BONE CELLS, CALCIFICATION, AND CALCIUM HOMEOSTASIS

Background: The currently available bone turnover markers are mostly derived from osteoblasts or osteoclasts. Protein markers derived from osteocytes, the most abundant bone cells that can regulate bone turnover activities by other cells, are less explored. Objective: This study aimed to compare the circulating markers of osteocytes and calcium homeostasis between Malaysian postmenopausal women with and without osteoporosis. Method: Postmenopausal women with (n=20) or without osteoporosis (n=20) as determined by dual-energy X-ray absorptiometry were randomly drawn from a bone health cohort. Their fasting blood was collected and assayed by a multiplex immunoassay panel. Results: The results showed that osteoprotegerin and sclerostin levels were significantly lower among postmenopausal women with osteoporosis than the normal control. No significant differences in other markers were observed between the two groups. Sclerostin level correlated positively with spine bone mineral density (BMD), while 25-hydroxyvitamin D correlated negatively with hip BMD in the control group. No significant correlation was observed between other markers with spine or hip BMD. Conclusion: These data provide an insight into the possible roles of osteocyte markers, especially osteoprotegerin and sclerostin in classifying subjects with osteoporosis. However, the lack of association between these markers and BMD indicates that osteoporosis is a complex and multifactorial condition.

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Both mercury and cadmium directly influence calcium homeostasis resulting from the suppression of scale bone cells: the scale is a good model for the evaluation of heavy metals in bone metabolism

Journal of Bone and Mineral Metabolism ◽

10.1007/s00774-004-0505-3 ◽

2004 ◽

Vol 22 (5) ◽

Cited By ~ 41

Author(s):

Nobuo Suzuki ◽

Megumi Yamamoto ◽

Kazuo Watanabe ◽

Akira Kambegawa ◽

Atsuhiko Hattori

Keyword(s):

Heavy Metals ◽

Bone Metabolism ◽

Calcium Homeostasis ◽

Bone Cells

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FGF23 as a calciotropic hormone

F1000Research ◽

10.12688/f1000research.7189.1 ◽

2015 ◽

Vol 4 ◽

pp. 1472 ◽

Cited By ~ 7

Author(s):

María E. Rodríguez-Ortiz ◽

Mariano Rodríguez

Keyword(s):

Vitamin D ◽

Parathyroid Hormone ◽

Growth Factor ◽

Fibroblast Growth Factor ◽

Calcium Homeostasis ◽

Bone Cells ◽

Mineral Metabolism ◽

Fibroblast Growth Factor 23 ◽

Calcium Deficiency ◽

Fibroblast Growth

Maintaining mineral metabolism requires several organs and hormones. Fibroblast growth factor 23 (FGF23) is a phosphatonin produced by bone cells that reduces renal production of calcitriol – 1,25(OH)2D3 – and induces phosphaturia. The consequences of a reduction in 1,25(OH)2D3 involve changes in calcium homeostasis. There are several factors that regulate FGF23: phosphorus, vitamin D, and parathyroid hormone (PTH). More recently, several studies have demonstrated that calcium also modulates FGF23 production. In a situation of calcium deficiency, the presence of 1,25(OH)2D3 is necessary to optimize intestinal absorption of calcium, and FGF23 is decreased to avoid a reduction in 1,25(OH)2D3 levels.

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Pathology of Bone Cells in Pigs with Experimental Turbinate Osteoporosis (Atrophic Rhinitis)

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100065560 ◽

1971 ◽

Vol 29 ◽

pp. 304-305

Author(s):

A. W. Fetter ◽

C. C. Capen

Keyword(s):

Mucous Membrane ◽

Bone Cells ◽

Atrophic Rhinitis ◽

Infectious Agents ◽

Metabolic Disturbances ◽

Progressive Reduction ◽

Naturally Occurring ◽

Fundamental Cause ◽

Osteocytic Osteolysis ◽

Uncertain Etiology

Atrophic rhinitis in swine is a disease of uncertain etiology in which infectious agents, hereditary predisposition, and metabolic disturbances have been reported to be of primary etiologic importance. It shares many similarities, both clinically and pathologically, with ozena in man. The disease is characterized by deformity and reduction in volume of the nasal turbinates. The fundamental cause for the localized lesion of bone in the nasal turbinates has not been established. Reduced osteogenesis, increased resorption related to inflammation of the nasal mucous membrane, and excessive resorption due to osteocytic osteolysis stimulated by hyperparathyroidism have been suggested as possible pathogenetic mechanisms.The objectives of this investigation were to evaluate ultrastructurally bone cells in the nasal turbinates of pigs with experimentally induced atrophic rhinitis, and to compare these findings to those in control pigs of the same age and pigs with the naturally occurring disease, in order to define the fundamental lesion responsible for the progressive reduction in volume of the osseous core.

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