate the effect of anti-metabolic drugs to injured BM ECs, the glycolysis inhibitor 3PO and PPARd agonist GW501516 were administrated to the cultivated BM ECs treated by 5-FU , hydrogen peroxide or derived from PGF. Results: We demonstrated that the glycolysis in BM ECs could be induced by the treatment with either 5-FU or hydrogen peroxide in vitro, consistent with the dysfunction(impaired migration, angiogenesis, and higher level of apoptosis) of BM ECs, which could be attenuated by glycolysis restoration. Mechanistically, we revealed that the aberrant glycolysis and dysfunction of BM ECs could be triggered by PPARd knockdown in vitro, while the PPARd were down-regulated by either 5-FU or hydrogen peroxide treatment in vitro, Furthermore, PPARd agonist GW501516 treatment attenuated the perturbed function and number of injured BM ECs treated by either 5-FU or hydrogen peroxide. Subsequently, the prospective case-control study demonstrated elevated expressions of the glycolytic activator PFKFB3 and decreased PPARd were observed in BM ECs of PGF patients, when compared with those of GGF patients and HD, indicating that BM ECs of PGF patients have a hyper-glycolytic metabolism. Moreover, either glycolysis (PFKFB3) inhibitor 3PO or PPARd agonist GW501516 treatment reduced the aberrant glycolysis and improved the number and function of BM ECs derived from patients with PGF in vitro, revealing the critical role of defective glycolysis in the impaired BM ECs of PGF. Summary / Conclusions: These findings reveal that hyper-glycolysis mediated by PPARd inhibition is involved in the dysfunction of BM ECs after injury. Defective glycolysis may contribute to the pathobiology of BM ECs of PGF patients, which could be attenuated by glycolysis inhibitor 3PO or PPARd agonist GW501516 in vitro. Our findings might merit further consideration of targeting BM ECs glycolysis or PPARd as a promising therapeutic approach for PGF patients post-allotransplant in the future. Disclosures No relevant conflicts of interest to declare.

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22

Gromova, О. А., А. М. Lila, I. Yu Torshin, and I. А. Reier. "Application of chondroprotective agents to inhibit osteodestructive processes in the subchondral bone in patients with osteoarthritis." FARMAKOEKONOMIKA. Modern Pharmacoeconomics and Pharmacoepidemiology 15, no. 1 (March 15, 2022): 107–18. http://dx.doi.org/10.17749/2070-4909/farmakoekonomika.2022.126.

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Background. Osteoarthritis (OA) is associated with an activation of local inflammation and involves subchondral tissue of the joint.Objective: to conduct a systemic analysis of the publications on the association between OA and metabolic disorders in bones.Material and methods. The authors analyzed 3,926 publications on the studies of OA and metabolic disorders in bones tissue by the method of a topologic theory of recognition selected by the request “osteoarthritis AND (bone resorption OR osteopenia OR osteoporosis)” in the database of biomedical publications PubMed/MEDLINE. The control sampling included 4,000 articles randomly selected out of 97,331 found by the request “osteoarthritis NOT bone NOT resorption NOT osteopenia NOT osteoporosis” (i.e. publications on OA that do not cover issues of bone metabolism).Results. The associations between cartilaginous pathology and bone tissue destruction are mediated by anti-inflammatory cytokines, osteoblast and osteoclast balance impairments, steroid hormone imbalance, and carbohydrate metabolism. Bone metabolism disorders are associated with an intensification of OA-associated pain syndrome. Chondroprotective agents (chondroitin sulfate (CS), glucosamine sulfate (GS), and undenaturated collagen) block the activity of anti-inflammatory cytokines (NF-κB and toll-receptors), stimulate the activity of osteoblasts (bone tissue synthesizing cells), and decrease the excessive activity of osteoclasts (cells that degrade bone tissue).Conclusion. Pharmaceutically standardized forms of CS and GS can be used for the normalization of bone metabolism along with safe osteoptotective means (vitamin D, calcium, etc.) in patients with OA.

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23

Gallagher, J. A., J. P. Dillon, and C. E. Sheard. "Rhinoceros bone cells in culture." Bone 7, no. 4 (1986): 313. http://dx.doi.org/10.1016/8756-3282(86)90247-4.

