Journal articles: 'Bone formation/resorption'

1

Li, Binbin, and Shifeng Yu. "Genistein Prevents Bone Resorption Diseases by Inhibiting Bone Resorption and Stimulating Bone Formation." Biological & Pharmaceutical Bulletin 26, no. 6 (2003): 780–86. http://dx.doi.org/10.1248/bpb.26.780.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Slootweg, M. C., W. W. Most, E. van Beek, L. P. C. Schot, S. E. Papapoulos, and C. W. G. M. Löwik. "Osteoclast formation together with interleukin-6 production in mouse long bones is increased by insulin-like growth factor-I." Journal of Endocrinology 132, no. 3 (March 1992): 433–38. http://dx.doi.org/10.1677/joe.0.1320433.

Full text

Abstract:

ABSTRACT Insulin-like growth factor-I (IGF-I) is a potent stimulator of bone formation. Whether this growth factor also induces bone resorption has not been studied in detail. We used two organ culture systems to examine the direct effect of IGF-I on bone resorption. Fetal mouse radii/ulnae, containing mature osteoclasts, showed no response to IGF-I, indicating that osteoclastic activity is not influenced by IGF-I. Fetal mouse metacarpals/metatarsals, containing just osteoclast precursors and progenitors, showed an increase in resorption in response to IGF-I, indicating that IGF-I stimulates the formulation of osteoclast precursors/progenitors and thereby increases the number of osteoclasts. Interleukin-6 (IL-6) has been hypothesized to be a mediator of bone resorptive agents such as parathyroid hormone (PTH). Both radii/ulnae and metacarpals/metatarsals reacted to IGF-I with an increase in IL-6 production. IL-6 production by UMR-106 osteogenic osteosarcoma cells was positively modulated by IGF-I, indicating that osteoblasts are likely to be the cells responsible for increased IL-6 production by the bones, and that IL-6 might be a mediatory of IGF-I-stimulated bone resorption. Journal of Endocrinology (1992) 132, 433–438

APA, Harvard, Vancouver, ISO, and other styles

3

Yavropoulou, Maria P., Helen P. Vafiadou, Olympia E. Anastasiou, Vasiliki Tsavdaridou, Georgia H. Kokaraki, and John G. Yovos. "Pioglitazone affects bone resorption but not bone formation." Bone 42 (March 2008): S91. http://dx.doi.org/10.1016/j.bone.2007.12.173.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Kitaura, Hideki, Aseel Marahleh, Fumitoshi Ohori, Takahiro Noguchi, Wei-Ren Shen, Jiawei Qi, Yasuhiko Nara, Adya Pramusita, Ria Kinjo, and Itaru Mizoguchi. "Osteocyte-Related Cytokines Regulate Osteoclast Formation and Bone Resorption." International Journal of Molecular Sciences 21, no. 14 (July 21, 2020): 5169. http://dx.doi.org/10.3390/ijms21145169.

Full text

Abstract:

The process of bone remodeling is the result of the regulated balance between bone cell populations, namely bone-forming osteoblasts, bone-resorbing osteoclasts, and the osteocyte, the mechanosensory cell type. Osteoclasts derived from the hematopoietic stem cell lineage are the principal cells involved in bone resorption. In osteolytic diseases such as rheumatoid arthritis, periodontitis, and osteoporosis, the balance is lost and changes in favor of bone resorption. Therefore, it is vital to elucidate the mechanisms of osteoclast formation and bone resorption. It has been reported that osteocytes express Receptor activator of nuclear factor κΒ ligand (RANKL), an essential factor for osteoclast formation. RANKL secreted by osteocytes is the most important factor for physiologically supported osteoclast formation in the developing skeleton and in pathological bone resorption such as experimental periodontal bone loss. TNF-α directly enhances RANKL expression in osteocytes and promotes osteoclast formation. Moreover, TNF-α enhances sclerostin expression in osteocytes, which also increases osteoclast formation. These findings suggest that osteocyte-related cytokines act directly to enhance osteoclast formation and bone resorption. In this review, we outline the most recent knowledge concerning bone resorption-related cytokines and discuss the osteocyte as the master regulator of bone resorption and effector in osteoclast formation.

APA, Harvard, Vancouver, ISO, and other styles

5

Franco, Leonardo, and Mario Alejandro Ortíz Salazar. "Biochemical markers of bone metabolism." Revista Estomatología 18, no. 1 (September 28, 2017): 30–34. http://dx.doi.org/10.25100/re.v18i1.5707.

Full text

Abstract:

The quantity and quality of bone tissue renewal are dependent on the generation of new bone (deposition) mediated by osteoblasts and the loss (resorption) mediated by osteoclasts. For each of these processes there are important markers that can be measured in serum or urine. Resorption markers are products of metabolic degradation of bone matrix in particu-lar of the type I collagen (hydroxyproline, pyridinoline and deoxypyridinoline). In addition, the resorptive activity can also be evaluated through the tartrate resistant acid phosphatase (TRAP) and calcium-creatinine ratio in urine. Bone formation markers are collagen proteins (ALP, OCN), non collagen (ONC, OPN, BSP) or fragments of collagen synthesis (procollagen peptides).

APA, Harvard, Vancouver, ISO, and other styles

6

Erjavec, Igor, Jelena Brkljacic, Slobodan Vukicevic, Boris Jakopovic, and Ivan Jakopovich. "Mushroom Extracts Decrease Bone Resorption and Improve Bone Formation." International Journal of Medicinal Mushrooms 18, no. 7 (2016): 559–69. http://dx.doi.org/10.1615/intjmedmushrooms.v18.i7.10.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Yamaguchi, Masayoshi. "Role of zinc in bone formation and bone resorption." Journal of Trace Elements in Experimental Medicine 11, no. 2-3 (1998): 119–35. http://dx.doi.org/10.1002/(sici)1520-670x(1998)11:2/3<119::aid-jtra5>3.0.co;2-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Buckland, Jenny. "Dual role for Wnt4: bone formation and bone resorption." Nature Reviews Rheumatology 10, no. 10 (August 26, 2014): 575. http://dx.doi.org/10.1038/nrrheum.2014.146.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Hirayama, T., A. Sabokbar, and NA Athanasou. "Effect of corticosteroids on human osteoclast formation and activity." Journal of Endocrinology 175, no. 1 (October 1, 2002): 155–63. http://dx.doi.org/10.1677/joe.0.1750155.

Full text

Abstract:

Chronic corticosteroid treatment is known to induce bone loss and osteoporosis. Osteoclasts are specialised bone-resorbing cells that are formed from mononuclear phagocyte precursors that circulate in the monocyte fraction. In this study we have examined the effect of the synthetic glucocorticoid, dexamethasone, on human osteoclast formation and bone-resorbing activity. Human monocytes were cultured for up to 21 days on glass coverslips and dentine slices, with soluble receptor activator for nuclear factor kappaB ligand (RANKL; 30 ng/ml) and human macrophage-colony stimulating factor (M-CSF; 25 ng/ml) in the presence and absence of dexamethasone (10(-8) M). The addition of dexamethasone over a period of 7 and 14 days of culture of monocytes (during which cell proliferation and differentiation predominantly occurred) resulted in a marked increase in the formation of tartrate-resistant acid phosphatase-positive multinucleated cells and an increase in lacunar resorption. The addition of dexamethasone to monocyte cultures after 14 days (when resorptive activity of osteoclasts had commenced) reduced the extent of lacunar resorption compared with cultures to which no dexamethasone had been added. The addition of dexamethasone to osteoclasts isolated from giant cell tumours of bone significantly inhibited resorption pit formation. Our findings indicate that dexamethasone has a direct effect on osteoclast formation and activity, stimulating the proliferation and differentiation of human osteoclast precursors and inhibiting the bone-resorbing activity of mature osteoclasts.

APA, Harvard, Vancouver, ISO, and other styles

10

Lean, J. M., J. W. M. Chow, and T. J. Chambers. "The rate of cancellous bone formation falls immediately after ovariectomy in the rat." Journal of Endocrinology 142, no. 1 (July 1994): 119–25. http://dx.doi.org/10.1677/joe.0.1420119.

