Osteoclast, a huge coenocytes,originates from mononuclear macrophages or monocytic series hematopoietic precursor cell, plays an important role in the progree of bone resorption. Formation and abnormal activity of osteoclast may cause osteoprosis, rheumatoid arthritis and aseptic loosening after arthroplasty. Therefore, osteoclast is the target for treating these disease. At present, a lot of study on formation of osteoclast were reported, but the study on how to identify and degradation of bone tissue is not yet reported. Bone mineral are seen as important component of identifing osteoclast, and the research suggested that bone matrix is not the essential ingredients of activiting osteoclast, petri dish covered by vitronectin also can make osteoclast occure certain form of bone resorption, vitronectin plays an significant role in activiting osteoclast. Otherwise, the research found that swallowing and secretion of bone matrix degradation products is benefit for differentiation of osteoclast and maintain of function, and this may be therapeutic target for treatment of musculoskeletal disorders.
Animals ; Bone Matrix ; metabolism ; Bone Resorption ; Humans ; Osteoclasts ; physiology

Bone is a dynamic tissue undergoing life-long remodeling, a process of bone resorption by osteoclast and bone formation by osteoblast, regulated by diverse hormones including estrogen. Recently, several pituitary hormones have been identified as a modulator of this process. Here, we reviewed the role of thyroid stimulating hormone signaling per se in bone metabolism.
Bone Remodeling ; Bone Resorption ; Estrogens ; Metabolism* ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Pituitary Hormones ; Thyroid Gland* ; Thyrotropin*

Bone is a dynamic tissue undergoing life-long remodeling, a process of bone resorption by osteoclast and bone formation by osteoblast, regulated by diverse hormones including estrogen. Recently, several pituitary hormones have been identified as a modulator of this process. Here, we reviewed the role of thyroid stimulating hormone signaling per se in bone metabolism.
Bone Remodeling ; Bone Resorption ; Estrogens ; Metabolism* ; Osteoblasts ; Osteoclasts ; Osteogenesis ; Pituitary Hormones ; Thyroid Gland* ; Thyrotropin*

PURPOSE: Growth hormone(GH) plays a major role in postnatal longitudinal bone growth. Exogenous growth hormone leads to stimulation of bone resorption as well as formation. The aim of this study is to observe the changes in the indices of bone metabolism and the correlation between growth velocity and changes in the levels of bone markers with GH treatment in children with GH deficiency(GHD). METHODS: Blood samples were collected from 12 patients before and 6 and 12 months after GH therapy. We measured bone-specific alkaline phosphatase(B-ALP), osteocalcin, and carboxy- terminal propeptide of type I collagen(PICP) as markers for bone formation, and cross-linked C-telopeptide of type I collagen(ICTP) as a marker for bone resorption. RESULTS: All patients showed significant increases in both height velocity(P<0.001), and height SD score(P<0.001) with GH therapy. The concentration of B-ALP increased after 12 mos of GH therapy(P<0.05). The maximal osteocalcin levels reached at 6 months of therapy(P<0.05), and decreased to near baseline level afterward. The concentration of PICP and ICTP significantly increased after 12 months of GH therapy(P<0.05). The percent of increase in serum B-ALP level during the first 6 months of GH treatment significantly correlated with increase in height SD score during the first year of GH therapy(P<0.005). CONCLUSION: GH treatment in children with GHD leads to activation of osteoclasts and osteoblasts as evidenced by increased biochemical markers of bone resorption and formation. The changes in the serum level of B-ALP during the first 6 months of therapy appears to be a useful marker for predicting growth responses during the first year of GH therapy.
Biomarkers ; Bone Development ; Bone Resorption ; Child* ; Growth Hormone* ; Humans ; Metabolism* ; Osteoblasts ; Osteocalcin ; Osteoclasts ; Osteogenesis

Animals ; Bone Regeneration ; Bone Resorption ; Cells, Cultured ; Disease Models, Animal ; Humans ; Jaw ; metabolism ; Osteoblasts ; Osteoclasts