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24

Adams⁎, G. B. "Hematopoietic stem cells and bone☆." Bone 47 (June 2010): S22. http://dx.doi.org/10.1016/j.bone.2010.04.025.

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25

Yankova, I., A. Shinkov, and R. Kovatcheva. "Changes in Bone Metabolism and Structure in Primary Hyperparathyroidism." Acta Medica Bulgarica 47, no. 4 (November 1, 2020): 75–80. http://dx.doi.org/10.2478/amb-2020-0050.

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AbstractParathyroid hormone (PTH) is a key regulator of bone turnover. Depending on the duration of action, the hormone causes catabolic and anabolic effects by binding with specific receptors (PTHR1) in the bone. Various cells expressing PTHR1 on their surface are involved in the process – osteoblasts, osteocytes, bone marrow stromal cells, T-lymphocytes and macrophages. In physiological conditions PTH balances the bone metabolism. Intermittent pharmacological doses of PTH lead to the prevalence of bone formation and are used in the treatment of osteoporosis. Persistently elevated levels of PTH stimulate bone resorption by impacting mainly the cortical bone. New imaging and analysis techniques show that high PTH levels can also have an adverse effect on trabecular microarchitecture. Primary hyperparathyroidism (PHPT) is a disease characterized by increased bone metabolism, decreased bone mineral density (BMD), inadequate osteoid mineralization and an increased risk of fractures. Prolonged overproduction of PTH leads to stimulation of bone resorption and defects in bone formation, mainly causing loss of cortical bone mass, while in the trabecular bone predominate demineralization processes. One explanation of these findings is the enhanced stimulation of RANKL expression by osteoblasts with decreased OPG expression and bone formation at the same time.

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26

Riddle, Ryan C., and Thomas L. Clemens. "Bone Cell Bioenergetics and Skeletal Energy Homeostasis." Physiological Reviews 97, no. 2 (April 2017): 667–98. http://dx.doi.org/10.1152/physrev.00022.2016.

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The rising incidence of metabolic diseases worldwide has prompted renewed interest in the study of intermediary metabolism and cellular bioenergetics. The application of modern biochemical methods for quantitating fuel substrate metabolism with advanced mouse genetic approaches has greatly increased understanding of the mechanisms that integrate energy metabolism in the whole organism. Examination of the intermediary metabolism of skeletal cells has been sparked by a series of unanticipated observations in genetically modified mice that suggest the existence of novel endocrine pathways through which bone cells communicate their energy status to other centers of metabolic control. The recognition of this expanded role of the skeleton has in turn led to new lines of inquiry directed at defining the fuel requirements and bioenergetic properties of bone cells. This article provides a comprehensive review of historical and contemporary studies on the metabolic properties of bone cells and the mechanisms that control energy substrate utilization and bioenergetics. Special attention is devoted to identifying gaps in our current understanding of this new area of skeletal biology that will require additional research to better define the physiological significance of skeletal cell bioenergetics in human health and disease.

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Yin, Wenzhen, Ziru Li, and Weizhen Zhang. "Modulation of Bone and Marrow Niche by Cholesterol." Nutrients 11, no. 6 (June 21, 2019): 1394. http://dx.doi.org/10.3390/nu11061394.

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Bone is a complex tissue composing of mineralized bone, bone cells, hematopoietic cells, marrow adipocytes, and supportive stromal cells. The homeostasis of bone and marrow niche is dynamically regulated by nutrients. The positive correlation between cardiovascular disease and osteoporosis risk suggests a close relationship between hyperlipidemia and/or hypercholesterolemia and the bone metabolism. Cholesterol and its metabolites influence the bone homeostasis through modulating the differentiation and activation of osteoblasts and osteoclasts. The effects of cholesterol on hematopoietic stem cells, including proliferation, migration, and differentiation, are also well-documented and further relate to atherosclerotic lesions. Correlation between circulating cholesterol and bone marrow adipocytes remains elusive, which seems opposite to its effects on osteoblasts. Epidemiological evidence has demonstrated that cholesterol deteriorates or benefits bone metabolism depending on the types, such as low-density lipoprotein (LDL) or high-density lipoprotein (HDL) cholesterol. In this review, we will summarize the latest progress of how cholesterol regulates bone metabolism and bone marrow microenvironment, including the hematopoiesis and marrow adiposity. Elucidation of these association and factors is of great importance in developing therapeutic options for bone related diseases under hypercholesterolemic conditions.