Full text

Abstract:

Abstract We have recently found that administration of oestradiol-17β (OE2) to rats stimulates trabecular bone formation. It is not known, however, whether oestrogen has a similar action on bone formation rate under physiological circumstances. Oestrogen is known to suppress bone resorption, and oestrogen-deficient states in the rat, as in humans, are associated with an increase in bone resorption that entrains an increase in bone formation. To see if the latter masks a relative reduction in bone formation, due to oestrogen deficiency, we measured bone formation very early after ovariectomy, before the resorption-induced increase in bone formation becomes established. To do this, rats were administered fluorochrome labels before and after ovariectomy, spaced at weekly intervals in the first, and 3-day intervals in the second experiment. In both experiments there was a decrease in indices of bone formation in the labelling interval immediately following ovariectomy such that, using the shorter fluorochrome intervals, the mineral apposition rate fell to 69%, the double-labelled surface to 45%, and the bone formation rate to 36% of sham-ovariectomized levels. The reduction was not sustained in the subsequent label intervals, presumably masked by the increase in bone formation attributable to increased resorption. These results suggest that if bone formation is assessed before this resorption-entrained increase in bone formation occurs, oestrogen deficiency is associated with a reduction in dynamic indices of bone formation. Thus, these experiments suggest that oestrogen stimulates bone formation under physiological circumstances, and that the osteopaenia that follows oestrogen deficiency may be attributable not only to an increase in bone resorption, but also to a relative deficiency in bone formation. Journal of Endocrinology (1994) 142, 119–125

APA, Harvard, Vancouver, ISO, and other styles

11

Suda, Tatsuo, and Naoyuki Takahashi. "Control mechanism of bone formation and resorption." Ensho 9, no. 5 (1989): 359–67. http://dx.doi.org/10.2492/jsir1981.9.359.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Andersen, Thomas L., Mohamed E. Abdelgawad, Helene B. Kristensen, Ellen M. Hauge, Lars Rolighed, Jens Bollerslev, Per Kjærsgaard-Andersen, and Jean-Marie Delaisse. "Understanding Coupling between Bone Resorption and Formation." American Journal of Pathology 183, no. 1 (July 2013): 235–46. http://dx.doi.org/10.1016/j.ajpath.2013.03.006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Marcus, R. "Biochemical assessment of bone resorption and formation." Bone 18, no. 1 (January 1996): S15—S16. http://dx.doi.org/10.1016/8756-3282(95)00375-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Piec, Grazyna, Jelena Mirkovitch, Silvia Palacio, Peter F. Mühlradt, and Rolf Felix. "Effect of MALP-2, a Lipopeptide fromMycoplasma fermentans, on Bone Resorption In Vitro." Infection and Immunity 67, no. 12 (December 1, 1999): 6281–85. http://dx.doi.org/10.1128/iai.67.12.6281-6285.1999.

Full text

Abstract:

ABSTRACT Mycoplasmas may be associated with rheumatoid arthritis in various animal hosts. In humans, mycoplasma arthritis has been recorded in association with hypogammaglobulinemia. Mycoplasma fermentans is one mycoplasma species considered to be involved in causing arthritis. To clarify which mycoplasmal compounds contribute to the inflammatory, bone-destructive processes in arthritis, we used a well-defined lipopeptide, 2-kDa macrophage-activating lipopeptide (MALP-2) from M. fermentans, as an example of a class of macrophage-activating compounds ubiquitous in mycoplasmas, to study its effects on bone resorption. MALP-2 stimulated osteoclast-mediated bone resorption in murine calvaria cultures, with a maximal effect at around 2 nM. Anti-inflammatory drugs inhibited MALP-2-mediated bone resorption by about 30%. This finding suggests that MALP-2 stimulates bone resorption partially by stimulating the formation of prostaglandins. Since interleukin-6 (IL-6) stimulates bone resorption, we investigated IL-6 production in cultured calvaria. MALP-2 stimulated the liberation of IL-6, while no tumor necrosis factor was detectable. Additionally, MALP-2 stimulated low levels of NO in calvaria cultures, an effect which was strongly increased in the presence of gamma interferon, causing an inhibition of bone resorption. MALP-2 stimulated the bone-resorbing activity of osteoclasts isolated from long bones of newborn rats and cultured on dentine slices without affecting their number. In bone marrow cultures, MALP-2 inhibited the formation of osteoclasts. It appears that MALP-2 has two opposing effects: it increases the bone resorption in bone tissue by stimulation of mature osteoclasts but inhibits the formation of new ones.

APA, Harvard, Vancouver, ISO, and other styles

15

Dacquin, Romain, Rachel A. Davey, Catherine Laplace, Régis Levasseur, Howard A. Morris, Steven R. Goldring, Samuel Gebre-Medhin, Deborah L. Galson, Jeffrey D. Zajac, and Gérard Karsenty. "Amylin inhibits bone resorption while the calcitonin receptor controls bone formation in vivo." Journal of Cell Biology 164, no. 4 (February 16, 2004): 509–14. http://dx.doi.org/10.1083/jcb.200312135.

Full text

Abstract:

Amylin is a member of the calcitonin family of hormones cosecreted with insulin by pancreatic β cells. Cell culture assays suggest that amylin could affect bone formation and bone resorption, this latter function after its binding to the calcitonin receptor (CALCR). Here we show that Amylin inactivation leads to a low bone mass due to an increase in bone resorption, whereas bone formation is unaffected. In vitro, amylin inhibits fusion of mononucleated osteoclast precursors into multinucleated osteoclasts in an ERK1/2-dependent manner. Although Amylin +/− mice like Amylin-deficient mice display a low bone mass phenotype and increased bone resorption, Calcr +/− mice display a high bone mass due to an increase in bone formation. Moreover, compound heterozygote mice for Calcr and Amylin inactivation displayed bone abnormalities observed in both Calcr +/− and Amylin +/− mice, thereby ruling out that amylin uses CALCR to inhibit osteoclastogenesis in vivo. Thus, amylin is a physiological regulator of bone resorption that acts through an unidentified receptor.

APA, Harvard, Vancouver, ISO, and other styles

16

Zhong, Qing, Takashi Itokawa, Supriya Sridhar, Ke-Hong Ding, Ding Xie, Baolin Kang, Wendy B. Bollag, et al. "Effects of glucose-dependent insulinotropic peptide on osteoclast function." American Journal of Physiology-Endocrinology and Metabolism 292, no. 2 (February 2007): E543—E548. http://dx.doi.org/10.1152/ajpendo.00364.2006.

Full text

Abstract:

Acute nutrient ingestion leads to a rapid inhibition of bone resorption while effects on makers of bone formation are less marked or absent, suggesting that there is a transient shift toward skeletal accretion in the immediate postprandial period. The cellular bases for these effects are not clear. Glucose-dependent insulinotropic peptide (GIP), a known modulator of glucose-induced insulin secretion, is secreted from intestinal endocrine cells in response to nutrient ingestion. In addition to the effect of GIP on pancreatic β-cells, GIP receptors are expressed by osteoblastic cells in bone, suggesting a role for this incretin hormone in bone formation. To determine whether GIP also plays a role in the anti-resorptive effect of nutrient ingestion, osteoclasts were analyzed for the presence of GIP receptors by PCR, immunohistochemical and immunocytochemical analyses of bone tissue, and freshly isolated mature osteoclasts and osteoclast-like cells cultured in vitro. Osteoclast function was assessed by fetal long bone resorption assay and by use of the Osteologic disc assay. Our results demonstrate that GIP receptor transcripts and protein are present in osteoclasts. In addition, with the use of an in vitro organ culture system and mature osteoclasts, GIP was found to inhibit bone resorption in the organ culture system and the resorptive activity of mature osteoclasts. These data are consistent with the hypothesis that GIP inhibits bone breakdown through a direct effect on osteoclast-resorptive activity and suggest one mechanism for the postprandial reduction in markers of bone breakdown.

APA, Harvard, Vancouver, ISO, and other styles

17

Kitaura, Hideki, Saika Ogawa, Fumitoshi Ohori, Takahiro Noguchi, Aseel Marahleh, Yasuhiko Nara, Adya Pramusita, et al. "Effects of Incretin-Related Diabetes Drugs on Bone Formation and Bone Resorption." International Journal of Molecular Sciences 22, no. 12 (June 19, 2021): 6578. http://dx.doi.org/10.3390/ijms22126578.