Platelet-derived growth factor(PDGF) and lipopolysaccharide(LPS) may be the important regualtors of bone metabolism. Exogenous PDGF is recognized to have a stimulating effect on bone resorption in organ culture, but to stimulate the formation of new bone ultimately. LPS is known to be a stimulating agent on the osteoclastic activity. The purpose of this study was to evaluate the effects and the interaction of PDGF and LPS on periodontal ligament(PDL) cells which have important roles in bone remodeling. Cultured human periodontal ligament cells were treated with various concentration of PDGF and/or LPS. The cellular viability was measured by Microtitration(MTT) assay according to the lapse time of culture. The obtained results were as follows: 1. The viability of PDL cells was not different from the control in O.lng/ml of PDGF, but was significantly increased to be over the level of control in lng/ml of PDGF at the second day of culture, and in lOng/ml of PDGF at the second and the third day of culture. 2. The cellular viability was decreased in O.5microgram/ml or 5microgram/ml of LPS at the third day of culture. 3. Incubation with both 1ng/ml or 10ng/ml of PDGF and 0.5microgram/ml or 5microgram/ml of LPS resulted in the increased cellular viability at the third day, which. was greater than LPS only treated group. It was greater than even the control group in lOng/ml of PDGF. From the above findings, we could summarize that the admixture of PDGF and LPS could not less increase the viability of the human periodontal ligament cells than PDGF only.
Bone Remodeling ; Bone Resorption ; Humans* ; Metabolism ; Organ Culture Techniques ; Osteoclasts ; Periodontal Ligament*

Bone is a dynamic tissue which is constantly remodelled by subsequent cycles of bone resorption and formation. Glucocorticoid and vitamine D3 are known as regulating substances in bone metabolism. In vitro experiments using bone tissue, it was suggested that glucoccorticoid inhibits bone resorption, whereas the effect of glucocorticoid on bone formation are complex- increasing or decreasing effect. The active form of vitamin D3, 1,25-dihydroxycholecalciferol [1.25-(OH)2D3], has been reported to stimulate osteoblastic activities including the production of ALP, type I collagen, and osteoclacin. The purpose of this study was to evaluate the effect of admixture of vitamin D3 and dexamethasone, one of glucocorticoids, on osteblastic cell line(MC3T#-E1). Alkaline phosphatase(ALP) and MTT assay were conducted in the cultivated cells with 1, 10, 100nm/ml of 1,25-(OH)2D3 and/or 10nM/ml, 100nM/ml, 1micrometer/ml of dexamethasone. The observed results were as follows. 1. The activity of osteoblastic cells with 1micrometer/ml of dexamethasone was significantly increased at 1-day cultivation with comparison to control group, but was decreased afterwards. But the activity of ALP was greatest in 1micrometer/ml of dexamethasone and increased with time lapsed. 2. The activity of osteoblastic cells with vitamin D3 was significantly increased dose-dependently at 1-day cultivation, but was significantly decreased in 10nM/ml or 100nM/ml at 2-day or 3-day cultivation, and was greatest in 100nM/ml at 3-day cultivation. 3. In case of admixture of dexamethasone and vitamin D3 at 2-day cultivation, but was increased again at 3-day cultivation, which was greater than that in control or dexamethasone only group. The activity of ALP was decreased at 1-day cultivation, but was increased in the admixture of 10nM/ml or 100nM/ml of dexamethasone with 100nM/ml of vitamin D3 at 2-day cultivation, and was again decreased at 3-day cultivation.
Bone and Bones ; Bone Resorption ; Calcitriol ; Cholecalciferol ; Collagen Type I ; Dexamethasone* ; Glucocorticoids ; Metabolism ; Osteoblasts* ; Osteogenesis ; Vitamins*