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28

Tencerova, Michaela, Meshail Okla, and Moustapha Kassem. "Insulin Signaling in Bone Marrow Adipocytes." Current Osteoporosis Reports 17, no. 6 (November 20, 2019): 446–54. http://dx.doi.org/10.1007/s11914-019-00552-8.

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Abstract Purpose of Review The goal of this review is to discuss the role of insulin signaling in bone marrow adipocyte formation, metabolic function, and its contribution to cellular senescence in relation to metabolic bone diseases. Recent Findings Insulin signaling is an evolutionally conserved signaling pathway that plays a critical role in the regulation of metabolism and longevity. Bone is an insulin-responsive organ that plays a role in whole body energy metabolism. Metabolic disturbances associated with obesity and type 2 diabetes increase a risk of fragility fractures along with increased bone marrow adiposity. In obesity, there is impaired insulin signaling in peripheral tissues leading to insulin resistance. However, insulin signaling is maintained in bone marrow microenvironment leading to hypermetabolic state of bone marrow stromal (skeletal) stem cells associated with accelerated senescence and accumulation of bone marrow adipocytes in obesity. Summary This review summarizes current findings on insulin signaling in bone marrow adipocytes and bone marrow stromal (skeletal) stem cells and its importance for bone and fat metabolism. Moreover, it points out to the existence of differences between bone marrow and peripheral fat metabolism which may be relevant for developing therapeutic strategies for treatment of metabolic bone diseases.

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29

Rothem, David E., Lilah Rothem, Michael Soudry, Aviva Dahan, and Rami Eliakim. "Nicotine modulates bone metabolism-associated gene expression in osteoblast cells." Journal of Bone and Mineral Metabolism 27, no. 5 (May 13, 2009): 555–61. http://dx.doi.org/10.1007/s00774-009-0075-5.

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30

Jones, D. B., and J. T. Ryaby. "Pulsed magnetic fields affect differentiation not metabolism in bone cells." Bone 7, no. 5 (January 1986): 396. http://dx.doi.org/10.1016/8756-3282(86)90292-9.

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31

Grayson, Warren L., Bruce A. Bunnell, Elizabeth Martin, Trivia Frazier, Ben P. Hung, and Jeffrey M. Gimble. "Stromal cells and stem cells in clinical bone regeneration." Nature Reviews Endocrinology 11, no. 3 (January 6, 2015): 140–50. http://dx.doi.org/10.1038/nrendo.2014.234.

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32

Prideaux, Matt, Tom O'Connell та Yukiko Kitase. "THE ROLE OF PPARδ-DRIVEN β-OXIDATION IN BONE HEALTH DURING AGING". Innovation in Aging 6, Supplement_1 (1 листопада 2022): 410. http://dx.doi.org/10.1093/geroni/igac059.1611.

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Abstract Musculoskeletal disorders are a significant complication of aging, leading to increased morbidity and mortality. However, current understanding of the mechanisms by which aging affects skeletal health is limited. Osteocytes are the most numerous and long-lived bone cells and play key roles in maintaining bone mass by responding to anabolic signals such as mechanical loading. Energy metabolism is dysregulated in many cells with aging, however regulation of energy metabolism in osteocytes and how this is affected during aging and by mechanical loading remains undefined. To investigate this, we first used IDG-SW3 osteocyte cells to determine the effects of mechanical loading on osteocytes in vitro by applying fluid flow shear stress (FFSS). FFSS increased Pparδ and Cpt1 expression, key promoters of fatty acid β-oxidation (FAO). Pharmacological antagonism of PPARδ or CPT1 resulted in dysregulated expression of key bone remodeling genes and impaired ATP release in response to FFSS. In vivo, mechanical loading significantly increased FAO in tibia cortical bone. However, FAO was impaired in the bones from aged mice. To further elucidate the role of osteocyte FAO, we deleted PPARδ specifically in osteocytes (PPARδ cKO), which resulted in decreased FAO and bone volume in female PPARδ cKO mice. Lastly, treatment of aging mice with the PPARδ activator GW0742 resulted in significantly increased bone mineral content, density and trabecular bone volume. These findings suggest important functions of osteocyte energy metabolism during aging and with mechanical loading on bone and identify PPARδ-driven FAO as a novel therapeutic target for improving skeletal health with aging.