Full text

Abstract:

Patients with type 2 diabetes have an increased risk of fracture compared to the general population. Glucose absorption is accelerated by incretin hormones, which induce insulin secretion from the pancreas. The level of the incretin hormone, glucagon-like peptide-1 (GLP-1), shows an immediate postprandial increase, and the circulating level of intact GLP-1 is reduced rapidly by dipeptidyl peptidase-4 (DPP-4)-mediated inactivation. Therefore, GLP-1 receptor agonists and DPP-4 inhibitors are effective in the treatment of type 2 diabetes. However, these incretin-related diabetic agents have been reported to affect bone metabolism, including bone formation and resorption. These agents enhance the expression of bone markers, and have been applied to improve bone quality and bone density. In addition, they have been reported to suppress chronic inflammation and reduce the levels of inflammatory cytokine expression. Previously, we reported that these incretin-related agents inhibited both the expression of inflammatory cytokines and inflammation-induced bone resorption. This review presents an overview of current knowledge regarding the effects of incretin-related diabetes drugs on osteoblast differentiation and bone formation as well as osteoclast differentiation and bone resorption. The mechanisms by which incretin-related diabetes drugs regulate bone formation and bone resorption are also discussed.

APA, Harvard, Vancouver, ISO, and other styles

18

Gerber, Thomas, Cornelia Ganz, Werner Götz, Kai Helms, Christoph Harms, and Thomas Mittlmeier. "Nanostructured Bone Grafting Substitutes Versus Autologous Cancellous Bone – An Animal Experiment in Sheep." Key Engineering Materials 631 (November 2014): 202–6. http://dx.doi.org/10.4028/www.scientific.net/kem.631.202.

Full text

Abstract:

In an In vivo study the full synthetic bone substitute NanoBone® S (NBS) was analyzed using a standardized bone defect (6 x 12 x 24mm) model in the ovine tibial metaphysis. The defect on the left side was filled with NBS granules and on the right side, autologous bone, harvested from the hip of the same animal, was inserted. After six, 12 and 26 weeks sheep were sacrificed and the tibiae analyzed. Quantitative histomorphological analysis after six weeks showed a resorption of biomaterial from over 60 to 24 percent. In contrast the bone formation after 6, and 12 weeks revealed an osteoneogenesis of 19%, and 34%, respectively. Hematoxylin and eosin sections demonstrated multinucleated giant cells on the surface of the biomaterial and resorption lacunae, indicating osteoclastic resorptive activity.

APA, Harvard, Vancouver, ISO, and other styles

19

Marie, P. J., L. Cancela, N. Le Boulch, and L. Miravet. "Bone changes due to pregnancy and lactation: influence of vitamin D status." American Journal of Physiology-Endocrinology and Metabolism 251, no. 4 (October 1, 1986): E400—E406. http://dx.doi.org/10.1152/ajpendo.1986.251.4.e400.

Full text

Abstract:

The effects of pregnancy and lactation on endosteal bone formation and resorption were evaluated in vitamin D-depleted (-D) and vitamin D-repleted (+D) rats. Pregnancy induced a marked stimulation of osteoclastic bone resorption and of static and dynamic parameters of bone formation and mineralization. Bone resorption increased independently of vitamin D status and did not correlate with plasma 1,25-dihydroxyvitamin D3 [1,25(OH)2D] levels, but it was associated with increased plasma immunoreactive parathyroid hormone (iPTH) concentrations. Stimulation of the endosteal bone formation rate was mainly impaired in D-depleted rats, resulting in trabecular bone loss, which, in -D mother rats, was associated with decreased bone ash and total bone calcium. Lactation further stimulated bone resorption and reduced the trabecular bone volume; ash weight and bone calcium content were also decreased independently of the vitamin D status and changes in plasma iPTH levels. In presence of vitamin D, the bone formation rate increased fourfold during lactation but was unchanged in -D lactating rats. During lactation, vitamin D-depleted rats lost twofold more calcified bone than +D rats because of impaired mineralization. Thus, the present study shows that both the endosteal bone resorption and formation are stimulated by pregnancy and lactation and that vitamin D is required for normal bone mineralization during the reproductive period.

APA, Harvard, Vancouver, ISO, and other styles

20

BERRY, PATRICIA A., ROSE A. MACIEWICZ, FLAVIA M. CICUTTINI, MARK D. JONES, CAROLINE J. HELLAWELL, and ANITA E. WLUKA. "Markers of Bone Formation and Resorption Identify Subgroups of Patients with Clinical Knee Osteoarthritis Who Have Reduced Rates of Cartilage Loss." Journal of Rheumatology 37, no. 6 (April 15, 2010): 1252–59. http://dx.doi.org/10.3899/jrheum.091055.

Full text

Abstract:

Objective.To determine whether serum markers of bone formation and resorption, used individually or in combination, can be used to identify subgroups who lose cartilage volume at different rates over 2 years within a knee osteoarthritis (OA) population.Methods.Changes in cartilage volume over 2 years were measured in 117 subjects with knee OA using magnetic resonance imaging. We examined relationships between change in cartilage volume and baseline serum markers of bone formation [intact N-terminal propeptide of type I procollagen (PINP) and osteocalcin] and resorption [N-telopeptide of type I collagen (NTX-I), C-telopeptide of type I collagen (CTX-I), and C-telopeptide of type I collagen (ICTP).Results.The baseline markers of bone formation, PINP and osteocalcin (p = 0.02, p = 0.01, respectively), and the baseline markers of bone resorption, CTX-I and NTX-I (p = 0.02 for both), were significantly associated with reduced cartilage loss. There were no significant associations between baseline ratios of bone formation to resorption markers and cartilage loss. However, when subjects were divided into subgroups with high or low bone formation markers (based on levels of marker ≥ mean or < mean for the population, respectively), in the subgroup with high PINP there was a significant association between increasing bone resorption markers CTX-I and NTX-I and reduced cartilage loss (p = 0.02, p = 0.001, respectively). Similarly, in the subgroup with high osteocalcin, there was a significant association between increasing CTX-I and NTX-I and reduced cartilage loss (p = 0.02, p = 0.003, respectively). In contrast, in subgroups with low bone formation markers, no significant associations were obtained between markers of bone resorption and cartilage loss.Conclusion.Overall, the results suggest that higher bone remodeling (i.e., higher serum levels of bone formation and resorption) is associated with reduced cartilage loss. Considering markers of bone formation and resorption together, it is possible to identify subgroups within the OA population who have reduced rates of cartilage loss.

APA, Harvard, Vancouver, ISO, and other styles

21

Bacovsky, Jaroslav, Vlastimil Scudla, Marketa Vytrasova, Marie Budikova, and Miroslav Myslivecek. "Monitoring of bone resorption and bone formation in multiple myeloma." Biomedical Papers 146, no. 2 (December 1, 2002): 59–61. http://dx.doi.org/10.5507/bp.2002.012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Chen, Yu-Si, Qi Guo, Li-Juan Guo, Ting Liu, Xian-Ping Wu, Zhang-Yuan Lin, Hong-Bo He, and Tie-Jian Jiang. "GDF8 inhibits bone formation and promotes bone resorption in mice." Clinical and Experimental Pharmacology and Physiology 44, no. 4 (March 27, 2017): 500–508. http://dx.doi.org/10.1111/1440-1681.12728.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Huang, Willis, and Edward M. Schwarz. "Mechanisms of bone resorption and new bone formation in spondyloarthropathies." Current Rheumatology Reports 4, no. 6 (December 2002): 513–17. http://dx.doi.org/10.1007/s11926-002-0059-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Stechschulte, L. A., P. J. Czernik, Z. C. Rotter, F. N. Tausif, C. A. Corzo, D. P. Marciano, A. Asteian, et al. "PPARG Post-translational Modifications Regulate Bone Formation and Bone Resorption." EBioMedicine 10 (August 2016): 174–84. http://dx.doi.org/10.1016/j.ebiom.2016.06.040.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Bernhardt, Anne, Jana Bacova, Uwe Gbureck, and Michael Gelinsky. "Influence of Cu2+ on Osteoclast Formation and Activity In Vitro." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2451. http://dx.doi.org/10.3390/ijms22052451.

