The maintenance of bone homeostasis is critical for bone health. It is vulnerable to cause bone loss, even severely osteoporosis when the balance between bone formation and absorption is interrupted. Growing evidence has shown that energy metabolism disorders, such as abnormal glucose metabolism, irregular amino acid metabolism, and aberrant lipid metabolism, can damage bone homeostasis, causing or exacerbating bone mass loss and osteoporosis-related fractures. Here, we summarize the studies of energy metabolism in osteoblasts and osteoclasts and provide a better appreciation of how energy metabolism, especially glucose metabolism maintains bone homeostasis. With this knowledge, new avenues will be unraveled to understand and cue bone-related diseases such as osteoporosis.
Bone and Bones ; Energy Metabolism ; Osteoblasts ; Osteoclasts ; Osteogenesis

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

OBJECTIVETo detect the expression of RANKL and OPG protein in the giant cell lesions of jaw and to study the mechanism of this lesion.

METHODSRANKL and OPG were detected by immunohistochemistry (SP) in 24 paraffin-embedded and 2 frozen specimens of central giant cell lesion of jaw.

RESULTSRANKL signals were strongly positive in the vascular epithelial cells. They also could be found in fibrous stroma, bone matrix, and stromal spindle cells, even in some cytomembrane of multinucleated giant cells. OPG was detected in multinucleated giant cells and a fraction of round mononuclear cells.

CONCLUSIONSActive vascular epithelial cells are contributed to the formation of multinucleated giant cells through regulating RANKL, and RANKL could play its role by paracrine and autocrine, which might be inhibited by OPG.

Giant Cells ; metabolism ; pathology ; Humans ; Jaw Diseases ; metabolism ; pathology ; Osteoclasts ; metabolism ; Osteoprotegerin ; metabolism ; RANK Ligand ; metabolism

OBJECTIVETo study the integrin beta1 mRNA changes after orthodontic tooth movement in normal teeth and periodontitis teeth of rats.

METHODSThe OD of positively stained osteoclasts for integrin beta1 mRNA using in situ hybridzation was detected after orthodontic tooth movement in normal teeth and periodontitis teeth groups.

RESULTSIntegrin beta1 mRNA expression were detected on all osteoclasts in tooth movement samples of normal and periodontitis teeth. There were stronger positive signals after given orthodontic force in both of the two groups. But no differences were found after 0.5, 1, 2, 3, 5, 7, 10 days since orthodontic tooth movement. The integrin beta1 mRNA signals in normal tooth movement group were not different from that in periodontitis group.

CONCLUSIONThe integrin beta1 of osteoclasts may play a role in the stability and remodeling of periodontal ligament in orthodontic tooth movement. There were no difference in the OD of integrin beta1 mRNA staining in orthodontic tooth movement between normal teeth group and periodontitis teeth group.

Animals ; Integrin beta1 ; metabolism ; Osteoclasts ; Periodontal Ligament ; Periodontitis ; physiopathology ; RNA, Messenger ; metabolism ; Rats ; Tooth Movement Techniques

Gorham-Stout disease (GSD) is a sporadic chronic disease characterized by progressive bone dissolution, absorption, and disappearance along with lymphatic vessel infiltration in bone-marrow cavities. Although the osteolytic mechanism of GSD has been widely studied, the cause of lymphatic hyperplasia in GSD is rarely investigated. In this study, by comparing the RNA expression profile of osteoclasts (OCs) with that of OC precursors (OCPs) by RNA sequencing, we identified a new factor, semaphorin 3A (Sema3A), which is an osteoprotective factor involved in the lymphatic expansion of GSD. Compared to OCPs, OCs enhanced the growth, migration, and tube formation of lymphatic endothelial cells (LECs), in which the expression of Sema3A is low compared to that in OCPs. In the presence of recombinant Sema3A, the growth, migration, and tube formation of LECs were inhibited, further confirming the inhibitory effect of Sema3A on LECs in vitro. Using an LEC-induced GSD mouse model, the effect of Sema3A was examined by injecting lentivirus-expressing Sema3A into the tibiae in vivo. We found that the overexpression of Sema3A in tibiae suppressed the expansion of LECs and alleviated bone loss, whereas the injection of lentivirus expressing Sema3A short hairpin RNA (shRNA) into the tibiae caused GSD-like phenotypes. Histological staining further demonstrated that OCs decreased and osteocalcin increased after Sema3A lentiviral treatment, compared with the control. Based on the above results, we propose that reduced Sema3A in OCs is one of the mechanisms contributing to the pathogeneses of GSD and that expressing Sema3A represents a new approach for the treatment of GSD.
Animals ; Mice ; Endothelial Cells/metabolism* ; Lymphatic Vessels ; Osteoclasts/pathology* ; Osteolysis, Essential/pathology* ; Semaphorin-3A/metabolism*

Bisphosphonates inhibit bone resorption by affecting osteoclastic function and formation of osteoclasts from their precursor cells. Chondroclasts have the same origin and differentiation as osteoclasts. Thus, it is hypothesized that bisphosphonate can affect on cartilage metabolism. This study was aimed to elucidate effects of alendronate, a nitrogen containing bisphosphonate, on cartilage development in the tibial proximal and femoral distal epiphyseal plates in rats. Alendronate (1 mg/kg) was subcutaneously administered in growing rat pups for 10 days. Several parameters such as the number and size of chondroclasts, involved in cartilage resorption, size of secondary ossification center and thickness of cartilage cell layers were measured and analysed by histomorphometry. The size of the secondary ossification centers in the tibial proximal and femoral distal epiphysis was smaller in the alendronate treated group (p< 0.01). The number of osteoclasts in the both the ossification centers and chondroclasts beneath the epiphyseal plates was significantly decreased by alendronate treatment (p< 0.01). The size of chondroclasts was not significantly changed (p> 0.05). The thickness of proliferating cartilage layer was not changed, but by contrast, hypertrophied cartilage layer was increased in thickness by alendronate treatment. These findings suggest that bisphosphonates can affect cartilage cell metabolism in a chondroprotective way.
Alendronate ; Animals ; Bone Resorption ; Cartilage ; Diphosphonates ; Epiphyses ; Growth Plate* ; Knee Joint* ; Knee* ; Metabolism ; Nitrogen ; Osteoclasts ; Rats*

BACKGROUND: In this study, we examined the influence of exercise loading characteristics on bone metabolic responses and bone morphology in the growth phase and adulthood. METHODS: Running exercise (RUN) and jumping exercise (JUM) were used for the exercise loading in 28-day-old male Wistar rats. Bone metabolism was measured by blood osteocalcin (OC) and tartrate-resistant acid phosphatase (TRACP) levels. For bone morphology, the maximum bone length, bone weight, and bone strength of the femur and tibia were measured. RESULTS: A pre- and post-exercise loading comparison in the growth phase showed significantly increased OC levels in the RUN and JUM groups and significantly decreased TRACP levels in the JUM group. On the other hand, a pre- and post-exercise loading comparison in adulthood showed significantly decreased TRACP levels in the RUN and JUM groups. Femur lengths were significantly shorter in the RUN and JUM groups than in the control (CON) group, while bone weight was significantly greater in the JUM group than in the CON group. CONCLUSIONS: Exercise loading activates OC levels in the growth phase and suppresses TRACP levels in adulthood. On the other hand, these results suggest that excessive exercise loading may suppress bone length.
Acid Phosphatase ; Femur ; Hand ; Humans ; Male ; Metabolism* ; Osteoblasts ; Osteocalcin ; Osteoclasts ; Osteogenesis* ; Rats, Wistar ; Running ; Tibia

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