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33

Forsberg, Jonathan A., Thomas A. Davis, Eric A. Elster, and Jeffrey M. Gimble. "Burned to the Bone." Science Translational Medicine 6, no. 255 (September 24, 2014): 255fs37. http://dx.doi.org/10.1126/scitranslmed.3010168.

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Heterotopic ossification—a complication of severe burns, head or blast injuries, and orthopaedic trauma—can result from altered adenosine metabolism in mesenchymal stem cells in response to elevated extracellular ATP (Peterson et al., this issue).

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34

Chen, Qin, Krishna M. Sinha, Benoit de Crombrugghe, and Ralf Krahe. "Osteoblast-Specific Overexpression of Nucleolar Protein NO66/RIOX1 in Mouse Embryos Leads to Osteoporosis in Adult Mice." Journal of Osteoporosis 2023 (January 10, 2023): 1–10. http://dx.doi.org/10.1155/2023/8998556.

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In previous study, we showed that nucleolar protein 66 (NO66) is a chromatin modifier and negatively regulates Osterix activity as well as mesenchymal progenitor differentiation. Genetic ablation of the NO66 (RIOX1) gene in cells of the Prx1-expressing mesenchymal lineage leads to acceleration of osteochondrogenic differentiation and a larger skeleton in adult mice, whereas mesenchyme-specific overexpression of NO66 inhibits osteochondrogenesis resulting in dwarfism and osteopenia. However, the impact of NO66 overexpression in cells of the osteoblast lineage in vivo remains largely undefined. Here, we generated osteoblast-specific transgenic mice overexpressing a FLAG-tagged NO66 transgene driven by the 2.3 kB alpha-1type I collagen (Col1a1) promoter. We found that overexpression of NO66 in cells of the osteoblast lineage did not cause overt defects in developmental bones but led to osteoporosis in the long bones of adult mice. This includes decreased bone volume (BV), bone volume density (bone volume/total volume, BV/TV), and bone mineral density (BMD) in cancellous compartment of long bones, along with the accumulation of fatty droplets in bone marrow. Ex vivo culture of the bone marrow mesenchymal stem/stromal cells (BMSCs) from adult Col1a1-NO66 transgenic mice showed an increase in adipogenesis and a decrease in osteogenesis. Taken together, these data demonstrate a crucial role for NO66 in adult bone formation and homeostasis. Our Col1a1-NO66 transgenic mice provide a novel animal model for the mechanistic and therapeutic study of NO66 in osteoporosis.

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35

Shiraliyev, O. K., T. F. Mamedov, and Zh I. Gaghiyeva. "Hormones and osteoporosis." Problems of Endocrinology 40, no. 3 (December 15, 1994): 49–52. http://dx.doi.org/10.14341/probl12019.