OBJECTIVES: The purpose of this study was to investigate the influences of interruption and reinitiation of monthly minodronate therapy on the bone mineral density (BMD) and bone metabolism markers in postmenopausal women with osteoporosis. METHODS: Study patients were included if they had been administered monthly minodronate therapy for ≥6 months, interrupted the therapy, and reinitiated the therapy for ≥12 months. The BMD and bone metabolism markers were assessed at 4 time points: initiation, interruption, reinitiation and 1 year after reinitiation of therapy. RESULTS: A total of 23 patients were enrolled. The mean monthly minodronate treatment period was 23.8 ± 12.9 months following a mean interruption period of 11.9 ± 5.4 months. Once increased by monthly minodronate treatment for 2 years on average, the BMD of lumbar spine and radius did not significantly decrease even after an interruption for 1 year on average. However, the BMD of the femoral neck did decrease after interruption. The BMD of the lumbar spine and radius increased further after 1 year of monthly minodronate retreatment. The BMD of the femoral neck did not change. Once decreased after the treatment for an average of 2 years followed by an interruption for 1 year, bone metabolism markers increased gradually but did not recover to baseline levels. A potent suppressive effect on bone resorption was noted. The change rate was greater for the bone formation marker procollagen 1 N-terminal propeptide. CONCLUSIONS: Monthly minodronate treatment increases BMD and reduces bone metabolism markers. The effect lessens after treatment interruptions, and can be restored by retreatment.
Bone Density ; Bone Resorption ; Female ; Femur Neck ; Humans ; Metabolism ; Osteogenesis ; Osteoporosis ; Procollagen ; Radius ; Retreatment ; Spine

It has been well documented that exercise can improve bone metabolism, promote bone growth and development, and alleviate bone loss. MicroRNAs (miRNAs) are widely involved in the proliferation and differentiation of bone marrow mesenchymal stem cells, osteoblasts, osteoclasts and other bone tissue cells, and regulation of balance between bone formation and bone resorption by targeting osteogenic factors or bone resorption factors. Thus miRNAs play an important role in the regulation of bone metabolism. Recently, regulation of miRNAs are shown to be one of the ways by which exercise or mechanical stress promotes the positive balance of bone metabolism. Exercise induces changes of miRNAs expression in bone tissue and regulates the expression of related osteogenic factors or bone resorption factors, to further strengthen the osteogenic effect of exercise. This review summarizes relevant studies on the mechanism whereby exercise regulates bone metabolism via miRNAs, providing a theoretical basis for osteoporosis prevention and treatment with exercise.
Humans ; MicroRNAs/metabolism* ; Osteogenesis/genetics* ; Cell Differentiation ; Osteoblasts ; Bone Resorption/metabolism*

One of the sequelae of spinal cord trauma which start soon after the onset of injury is the loss of the calcium from bone. Bone mineral and matrix resorption causes negative calcium balance, and eventually osteoporosis. Etidronate disodium(etidronate) is an oral diphosphonate compound known to reduce bone resorption through the inhibition of osteoclasic activity. Since continuous oral treatment with high doses of etidronate may lead to the impairment of bone mineralization and the cessation of bone remodeling, a ideal therapeutic regimen consist of the intermittent cyclical administration of the diphosphonate in a dose that inhibits bone resorption. To assess the effect of etidronate on bone metabolism and bone mineral density after spinal cord injury, we studied two groups of 7 spinal cord injury(SCI) patients with etidronate and 7 SCI patients without etidronate. Seven patients of treatment group received oral etidronate (5 mg/kg/day) for 2 weeks followed by a 10-week period in which no drugs were given. This sequence was repeated 4 times, for a total of 48 weeks. The results showed that the patients receiving etidronate had siginificant decrease in the serum osteocalcin(OC), urine deoxypyridinoline(D-PYD) level but no increase in their mean bone density. We can carefully conclude that intermittent cyclical therapy with etidronate siginificantly reduces bone metabolic rate and inhibit bone mineral loss on osteoporosis in spinal cord injury patients.
Bone Density ; Bone Remodeling ; Bone Resorption ; Calcification, Physiologic ; Calcium ; Etidronic Acid* ; Humans ; Metabolism ; Osteoporosis* ; Spinal Cord Injuries* ; Spinal Cord*