Full text

Abstract:

Background: Copper-containing biomaterials are increasingly applied for bone regeneration due to their pro-angiogenetic, pro-osteogenetic and antimicrobial properties. Therefore, the effect of Cu2+ on osteoclasts, which play a major role in bone remodeling was studied in detail. Methods: Human primary osteoclasts, differentiated from human monocytes were differentiated or cultivated in the presence of Cu2+. Osteoclast formation and activity were analyzed by measurement of osteoclast-specific enzyme activities, gene expression analysis and resorption assays. Furthermore, the glutathione levels of the cells were checked to evaluate oxidative stress induced by Cu2+. Results: Up to 8 µM Cu2+ did not induce cytotoxic effects. Activity of tartrate-resistant acid phosphatase (TRAP) was significantly increased, while other osteoclast specific enzyme activities were not affected. However, gene expression of TRAP was not upregulated. Resorptive activity of osteoclasts towards dentin was not changed in the presence of 8 µM Cu2+ but decreased in the presence of extracellular bone matrix. When Cu2+ was added to mature osteoclasts TRAP activity was not increased and resorption decreased only moderately. The glutathione level of both differentiating and mature osteoclasts was significantly decreased in the presence of Cu2+. Conclusions: Differentiating and mature osteoclasts react differently to Cu2+. High TRAP activities are not necessarily related to high resorption.

APA, Harvard, Vancouver, ISO, and other styles

26

Malaval, Luc, Ndéyé Marième Wade-Guéye, Maya Boudiffa, Jia Fei, Ralph Zirngibl, Frieda Chen, Norbert Laroche, et al. "Bone sialoprotein plays a functional role in bone formation and osteoclastogenesis." Journal of Experimental Medicine 205, no. 5 (May 5, 2008): 1145–53. http://dx.doi.org/10.1084/jem.20071294.

Full text

Abstract:

Bone sialoprotein (BSP) and osteopontin (OPN) are both highly expressed in bone, but their functional specificities are unknown. OPN knockout (−/−) mice do not lose bone in a model of hindlimb disuse (tail suspension), showing the importance of OPN in bone remodeling. We report that BSP−/− mice are viable and breed normally, but their weight and size are lower than wild-type (WT) mice. Bone is undermineralized in fetuses and young adults, but not in older (≥12 mo) BSP−/− mice. At 4 mo, BSP−/− mice display thinner cortical bones than WT, but greater trabecular bone volume with very low bone formation rate, which indicates reduced resorption, as confirmed by lower osteoclast surfaces. Although the frequency of total colonies and committed osteoblast colonies is the same, fewer mineralized colonies expressing decreased levels of osteoblast markers form in BSP−/− versus WT bone marrow stromal cultures. BSP−/− hematopoietic progenitors form fewer osteoclasts, but their resorptive activity on dentin is normal. Tail-suspended BSP−/− mice lose bone in hindlimbs, as expected. In conclusion, BSP deficiency impairs bone growth and mineralization, concomitant with dramatically reduced bone formation. It does not, however, prevent the bone loss resulting from loss of mechanical stimulation, a phenotype that is clearly different from OPN−/− mice.

APA, Harvard, Vancouver, ISO, and other styles

27

Florencio-Silva, Rinaldo, Gisela Rodrigues da Silva Sasso, Estela Sasso-Cerri, Manuel Jesus Simões, and Paulo Sérgio Cerri. "Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells." BioMed Research International 2015 (2015): 1–17. http://dx.doi.org/10.1155/2015/421746.

Full text

Abstract:

Bone tissue is continuously remodeled through the concerted actions of bone cells, which include bone resorption by osteoclasts and bone formation by osteoblasts, whereas osteocytes act as mechanosensors and orchestrators of the bone remodeling process. This process is under the control of local (e.g., growth factors and cytokines) and systemic (e.g., calcitonin and estrogens) factors that all together contribute for bone homeostasis. An imbalance between bone resorption and formation can result in bone diseases including osteoporosis. Recently, it has been recognized that, during bone remodeling, there are an intricate communication among bone cells. For instance, the coupling from bone resorption to bone formation is achieved by interaction between osteoclasts and osteoblasts. Moreover, osteocytes produce factors that influence osteoblast and osteoclast activities, whereas osteocyte apoptosis is followed by osteoclastic bone resorption. The increasing knowledge about the structure and functions of bone cells contributed to a better understanding of bone biology. It has been suggested that there is a complex communication between bone cells and other organs, indicating the dynamic nature of bone tissue. In this review, we discuss the current data about the structure and functions of bone cells and the factors that influence bone remodeling.

APA, Harvard, Vancouver, ISO, and other styles

28

Hardy, R., and M. S. Cooper. "Bone loss in inflammatory disorders." Journal of Endocrinology 201, no. 3 (February 24, 2009): 309–20. http://dx.doi.org/10.1677/joe-08-0568.

Full text

Abstract:

Chronic inflammatory diseases of almost any cause are associated with bone loss. Bone loss is due to direct effects of inflammation, poor nutrition, reduced lean body mass, immobility and the effects of treatments, especially glucocorticoids. These mechanisms are complex and interrelated but are ultimately mediated through effects on the bone remodelling cycle. Inflammatory disease can increase bone resorption, decrease bone formation but most commonly impacts on both of these processes resulting in an uncoupling of bone formation from resorption in favour of excess resorption. This review will illustrate these interactions between inflammation and bone metabolism and discuss how these are, and might be, manipulated as therapies for inflammation related bone loss.

APA, Harvard, Vancouver, ISO, and other styles

29

Tani-Ishii, N., A. Tsunoda, T. Teranaka, and T. Umemoto. "Autocrine Regulation of Osteoclast Formation and Bone Resorption by IL-1α and TNFα." Journal of Dental Research 78, no. 10 (October 1999): 1617–23. http://dx.doi.org/10.1177/00220345990780100601.

Full text

Abstract:

Bone resorption is regulated by the cytokines within marrow cells that mediate osteoclast formation and activation. IL-1 and TNF induce bone resorption by stimulating the production of osteoclast-like multinucleated cells and by increasing the bone-resorbing activity of formed osteoclasts. This study was designed to detect IL-1 and TNF in osteoclasts in vitro and to determine whether these cytokines up-regulate osteoclast differentiation and bone resorption. The production of IL-1α, -β, and TNFa, β in osteoclasts was examined immunohistochemically and by in situ hybridization. In the co-culture of C57BL/6N mouse bone marrow and MC3T3-G2/PA6 cells, a colony of osteoclasts formed, and IL-1α and TNFa were detected. However, IL-1β and TNF β were not detected. To investigate the role of IL-1α and TNFα from osteoclasts, we enumerated TRAP-positive cells and measured the resorption pit areas in the presence of antibodies against IL-1α and TNFα. The addition of antibodies against IL-1α and TNFα to the co-culture system decreased the number of TRAP-positive colonies at seven days after incubation (anti-IL-1α, 25.0 ± 2.3%; anti-TNFα, 41.7 ± 3.7%; anti-IL-1α + anti-TNFα, 40.5 ± 1.3%; and control, 100%), and the ratio of mononuclear to multinuclear cells had changed (anti-IL-1α, 90:10; anti-TNFα, 75:25; anti-IL-1α+ anti-TNFα, 88:12; and control, 60:40). The total pit areas per dentin slice also decreased with the addition of antibodies (anti-IL-1α, 28,828; anti-TNFα, 49,249; anti-IL-1α + anti-TNFα, 30,685; and control, 303,139 mm2). These results suggest that local production of IL-la and TNFα by osteoclasts is an important mechanism for regulating the osteoclast differentiation and bone resorptive process.

APA, Harvard, Vancouver, ISO, and other styles

30

Na, WooJin, and Young-Hee Kang. "Aesculetin Inhibits Bone Resorption Through Down-Regulating Differentiation and Lysosomal Formation in Osteoclasts." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 442. http://dx.doi.org/10.1093/cdn/nzaa045_075.