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Osteoporosis and its complications - bone fractures - represent a significant medical and social problem. Due to osteoporosis, bone fractures occur annually in 1.3 million Americans and 40 thousand Canadians. In France, one in two, and in Australia, one in five women aged about 70 years, suffer from fractures caused by osteoporosis. The occurrence of osteoporosis in old women is due to a decrease in estrogen production. However, a decrease in bone mineral density occurs not only with age, but even more so with all conditions leading to a change in the balance of hormones of the hypothalamic-pituitary system, thyroid and parathyroid glands, and adrenal glands. In connection with the stated purpose of this work was a synthesis of literature data on the effect of hormones on the occurrence and development of osteoporosis. Bone tissue is a dynamic metabolically active system. Depending on the function performed, cortical and trabecular bone are distinguished. The first makes up three quarters of the entire skeletal mass, forms the diaphysis of the tubular bones, has a low porosity, performs the function of supporting soft tissues and transmitting muscle contraction from one part of the body to another. Trabecular bone tissue makes up one fourth of the mass of the skeleton, forms the bones of the axial skeleton and the epiphysis of the tubular bones, has high porosity and ensures normal vital activity of the bone marrow. To do this, in the trabecular bones there are cavities ranging in size from 500 to 1000 microns, located between bone plates 100-150 microns thick. The basis of the vital activity of bone tissue is the functioning of two types of cells: osteoclasts resorbing the bone, and osteoblasts responsible for its formation. The ancestors of these cells are not fully understood, although hematopoietic monocyte macrophages are considered the most probable for osteoclasts, and stromal cells for osteoblasts, from which preosteoblasts arise. Throughout life, there is a constant renewal of bones, manifested in the resorption of individual, very small sections of tissue, with the almost simultaneous formation of a new bone. This process is of great evolutionary importance, since it allows you to remove microtrauma and bone microcracks that arise during the life process. Annually 25% of the mass of the trabecular bones and only 2-3% of the cortical bones are renewed.

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36

Srivastava, Rupesh K., Leena Sapra, and Pradyumna K. Mishra. "Osteometabolism: Metabolic Alterations in Bone Pathologies." Cells 11, no. 23 (December 6, 2022): 3943. http://dx.doi.org/10.3390/cells11233943.

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Renewing interest in the study of intermediate metabolism and cellular bioenergetics is brought on by the global increase in the prevalence of metabolic illnesses. Understanding of the mechanisms that integrate energy metabolism in the entire organism has significantly improved with the application of contemporary biochemical tools for quantifying the fuel substrate metabolism with cutting-edge mouse genetic procedures. Several unexpected findings in genetically altered mice have prompted research into the direction of intermediate metabolism of skeletal cells. These findings point to the possibility of novel endocrine connections through which bone cells can convey their energy status to other metabolic control centers. Understanding the expanded function of skeleton system has in turn inspired new lines of research aimed at characterizing the energy needs and bioenergetic characteristics of these bone cells. Bone-forming osteoblast and bone-resorbing osteoclast cells require a constant and large supply of energy substrates such as glucose, fatty acids, glutamine, etc., for their differentiation and functional activity. According to latest research, important developmental signaling pathways in bone cells are connected to bioenergetic programs, which may accommodate variations in energy requirements during their life cycle. The present review article provides a unique perspective of the past and present research in the metabolic characteristics of bone cells along with mechanisms governing energy substrate utilization and bioenergetics. In addition, we discussed the therapeutic inventions which are currently being utilized for the treatment and management of bone-related diseases such as osteoporosis, rheumatoid arthritis (RA), osteogenesis imperfecta (OIM), etc., by modulating the energetics of bone cells. We further emphasized on the role of GUT-associated metabolites (GAMs) such as short-chain fatty acids (SCFAs), medium-chain fatty acids (MCFAs), indole derivates, bile acids, etc., in regulating the energetics of bone cells and their plausible role in maintaining bone health. Emphasis is importantly placed on highlighting knowledge gaps in this novel field of skeletal biology, i.e., “Osteometabolism” (proposed by our group) that need to be further explored to characterize the physiological importance of skeletal cell bioenergetics in the context of human health and bone related metabolic diseases.

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37

Ishijima, Muneaki, Kunikazu Tsuji, Susan R. Rittling, Teruhito Yamashita, Hisashi Kurosawa, David T. Denhardt, Akira Nifuji, Yoichi Ezura, and Masaki Noda. "Osteopontin is required for mechanical stress-dependent signals to bone marrow cells." Journal of Endocrinology 193, no. 2 (May 2007): 235–43. http://dx.doi.org/10.1677/joe.1.06704.