Full text

Abstract:

Abstract Objectives For the optimal resorption of mineralized bone extracellular matrix, osteoclasts require the generation of a resorption lacuna characterized by the presence of specific proteases and a low pH. Thus, bone resorption by osteoclasts highly rely on lysosomes, the organelles specialized in intra- and extracellular material degradation. Aesculetin, a derivative of coumarin, possesses anti-inflammatory and anti-bacterial effects. The purpose of this study was to identify that aesculetin inhibited osteoclast differentiation and bone resorption through down-regulating lysosomal formation. Methods Raw 264.7 cells were cultured for 5 days on α-MEM with 10% FBS in the absence or presence of 50 ng/ml RANKL and 1–10 μM aesculetin. Tartrate-resistance acid phosphatase (TRAP) staining and bone resorption assay were performed by using assay kits. Western blotting was conducted with antibodies of target proteins involved in activation and lysosome biogenesis of osteoclasts. Immunocytochemical analysis employed LysoTracker for lysosome staining and α-tubulin antibody conjugated with FITC. Results Aesculetin inhibited RANKL-treated formation of multinucleated osteoclasts with a reduction of TRAP activity. When 1–10 μM aesculetin was treated to RANKL-exposed osteoclasts, the bone resorption was highly suppressed in osteoclasts. In addition, aesculetin reduced cellular expression of carbonic anhydrase II, vacuolar-type H (+)-ATPase D2 and cathepsin K elevated by RANKL, all involved in the bone resorption. Furthermore, aesculetin curtailed cellular induction of autophagy-related (Atg)5, Atg7 and small GTPase Rab7 elevated by RANKL for lysosome transportation/secretion and bone resorption in osteoclasts. Conclusions Aesculetin was effective in retarding osteoclast differentiation and secretory lysosome formation for osteoclast resorption, indicating that this compound may be a potential agent for the treatment of osteoporosis. Funding Sources No funding sources to report.

APA, Harvard, Vancouver, ISO, and other styles

31

Fu, Chao, and Ruyi Shi. "Osteoclast biology in bone resorption: a review." STEMedicine 1, no. 4 (September 3, 2020): e57. http://dx.doi.org/10.37175/stemedicine.v1i4.57.

Full text

Abstract:

What we know about bone resorption has changed a lot in the last few decades. The osteoclast is the only cell to nibble and break down the bone, and in the formation and resorption of bone tissue, osteoclasts play an important role. Once the balance of bone formation and bone loss is out of control, diseases like osteopetrosis and osteoporosis occur. Bone resorption is a unique function of osteoblasts, which are multinucleated cells formed by the fusion of mononuclear progenitor cells of the monocyte/macrophage family. In the formation of osteoclasts, there are two main factors affecting this process, macrophage colony-stimulating factor (M-CSF) and ligand-activated receptor (RANKL) of nuclear factor kappa B (NF-κB). The identification of RANK-RANKL signaling and other classic signaling pathways such as Wnt and Notch, as the major signaling regulation in osteoclast differentiation, was a significant breakthrough in the field of osteoclastogenesis. In this review, we briefly describe the latest knowledge of osteoclast-induced bone resorption and cellular factors that regulate the activity of osteoclasts and cell fusion, for the purpose of understanding osteoclastogenesis and the development of drugs that enhance bone resorption to improve pathological bone diseases.

APA, Harvard, Vancouver, ISO, and other styles

32

Kenkre, JS, and JHD Bassett. "The bone remodelling cycle." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 55, no. 3 (March 4, 2018): 308–27. http://dx.doi.org/10.1177/0004563218759371.

Full text

Abstract:

The bone remodelling cycle replaces old and damaged bone and is a highly regulated, lifelong process essential for preserving bone integrity and maintaining mineral homeostasis. During the bone remodelling cycle, osteoclastic resorption is tightly coupled to osteoblastic bone formation. The remodelling cycle occurs within the basic multicellular unit and comprises five co-ordinated steps; activation, resorption, reversal, formation and termination. These steps occur simultaneously but asynchronously at multiple different locations within the skeleton. Study of rare human bone disease and animal models have helped to elucidate the cellular and molecular mechanisms that regulate the bone remodelling cycle. The key signalling pathways controlling osteoclastic bone resorption and osteoblastic bone formation are receptor activator of nuclear factor-κB (RANK)/RANK ligand/osteoprotegerin and canonical Wnt signalling. Cytokines, growth factors and prostaglandins act as paracrine regulators of the cycle, whereas endocrine regulators include parathyroid hormone, vitamin D, calcitonin, growth hormone, glucocorticoids, sex hormones, and thyroid hormone. Disruption of the bone remodelling cycle and any resulting imbalance between bone resorption and formation leads to metabolic bone disease, most commonly osteoporosis. The advances in understanding the cellular and molecular mechanisms underlying bone remodelling have also provided targets for pharmacological interventions which include antiresorptive and anabolic therapies. This review will describe the remodelling process and its regulation, discuss osteoporosis and summarize the commonest pharmacological interventions used in its management.

APA, Harvard, Vancouver, ISO, and other styles

33

Mamedova, Elizaveta O., Tatiana A. Grebennikova, Zhanna E. Belaya, and Liudmila Y. Rozhinskaya. "Sclerostin antibodies as novel anabolic therapy for osteoporosis." Osteoporosis and Bone Diseases 21, no. 3 (April 8, 2019): 21–29. http://dx.doi.org/10.14341/osteo10127.

Full text

Abstract:

Osteoporosis medications are divided into two groups: those inhibiting bone resorption and formation (bisphosphonates and denosumab), and those stimulating bone formation i.e. having an anabolic effect. The latter include teriparatide, parathyroid hormone 1-84 and abaloparatide, all of which stimulate bone resorption as well as bone formation, which limits their anabolic effect. The discovery of sclerostin – the key inhibitor of bone formation – has led to development of the concept that inhibition of this protein could stimulate bone formation. Romosozumab is a human monoclonal antibody to sclerostin that binds to sclerostin and enables Wnt-signaling pathway ligands and their co-receptors to interact with each other, which, in turn, leads to increased bone formation and bone mineral density. Unlike classical anabolic drugs in osteoporosis treatment, romosozumab stimulates bone formation and inhibits bone resorption. In clinical trials, romosozumab showed marked increase in lumbar spine and hip bone mineral density. Presented article contains information about pre-clinical and clinical studies of romosozumab.

APA, Harvard, Vancouver, ISO, and other styles

34

Langdahl, Bente, Serge Ferrari, and David W. Dempster. "Bone modeling and remodeling: potential as therapeutic targets for the treatment of osteoporosis." Therapeutic Advances in Musculoskeletal Disease 8, no. 6 (October 6, 2016): 225–35. http://dx.doi.org/10.1177/1759720x16670154.

Full text

Abstract:

The adult skeleton is renewed by remodeling throughout life. Bone remodeling is a process where osteoclasts and osteoblasts work sequentially in the same bone remodeling unit. After the attainment of peak bone mass, bone remodeling is balanced and bone mass is stable for one or two decades until age-related bone loss begins. Age-related bone loss is caused by increases in resorptive activity and reduced bone formation. The relative importance of cortical remodeling increases with age as cancellous bone is lost and remodeling activity in both compartments increases. Bone modeling describes the process whereby bones are shaped or reshaped by the independent action of osteoblast and osteoclasts. The activities of osteoblasts and osteoclasts are not necessarily coupled anatomically or temporally. Bone modeling defines skeletal development and growth but continues throughout life. Modeling-based bone formation contributes to the periosteal expansion, just as remodeling-based resorption is responsible for the medullary expansion seen at the long bones with aging. Existing and upcoming treatments affect remodeling as well as modeling. Teriparatide stimulates bone formation, 70% of which is remodeling based and 20–30% is modeling based. The vast majority of modeling represents overflow from remodeling units rather than de novo modeling. Denosumab inhibits bone remodeling but is permissive for modeling at cortex. Odanacatib inhibits bone resorption by inhibiting cathepsin K activity, whereas modeling-based bone formation is stimulated at periosteal surfaces. Inhibition of sclerostin stimulates bone formation and histomorphometric analysis demonstrated that bone formation is predominantly modeling based. The bone-mass response to some osteoporosis treatments in humans certainly suggests that nonremodeling mechanisms contribute to this response and bone modeling may be such a mechanism. To date, this has only been demonstrated for teriparatide, however, it is clear that rediscovering a phenomenon that was first observed more half a century ago will have an important impact on our understanding of how new antifracture treatments work.

APA, Harvard, Vancouver, ISO, and other styles

35

Vacher, Jean, Michael Bruccoleri, and Monica Pata. "Ostm1 from Mouse to Human: Insights into Osteoclast Maturation." International Journal of Molecular Sciences 21, no. 16 (August 5, 2020): 5600. http://dx.doi.org/10.3390/ijms21165600.

Full text

Abstract:

The maintenance of bone mass is a dynamic process that requires a strict balance between bone formation and resorption. Bone formation is controlled by osteoblasts, while osteoclasts are responsible for resorption of the bone matrix. The opposite functions of these cell types have to be tightly regulated not only during normal bone development, but also during adult life, to maintain serum calcium homeostasis and sustain bone integrity to prevent bone fractures. Disruption of the control of bone synthesis or resorption can lead to an over accumulation of bone tissue in osteopetrosis or conversely to a net depletion of the bone mass in osteoporosis. Moreover, high levels of bone resorption with focal bone formation can cause Paget’s disease. Here, we summarize the steps toward isolation and characterization of the osteopetrosis associated trans-membrane protein 1 (Ostm1) gene and protein, essential for proper osteoclast maturation, and responsible when mutated for the most severe form of osteopetrosis in mice and humans.

APA, Harvard, Vancouver, ISO, and other styles

36

Fuller, K., J. M. Owens, C. J. Jagger, A. Wilson, R. Moss, and T. J. Chambers. "Macrophage colony-stimulating factor stimulates survival and chemotactic behavior in isolated osteoclasts." Journal of Experimental Medicine 178, no. 5 (November 1, 1993): 1733–44. http://dx.doi.org/10.1084/jem.178.5.1733.

Full text

Abstract:

Macrophage colony-stimulating factor (M-CSF) is known to play an important role in osteoclast formation. However, its actions on mature cells have not been fully characterized. We now report that M-CSF dramatically stimulates osteoclastic motility and spreading; osteoclasts responded to a gradient of M-CSF with orientation, and random cell polarization occurred after isotropic exposure. M-CSF also supported the survival of osteoclasts by preventing apoptosis. Paradoxically, M-CSF inhibits bone resorption by isolated osteoclasts. We found that this was effected predominantly by reduction in the number of excavations. Thus, M-CSF showed a propensity to suppress resorption through a reduction in the proportion of cells that were resorbing bone. Our data suggest that apart from the established role of M-CSF in the provision of precursors for osteoclastic induction, a major role for M-CSF in bone resorption is to enhance osteoclastic survival, migration, and chemotaxis. It seems appropriate that during these processes resorptive functions should be suppressed. We suggest that M-CSF continues to modulate osteoclastic activity once osteoclasts are on resorptive sites, through regulation of the balance between resorption and migration, such that not only the quantity, but the spatial pattern of resorption can be controlled by adjacent M-CSF-secreting cells of osteoblastic lineage.

APA, Harvard, Vancouver, ISO, and other styles

37

Suda, Tatsuo. "The Control Mechanism of Bone Formation and Resorption." Journal of the Kyushu Dental Society 45, no. 4 (1991): 549–51. http://dx.doi.org/10.2504/kds.45.549.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Leah, Emma. "Nitroglycerin ointment boosts bone formation and reduces resorption." Nature Reviews Rheumatology 7, no. 4 (April 2011): 196. http://dx.doi.org/10.1038/nrrheum.2011.32.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Kim, Beom-Jun, Young-Sun Lee, Sun-Young Lee, Wook-Young Baek, Young Jin Choi, Sung Ah Moon, Seung Hun Lee, et al. "Osteoclast-secreted SLIT3 coordinates bone resorption and formation." Journal of Clinical Investigation 128, no. 4 (March 5, 2018): 1429–41. http://dx.doi.org/10.1172/jci91086.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Williams, S., A. Wakisaka, Q. Q. Zeng, J. Barnes, S. Seyedin, G. Martin, W. J. Wechter, and C. T. Liang. "Effect of Minocycline on Osteoporosis." Advances in Dental Research 12, no. 1 (November 1998): 71–75. http://dx.doi.org/10.1177/08959374980120012401.

Full text

Abstract:

The effect of oral minocycline on osteopenia in ovariectomized (OVX) old rats was examined in this study. Rats were divided into 4 groups: sham-operated, OVX followed by treatment with vehicle, minocycline, or 17β-estradiol. The treatment was initiated one day after OVX and proceeded for 8 wks. OVX reduced bone mineral density (BMD) in the whole femur and in the femoral regions that are enriched in trabecular bone. Treatment with minocycline or estrogen prevented a decrease in BMD. Femoral trabecular bone area, trabecular number, and trabecular thickness were reduced, and trabecular separation was increased by OVX. Treatment with minocycline or estrogen abolished the detrimental effects induced by OVX. OVX also reduced indices that reflect the interconnectivity of trabecular bone, and the loss of trabecular connectivity was prevented by treatment with minocycline or estrogen. Based on the levels of urinary pyridinoline, we showed that the effect of estrogen, but not minocycline, was primarily through its inhibitory effect on bone resorption. Analysis of bone turnover activity suggests that OVX increased parameters associated with bone resorption (eroded surface) and formation (osteoid surface, mineralizing surface, mineral apposition rate, and bone formation rate). Treatment with minocycline reduced bone resorption modestly and stimulated bone formation substantially. In contrast, treatment with estrogen drastically reduced parameters associated with both bone resorption and formation. We have concluded that oral minocycline can effectively prevent the decrease in BMD and trabecular bone through its dual effects on bone resorption and formation.

APA, Harvard, Vancouver, ISO, and other styles

41

Southmayd, Emily A., Nancy I. Williams, Rebecca J. Mallinson, and Mary Jane De Souza. "Energy Deficiency Suppresses Bone Turnover in Exercising Women With Menstrual Disturbances." Journal of Clinical Endocrinology & Metabolism 104, no. 8 (March 21, 2019): 3131–45. http://dx.doi.org/10.1210/jc.2019-00089.

Full text

Abstract:

Abstract Context In exercising women, energy deficiency can disrupt the balance of bone formation and resorption, resulting in bone loss and an altered rate of bone turnover, which may influence future bone mineral density and fracture risk. Objective To assess the effects of energy status and estrogen status on bone turnover. Design Cross-sectional. Setting The Women’s Health and Exercise Laboratory at Pennsylvania State University. Participants Exercising women (n = 109) operationally defined as energy deficient or replete based on total triiodothyronine concentration and as estrogen deficient or replete based on menstrual cycle history and reproductive hormone metabolites. Main Outcome Measures Bone formation index [procollagen type I N-terminal propeptide (P1NP) concentration corrected for average P1NP concentration in healthy reference group, i.e., [P1NP]i/median [P1NP]ref], bone resorption index [serum C-terminal telopeptide (sCTx) concentration corrected for average sCTx concentration in healthy reference group, i.e., [sCTx]i/median [sCTx]ref], bone balance (ratio of bone formation index to bone resorption index to indicate which process predominates), and bone turnover rate (collective magnitude of bone formation index and bone resorption index to indicate overall amount of bone turnover). Results The combination of energy and estrogen deficiency resulted in less bone formation and a lower rate of bone turnover compared with women who were estrogen deficient but energy replete. Regardless of estrogen status, energy deficiency was associated with decreased bone resorption as well. No main effects of estrogen status were observed. Conclusions The results highlight the critical role that adequate energy plays in the regulation of bone turnover, especially bone formation, in exercising women with menstrual disturbances.

APA, Harvard, Vancouver, ISO, and other styles

42

Jensen, Pia Rosgaard, Thomas Levin Andersen, Brenda L. Pennypacker, Le T. Duong, Lars H. Engelholm, and Jean-Marie Delaissé. "A supra-cellular model for coupling of bone resorption to formation during remodeling: lessons from two bone resorption inhibitors affecting bone formation differently." Biochemical and Biophysical Research Communications 443, no. 2 (January 2014): 694–99. http://dx.doi.org/10.1016/j.bbrc.2013.12.036.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Szulc, Pawel. "Biochemical Bone Turnover Markers and Osteoporosis in Older Men: Where Are We?" Journal of Osteoporosis 2011 (2011): 1–5. http://dx.doi.org/10.4061/2011/704015.