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Mechanical stress to bone plays a crucial role in the maintenance of bone homeostasis. It causes the deformation of bone matrix and generates strain force, which could initiate the mechano-transduction pathway. The presence of osteopontin (OPN), which is one of the abundant proteins in bone matrix, is required for the effects of mechanical stress on bone, as we have reported that OPN-null (OPN−/−) mice showed resistance to unloading-induced bone loss. However, cellular mechanisms underlying the phenomenon have not been completely elucidated. To obtain further insight into the role of OPN in mediating mechanical stress effect on bone, we examined in vitro mineralization and osteoclast-like cell formation in bone marrow cells obtained from hind limb bones of OPN−/− mice after tail suspension. The levels of mineralized nodule formation of bone marrow cells derived from the femora subjected to unloading were decreased compared with that from loaded control in wild-type mice. However, these were not decreased in cells from OPN−/− mice after tail suspension compared with that from loaded OPN−/− mice. Moreover, while spreading of osteoclast-like cells derived from bone marrow cells of the femora subjected to unloading was enhanced compared with that from loaded control in wild-type mice, this enhancement of spreading of these cells derived from the femora subjected to unloading was not recognized compared with those from loaded control in OPN−/− mice. These data provided cellular bases for the effect of the OPN deficiency on in vitro reduced mineralized nodule formation by osteoblasts and on enhancement of osteoclast spreading in vitro induced by the absence of mechanical stress. These in vitro results correlate well with the resistance to unloading-induced bone loss in OPN−/− mice in vivo, suggesting that OPN has an important role in the effects of unloading-induced alterations of differentiation of bone marrow into osteoblasts and osteoclasts.

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38

Nyssen-Behets, C., D. Xhema, T. Schubert, M. Schubert, B. Lengelé, C. Delloye, and D. Dufrane. "Improvement of bone tissue allograft by mesenchymal stem cells: Bone marrow vs adipose stem cells." Bone 47 (June 2010): S128. http://dx.doi.org/10.1016/j.bone.2010.04.284.

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39

Hoebertz, A., A. Townsend-Nicholson, R. Glass, G. Burnstock, and T. R. Arnett. "Expression of P2 receptors in bone and cultured bone cells." Bone 27, no. 4 (October 2000): 503–10. http://dx.doi.org/10.1016/s8756-3282(00)00351-3.

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40

Cornish, Jillian, Usha Bava, Karen E. Callon, Jizhong Bai, Dorit Naot, and Ian R. Reid. "Bone-bound bisphosphonate inhibits growth of adjacent non-bone cells." Bone 49, no. 4 (October 2011): 710–16. http://dx.doi.org/10.1016/j.bone.2011.07.020.

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41

Fujita, Takuo. "Calcium, cells and bone." Journal of Bone and Mineral Metabolism 6, no. 1 (March 1988): 1–2. http://dx.doi.org/10.1007/bf02378732.

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42

Wang, Chunyu, Li Tian, Kun Zhang, Yaxi Chen, Xiang Chen, Ying Xie, Qian Zhao, and Xijie Yu. "Interleukin-6 gene knockout antagonizes high-fat-induced trabecular bone loss." Journal of Molecular Endocrinology 57, no. 3 (October 2016): 161–70. http://dx.doi.org/10.1530/jme-16-0076.

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The purpose of the study was to determine the roles of interleukin-6 (IL6) in fat and bone communication. Male wild-type (WT) mice and IL6 knockout (IL6−/−) mice were fed with either regular diet (RD) or high-fat diet (HFD) for 12 weeks. Bone mass and bone microstructure were evaluated by micro-computed tomography. Gene expression related to lipid and bone metabolisms was assayed with real-time quantitative polymerase chain reaction. Bone marrow cells from both genotypes were induced to differentiate into osteoblasts or osteoclasts, and treated with palmitic acid (PA). HFD increased the body weight and fat pad weight, and impaired lipid metabolism in both WT and IL6−/− mice. The dysregulation of lipid metabolism was more serious in IL6−/− mice. Trabecular bone volume fraction, trabecular bone number and trabecular bone thickness were significantly downregulated in WT mice after HFD than those in the RD (P < 0.05). However, these bone microstructural parameters were increased by 53%, 34% and 40%, respectively, in IL6−/− mice than those in WT mice on the HFD (P < 0.05). IL6−/− osteoblasts displayed higher alkaline phosphatase (ALP) activity and higher mRNA levels of Runx2 and Colla1 than those in WT osteoblasts both in the control and PA treatment group (P < 0.05). IL6−/− mice showed significantly lower mRNA levels of PPARγ and leptin and higher mRNA levels of adiponectin in comparison with WT mice on HFD. In conclusion, these findings suggested that IL6 gene deficiency antagonized HFD-induced bone loss. IL6 might bridge lipid and bone metabolisms and could be a new potential therapeutic target for lipid metabolism disturbance-related bone loss.