Full text

Abstract:

In men aged less than 60, the association of serum and urinary levels of biochemical bone turnover markers (BTMs) and bone mineral density (BMD) is weak or not significant. After this age, higher BTM levels are correlated weakly, but significantly, with lower BMD and faster bone loss. Limited data from the cohort studies suggest that BTM measurement does not improve the prediction of fragility fractures in older men in comparison with age, BMD, history of falls and fragility fractures. Testosterone replacement therapy (TRT) decreases bone resorption. During TRT, bone formation markers slightly increase (direct effect on osteoblasts), then decrease (slowdown of bone turnover). Bisphosphonates (alendronate, risedronate, ibandronate, zoledronate) induce a rapid decrease in bone resorption followed by a milder decrease in bone formation. In men receiving antiresorptive therapy for prostate cancer, zoledronate, denosumab and toremifene decrease significantly levels of bone resorption and bone formation markers. Teriparatide induced a rapid increase in serum concentrations of bone formation markers followed by an increase in bone resorption. We need more studies on the utility of BTM measurement for the improvement of the persistence and adherence to the anti-osteoporotic treatment in men.

APA, Harvard, Vancouver, ISO, and other styles

44

Lee, Jin-Young, Da-Ae Kim, Eun-Young Kim, Eun-Ju Chang, So-Jeong Park, and Beom-Jun Kim. "Lumican Inhibits Osteoclastogenesis and Bone Resorption by Suppressing Akt Activity." International Journal of Molecular Sciences 22, no. 9 (April 29, 2021): 4717. http://dx.doi.org/10.3390/ijms22094717.

Full text

Abstract:

Lumican, a ubiquitously expressed small leucine-rich proteoglycan, has been utilized in diverse biological functions. Recent experiments demonstrated that lumican stimulates preosteoblast viability and differentiation, leading to bone formation. To further understand the role of lumican in bone metabolism, we investigated its effects on osteoclast biology. Lumican inhibited both osteoclast differentiation and in vitro bone resorption in a dose-dependent manner. Consistent with this, lumican markedly decreased the expression of osteoclastogenesis markers. Moreover, the migration and fusion of preosteoclasts and the resorptive activity per osteoclast were significantly reduced in the presence of lumican, indicating that this protein affects most stages of osteoclastogenesis. Among RANKL-dependent pathways, lumican inhibited Akt but not MAP kinases such as JNK, p38, and ERK. Importantly, co-treatment with an Akt activator almost completely reversed the effect of lumican on osteoclast differentiation. Taken together, our findings revealed that lumican inhibits osteoclastogenesis by suppressing Akt activity. Thus, lumican plays an osteoprotective role by simultaneously increasing bone formation and decreasing bone resorption, suggesting that it represents a dual-action therapeutic target for osteoporosis.

APA, Harvard, Vancouver, ISO, and other styles

45

Ryu, Seung Min, Myun Whan Ahn, Chul Hyun Park, Gun Woo Lee, In Hwan Song, Hyo Sae Ahn, Jooseong Kim, and Sukyoung Kim. "Effect of water glass coating of tricalcium phosphate granules on in vivo bone formation." Journal of Biomaterials Applications 33, no. 5 (November 2018): 662–72. http://dx.doi.org/10.1177/0885328218808038.

Full text

Abstract:

Background Recently, some authors introduced a water glass (WG, sodium-silicate glass; Na2O·SiO2·nH2O) coating over tricalcium phosphate (TCP) bioceramic to modulate its resorption rate and enhance the bone cell behaviors. In this study, four different types of granular samples were prepared to evaluate the ability of new bone formation in vivo using micro-computed tomography and histology. Methods Four types sample groups: group A (pure HA as a negative resorption control); group B (pure TCP as a positive resorption control); group C (WG-coated TCP as an early resorption model); and group D (same as group C but heat-treated at 500°C as a delayed resorption model). Cylindrical tube-type carriers with holes were fabricated with HA by extrusion and sintering. Each carrier was filled densely with each granular sample. Four types of tubes were implanted into the medial femoral condyle and medial tibial condyle of New Zealand White rabbits. Results The HA group (A) showed the lowest amount of new bone formation. All the TCP sample groups (B, C, and D) showed more new bone formation. On the other hand, among the TCP groups, group C (early resorption model) showed slightly more bone formation. The amount of residual bioceramics was most abundant in the HA group (A). All the TCP sample groups showed less residual bioceramics than group A. Among the TCP groups, group C showed slightly more residual bioceramics. Group B showed the lowest amount of residual bioceramics. Conclusions The WG-coated TCP sample (group C) is the best bone substitute candidate because of its proper biodegradation rate and the Si ions release because the WG-coated layer reduces the material resorption and enhances the new bone formation. That is, the WG-coated TCP is believed to be the best material for the application of an artificial bone substitute material.

APA, Harvard, Vancouver, ISO, and other styles

46

Ueland, Thor. "GH/IGF-I and bone resorption in vivo and in vitro." European Journal of Endocrinology 152, no. 3 (March 2005): 327–32. http://dx.doi.org/10.1530/eje.1.01874.

Full text

Abstract:

IGF-I may act as one of several coupling agents by activating bone formation and bone resorption. In vivo studies in normal subjects, postmenopausal women and patients with excess or diminished GH production (acromegaly and GHD) indicate that both GH and IGF-I activate osteoclasts, but that GH has a more pronounced effect, independently of IGF-I. In vitro, GH and IGF receptors have been demonstrated on osteoclasts and both GH and IGF-I may directly modify osteoclast function and activity. In addition to direct effects on osteoclasts, GH and IGF-I may affect bone resorption indirectly by stimulating release of paracrine mediators that regulate osteoclastic resorption (cytokines). Critical for the bone resorptive process is the balance between OPG and RANKL, which is regulated by many systemic factors. In vivo and in vitro, GH/IGF-I may modulate this balance but these studies are difficult to interpret, reflecting the complexity of this system. Increased OPG expression may possibly protect against GH/IGF-I-induced bone resorption and potentially be important for the long-term beneficial effects of GH replacement. Further studies investigating the OPG/RANKL ratio and system in experimental and transgenic GH/IGF models may clarify these issues.

APA, Harvard, Vancouver, ISO, and other styles

47

Elefteriou, Florent, Shu Takeda, Xiuyun Liu, Dawna Armstrong, and Gerard Karsenty. "Monosodium Glutamate-Sensitive Hypothalamic Neurons Contribute to the Control of Bone Mass." Endocrinology 144, no. 9 (September 1, 2003): 3842–47. http://dx.doi.org/10.1210/en.2003-0369.

Full text

Abstract:

Abstract Using chemical lesioning we previously identified hypothalamic neurons that are required for leptin antiosteogenic function. In the course of these studies we observed that destruction of neurons sensitive to monosodium glutamate (MSG) in arcuate nuclei did not affect bone mass. However MSG treatment leads to hypogonadism, a condition inducing bone loss. Therefore the normal bone mass of MSG-treated mice suggested that MSG-sensitive neurons may be implicated in the control of bone mass. To test this hypothesis we assessed bone resorption and bone formation parameters in MSG-treated mice. We show here that MSG-treated mice display the expected increase in bone resorption and that their normal bone mass is due to a concomitant increase in bone formation. Correction of MSG-induced hypogonadism by physiological doses of estradiol corrected the abnormal bone resorptive activity in MSG-treated mice and uncovered their high bone mass phenotype. Because neuropeptide Y (NPY) is highly expressed in MSG-sensitive neurons we tested whether NPY regulates bone formation. Surprisingly, NPY-deficient mice had a normal bone mass. This study reveals that distinct populations of hypothalamic neurons are involved in the control of bone mass and demonstrates that MSG-sensitive neurons control bone formation in a leptin-independent manner. It also indicates that NPY deficiency does not affect bone mass.

APA, Harvard, Vancouver, ISO, and other styles

48

Faraz, Shahdabul, Roger N. Pearse, Sujitha Yadlapati, David Jayabalan, Adriana C. Rossi, Tomer M. Mark, Ruben Niesvizky, and Joseph Lane. "The Clinical Utility of Bone Resorption and Bone Formation Markers in Multiple Myeloma." Blood 126, no. 23 (December 3, 2015): 5373. http://dx.doi.org/10.1182/blood.v126.23.5373.5373.