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43

Singer, Frederick R., Barbara G. Mills, Helen E. Gruber, Jolene J. Windle, and G. David Roodman. "Ultrastructure of Bone Cells in Paget's Disease of Bone." Journal of Bone and Mineral Research 21, S2 (December 2006): P51—P54. http://dx.doi.org/10.1359/jbmr.06s209.

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44

Martin, Shailer B., William S. Reiche, Nicholas A. Fifelski, Alexander J. Schultz, Spencer J. Stanford, Alexander A. Martin, Danielle L. Nack, Bernhard Radlwimmer, Michael P. Boyer, and Elitsa A. Ananieva. "Leucine and branched-chain amino acid metabolism contribute to the growth of bone sarcomas by regulating AMPK and mTORC1 signaling." Biochemical Journal 477, no. 9 (May 5, 2020): 1579–99. http://dx.doi.org/10.1042/bcj20190754.

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Osteosarcoma and chondrosarcoma are sarcomas of the bone and the cartilage that are primarily treated by surgical intervention combined with high toxicity chemotherapy. In search of alternative metabolic approaches to address the challenges in treating bone sarcomas, we assessed the growth dependence of these cancers on leucine, one of the branched-chain amino acids (BCAAs), and BCAA metabolism. Tumor biopsies from bone sarcoma patients revealed differential expression of BCAA metabolic enzymes. The cytosolic branched-chain aminotransferase (BCATc) that is commonly overexpressed in cancer cells, was down-regulated in chondrosarcoma (SW1353) in contrast with osteosarcoma (143B) cells that expressed both BCATc and its mitochondrial isoform BCATm. Treating SW1353 cells with gabapentin, a selective inhibitor of BCATc, further revealed that these cells failed to respond to gabapentin. Application of the structural analog of leucine, N-acetyl-leucine amide (NALA) to disrupt leucine uptake, indicated that all bone sarcoma cells used leucine to support their energy metabolism and biosynthetic demands. This was evident from the increased activity of the energy sensor AMP-activated protein kinase (AMPK), down-regulation of complex 1 of the mammalian target of rapamycin (mTORC1), and reduced cell viability in response to NALA. The observed changes were most profound in the 143B cells, which appeared highly dependent on cytosolic and mitochondrial BCAA metabolism. This study thus demonstrates that bone sarcomas rely on leucine and BCAA metabolism for energy and growth; however, the differential expression of BCAA enzymes and the presence of other carbon sources may dictate how efficiently these cancer cells take advantage of BCAA metabolism.

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45

Allain, T. J., T. J. Chambers, A. M. Flanagan, and A. M. McGregor. "Tri-iodothyronine stimulates rat osteoclastic bone resorption by an indirect effect." Journal of Endocrinology 133, no. 3 (June 1992): 327–31. http://dx.doi.org/10.1677/joe.0.1330327.

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ABSTRACT Tri-iodothyronine (T3) increases bone resorption in vivo and in vitro. In order to understand further the mechanisms by which this occurs we studied the effects of T3 at concentrations in the range of 1 pmol/l–1 μmol/l on bone resorption by osteoclasts isolated from neonatal rat long bones. Osteoclasts were disaggregated and incubated either with or without UMR 106 cells or with mixed bone cells. We found that there was no effect of T3 on bone resorption by osteoclasts incubated alone or co-cultured with UMR 106 cells. However, in culture with mixed bone cells there was a significant relationship between the concentration of T3 and bone resorption (r = 0·54, P= 0·01) The greatest effect was observed at a T3 concentration of 1 μmol/l at which a 1·8-fold increase in resorption was seen compared with control (P <0·005; paired t-test). We conclude that the ability of T3 to increase osteoclastic bone resorption is not due to a direct action of T3 on osteoclasts but is mediated by another cell present in bone. The observation that UMR 106 cells are unable to mediate this effect suggests that either the mediating cell is not osteoblastic or the phenotype of UMR 106 does not conform to the phenotype of osteoblastic cells that mediate the T3 responsiveness of bone. Journal of Endocrinology (1992) 133, 327–331

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46

Anastasilakis, Athanasios D., Marina Tsoli, Gregory Kaltsas, and Polyzois Makras. "Bone metabolism in Langerhans cell histiocytosis." Endocrine Connections 7, no. 7 (July 2018): R246—R253. http://dx.doi.org/10.1530/ec-18-0186.

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Langerhans cell histiocytosis (LCH) is a rare disease of not well-defined etiology that involves immune cell activation and frequently affects the skeleton. Bone involvement in LCH usually presents in the form of osteolytic lesions along with low bone mineral density. Various molecules involved in bone metabolism are implicated in the pathogenesis of LCH or may be affected during the course of the disease, including interleukins (ILs), tumor necrosis factor α, receptor activator of NF-κB (RANK) and its soluble ligand RANKL, osteoprotegerin (OPG), periostin and sclerostin. Among them IL-17A, periostin and RANKL have been proposed as potential serum biomarkers for LCH, particularly as the interaction between RANK, RANKL and OPG not only regulates bone homeostasis through its effects on the osteoclasts but also affects the activation and survival of immune cells. Significant changes in circulating and lesional RANKL levels have been observed in LCH patients irrespective of bone involvement. Standard LCH management includes local or systematic administration of corticosteroids and chemotherapy. Given the implication of RANK, RANKL and OPG in the pathogenesis of the disease and the osteolytic nature of bone lesions, agents aiming at inhibiting the RANKL pathway and/or osteoclastic activation, such as bisphosphonates and denosumab, may have a role in the therapeutic approach of LCH although further clinical investigation is warranted.

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47

Omata, Yasunori, Michael Frech, Taku Saito, Georg Schett, Mario M. Zaiss, and Sakae Tanaka. "Inflammatory Arthritis and Bone Metabolism Regulated by Type 2 Innate and Adaptive Immunity." International Journal of Molecular Sciences 23, no. 3 (January 20, 2022): 1104. http://dx.doi.org/10.3390/ijms23031104.

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While type 2 immunity has traditionally been associated with the control of parasitic infections and allergic reactions, increasing evidence suggests that type 2 immunity exerts regulatory functions on inflammatory diseases such as arthritis, and also on bone homeostasis. This review summarizes the current evidence of the regulatory role of type 2 immunity in arthritis and bone. Key type 2 cytokines, like interleukin (IL)-4 and IL-13, but also others such as IL-5, IL-9, IL-25, and IL-33, exert regulatory properties on arthritis, dampening inflammation and inducing resolution of joint swelling. Furthermore, these cytokines share anti-osteoclastogenic properties and thereby reduce bone resorption and protect bone. Cellular effectors of this action are both T cells (i.e., Th2 and Th9 cells), but also non-T cells, like type 2 innate lymphoid cells (ILC2). Key regulatory actions mediated by type 2 cytokines and immune cells on both inflammation as well as bone homeostasis are discussed.

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48

Imai, K., M. W. Neuman, T. Kawase, and S. Saito. "Calcium in osteoblast-enriched bone cells." Bone 13, no. 3 (May 1992): 217–23. http://dx.doi.org/10.1016/8756-3282(92)90200-g.

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49

Montjovent, Marc-Olivier, Nathalie Burri, Silke Mark, Ermanno Federici, Corinne Scaletta, Pierre-Yves Zambelli, Patrick Hohlfeld, Pierre-François Leyvraz, Lee L. Applegate, and Dominique P. Pioletti. "Fetal bone cells for tissue engineering." Bone 35, no. 6 (December 2004): 1323–33. http://dx.doi.org/10.1016/j.bone.2004.07.001.

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50

Schett, G. "T and B cells and bone." Bone 48 (May 2011): S56—S57. http://dx.doi.org/10.1016/j.bone.2011.03.030.

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