Full text

Abstract:

Abstract Introduction: While bone resorption markers such as urinary N-terminal telopeptide (NTx) have long been used in research, serum C-terminal telopeptide (CTx) has become the preferred marker of bone status in multiple myeloma (MM). A full understanding of the clinical utility of CTx, as well as the bone formation markers osteocalcin (OC) and bone-specific alkaline phosphatase (BSAP), in MM is still lacking. In this study, we evaluated levels of CTx, OC, and BSAP in a cohort of MM patients to better understand their roles. Methods: One set of CTx, OC, and BSAP data was obtained by random sampling in patients during a 60-day window at the Weill Cornell Medical College Myeloma Center. Bone marker changes were assessed with respect to type of myeloma therapy, response status, use of anti-resorptive therapy, and presence of osteolytic lesions or fractures. Additionally, we tested the ability of the bone markers to isolate a high fracture risk group, as defined by radiologic evidence of impending fracture. The Wilcoxon-Mann-Whitney test was used to assess clinical variables, and a 2-sided t value of less than 0.05 indicated statistical significance. Results: 50 patients were identified with bone marker data, of which 47 had MM and 3 had MM precursor diseases. The mean age was 64 years, with 25 males and 25 females. All three markers CTx (p=0.001), OC (p=0.004), and BSAP (p<0.001) significantly decreased with myeloma therapy initiation. Only CTx, however, was significantly lower in patients who achieved a partial response or greater, compared to non-responders (p=0.010). Moreover, only CTx decreased significantly in patients using anti-resorptive therapy within one year of bone marker date (p=0.006). Both CTx (p=0.011) and BSAP (p=0.005) were significantly higher in patients with more than 5 osteolytic lesions compared to those without such lesions. Additionally, only CTx predicted which patients were at risk for impending fracture (p<0.001). Of 8 patients in this high-risk group for fractures, 2 developed new pathological fractures within 1 month of the CTx test. CTx values were significantly higher in patients who were taking both proteasome inhibitor (PI) and alkylating agents compared to those only taking PIs (p<0.001). Choice of PI also affected levels of bone markers, with patients receiving bortezomib having significantly higher levels of CTx (p=0.019) than those on carfilzomib. BSAP levels were similarly higher, with a trend toward significance (p=0.064). Discussion: Of the evaluated bone markers, only CTx correlated with response to anti-MM therapy and risk of impending fracture. Additionally, CTx reflects the extent of bone disease. CTx levels decreased with use of anti-resorptive therapy within one year of bone marker date, but not with longer time points. This suggests the clinical benefit of at least annual dosing of anti-resorptive therapy and indicates the dynamic nature of this marker. The high CTx values in the PI plus alkylating group may also suggest that PI alone is more effective in addressing bone disease in such patients. Differences in CTx between individual proteasome inhibitors points to agent-specific effects of PI on bone remodeling, which warrant further investigation. The potential increase in BSAP with bortezomib versus carfilzomib treatment is consistent with recent findings, which show that bortezomib promotes osteoblastic differentiation and bone formation. As opposed to our CTx data, OC and BSAP did not prognosticate disease response or future fractures or correlate with use of anti-resorptive therapy, suggesting limited utility of these bone formation markers in MM. Table 1. Bone Marker Category MM Therapy Initiation MM Therapy Responders ART Use Within 1 Year ART Use Before 1 Year Lytic Lesions Present 5+ lytic Lesions Present Risk of Future Fracture PI Plus Alkylator CTx Bone Resorption ↓↓ ↓ ↓↓ NS ↑ ↑↑ ↑↑ ↑↑↑ OC Bone Formation ↓↓ NS NS NS NS NS NS NS BSAP Bone Formation ↓↓ NS NS NS ↑ ↑↑ NS ↑ Abbreviations: CTx, C-terminal telopeptide; OC, osteocalcin; BSAP, bone-specific alkaline phosphatase; MM, multiple myeloma; ART, anti-resorptive therapy; NS, not significant; PI, proteasome inhibitor. Single arrow represents a change by a factor of less than 2. Double arrows represent a change by a factor of greater than 2. Triple arrows represent a change by a factor of greater than 3. Disclosures Pearse: Celegen: Consultancy. Rossi:Calgene: Speakers Bureau. Mark:Calgene: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau. Niesvizky:Celgene: Consultancy, Speakers Bureau. Lane:Agnovos Healthcare, LLC: Consultancy; Bone Therapeutics: Membership on an entity's Board of Directors or advisory committees; CollPlant Holdings, Ltd.: Consultancy; D'Fine, Inc.: Consultancy; Gradtys: Membership on an entity's Board of Directors or advisory committees; ISTO Technologies, Inc: Membership on an entity's Board of Directors or advisory committees; Kuros: Membership on an entity's Board of Directors or advisory committees; Royal Consulting & Marketing: Consultancy.

APA, Harvard, Vancouver, ISO, and other styles

49

Tumber, A., S. Papaioannou, J. Breckon, MC Meikle, JJ Reynolds, and PA Hill. "The effects of serine proteinase inhibitors on bone resorption in vitro." Journal of Endocrinology 178, no. 3 (September 1, 2003): 437–47. http://dx.doi.org/10.1677/joe.0.1780437.

Full text

Abstract:

The aims of this study were to identify the role and sites of action of serine proteinases (SPs) in bone resorption, a process which involves a cascade of events, the central step of which is the removal of bone matrix by osteoclasts (OCs). This resorbing activity, however, is also determined by recruitment of new OCs to future resorption sites and removal of the osteoid layer by osteoblasts (OBs), which enables OCs to gain access to the underlying mineralized bone. The resorption systems we have studied consisted of (i) neonatal calvarial explants, (ii) isolated OCs cultured on ivory slices, (iii) mouse OBs cultured on either radiolabelled type I collagen films or bone-like matrix, (iv) bone marrow cultures to assess OC formation and (v) 17-day-old fetal mouse metatarsal bone rudiments to assess OC migration and fusion. Two separate SP inhibitors, aprotinin and alpha(2)-antiplasmin dose-dependently inhibited (45)Ca release from neonatal calvarial explants: aprotinin (10(-6) M) was the most effective SP inhibitor, producing a maximum inhibitory effect of 55.9%.Neither of the SP inhibitors influenced either OC formation or OC resorptive activity. In contrast, each SP inhibitor dose-dependently inhibited OB-mediated degradation of both type I collagen fibrils and non-mineralized bone matrix. In 17-day-old metatarsal explants aprotinin produced a 55% reduction in the migration of OCs from the periosteum to the mineralized matrix after 3 days in culture but after 6 days in culture aprotinin was without effect on OC migration. Primary mouse osteoblasts expressed mRNA for urokinase type plasminogen activator (uPA), tIssue type plasminogen activator (tPA), the type I receptor for uPA, plasminogen activator inhibitor types I and II and the broad spectrum serine proteinase inhibitor, protease nexin I. In situ hybridization demonstrated expression of tPA and uPA in osteoclasts disaggregated from 6-day-old mouse long bones. We propose that the regulation of these various enzyme systems within bone tIssue determines the sites where bone resorption will be initiated.

APA, Harvard, Vancouver, ISO, and other styles

50

Roy, Michèle, and Sophie Roux. "Rab GTPases in Osteoclastic Bone Resorption and Autophagy." International Journal of Molecular Sciences 21, no. 20 (October 16, 2020): 7655. http://dx.doi.org/10.3390/ijms21207655.

Full text

Abstract:

Small guanosine triphosphate hydrolases (GTPases) of the Rab family are involved in plasma membrane delivery, fusion events, and lysosomal and autophagic degradation pathways, thereby regulating signaling pathways and cell differentiation and function. Osteoclasts are bone-resorbing cells that maintain bone homeostasis. Polarized vesicular trafficking pathways result in the formation of the ruffled border, the osteoclast’s resorptive organelle, which also assists in transcytosis. Here, we reviewed the different roles of Rab GTPases in the endomembrane machinery of osteoclasts and in bone diseases caused by the dysfunction of these proteins, with a particular focus on autophagy and bone resorption. Understanding the molecular mechanisms underlying osteoclast-related bone disease development is critical for developing and improving therapies.

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Bone formation/resorption'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles