Journal articles: 'Bone resorption'

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Carron, CP, DM Meyer, VW Engleman, JG Rico, PG Ruminski, RL Ornberg, WF Westlin, and GA Nickols. "Peptidomimetic antagonists of alphavbeta3 inhibit bone resorption by inhibiting osteoclast bone resorptive activity, not osteoclast adhesion to bone." Journal of Endocrinology 165, no. 3 (June 1, 2000): 587–98. http://dx.doi.org/10.1677/joe.0.1650587.

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Osteoclasts are actively motile on bone surfaces and undergo alternating cycles of migration and resorption. Osteoclast interaction with the extracellular matrix plays a key role in the osteoclast resorptive process and a substantial body of evidence suggests that integrin receptors are important in osteoclast function. These integrin receptors bind to the Arg-Gly-Asp (RGD) sequence found in a variety of extracellular matrix proteins and it is well established that the interaction of osteoclast alpha v beta 3 integrin with the RGD motif within bone matrix proteins is important in osteoclast-mediated bone resorption. In this study, we characterized the effects of two synthetic peptidomimetic antagonists of alpha v beta 3, SC-56631 and SC-65811, on rabbit osteoclast adhesion to purified matrix proteins and bone, and on bone resorption in vitro. SC-56631 and SC-65811 are potent inhibitors of vitronectin binding to purified alpha v beta 3. Both SC-56631 and SC-65811 inhibited osteoclast adhesion to osteopontin- and vitronectin-coated surfaces and time-lapse video microscopy showed that osteoclasts rapidly retract from osteopontin-coated surfaces when exposed to SC-56631 and SC-65811. SC-56631 and SC-65811 blocked osteoclast-mediated bone resorption in a dose-responsive manner. Further analysis showed that SC-65811 and SC-56631 reduced the number of resorption pits produced per osteoclast and the average pit size. SC-65811 was a more potent inhibitor of bone resorption and the combination of reduced pit number and size led to a 90% inhibition of bone resorption. Surprisingly, however, osteoclasts treated with SC-65811, SC-56631 or the disintegrin echistatin, at concentrations that inhibit bone resorption did not inhibit osteoclast adhesion to bone. These results suggest that alphavbeta3 antagonists inhibited bone resorption by decreasing osteoclast bone resorptive activity or efficiency but not by inhibiting osteoclast adhesion to bone per se.

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Chu, Pei-Wen, Yu-Hsu Chen, Chien-Hui Chen, and Shau-Kwaun Chen. "Inflammatory environments disrupt both bone formation and bone resorption." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 224.46. http://dx.doi.org/10.4049/jimmunol.204.supp.224.46.

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Abstract Inflammation has been associated with bone diseases such as osteoporosis and osteoarthritis. Bone loss were reported in the patients of several inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease. However, how inflammation influence bone metabolism remains elusive. The bone loss in inflammatory environments are widely considered as the results of osteoclast overactivation which leads to excessive bone resorption. We previously discovered that osteoclasts induced from RAW macrophage treated with RANKL exhibited different cell properties and gene expression profile with undifferentiated macrophage. In this research we examined the excessive bone resorption hypothesis in in vitro systems. RANKL stimulated differentiation of RAW cells into bone-resorptive osteoclasts, and induction of pre-osteoblasts (MC-3T3 E1) into mature osteoblasts are utilized in this research. Inflammatory environments are mimic by treating cultured osteoclast or osteoblast with conditioned medium collected from bone marrow derived macrophage primed with LPS or interferon-γ. The pro-inflammatory cytokines inhibit the proliferation and disrupt the expression of genes that are needed for bone formation, such as osteocalcin and collagen. On the other hand, inflammatory environments did not activate osteoclast, nor promote bone resorption. Instead, pro-inflammatory cytokines inhibit osteoclastogenesis and bone resorption, induce mitochondrial dysfunctions and lead to apoptosis of osteoclast. These results indicated that the bone loss developed in the inflammatory environments might be due to the disruption of both bone formation and bone resorption.

3

Chambers, T. J., and K. Fuller. "Bone cells predispose bone surfaces to resorption by exposure of mineral to osteoclastic contact." Journal of Cell Science 76, no. 1 (June 1, 1985): 155–65. http://dx.doi.org/10.1242/jcs.76.1.155.

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The cell-free endocranial surface of young adult rat parietal bones was used as a substrate for osteoclastic bone resorption, either without prior treatment, or after incubation of the parietal bones with collagenase or neonatal rat calvarial cells. Untreated, the endocranial surface consisted of unmineralized organic fibres; incubation with calvarial cells or collagenase caused disruption and removal of these fibres, with extensive exposure of bone mineral on the endocranial surface, without morphologically detectable mineral dissolution. Neonatal rabbit osteoclasts resorbed bone to a greater extent from parietal bones pre-incubated with calvarial cells or collagenase than from untreated bones; mineral exposure and subsequent osteoclastic resorption were both increased if calvarial cells were incubated with parathyroid hormone; removal of bone mineral after incubation with calvarial cells removed the predisposition to osteoclastic resorption. These experiments demonstrate that calvarial cells are capable of osteoid destruction, and indicate that one mechanism by which osteoblasts induce osteoclastic bone resorption may be through digestion of the unmineralized organic material that covers bone surfaces, to expose the underlying resorption-stimulating bone mineral to osteoclastic contact.

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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.

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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

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Towhidul Alam, A. S. M., Christopher L. H. Huang, David R. Blake, and Mone Zaidi. "A hypothesis for the local control of osteoclast function by Ca2+, nitric oxide and free radicals." Bioscience Reports 12, no. 5 (October 1, 1992): 369–80. http://dx.doi.org/10.1007/bf01121500.

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Several important conclusions have recently emerged from in vitro studies on the resorptive cell of bone, the osteoclast. First, it has been established that osteoclast function is modulated locally, by changes in the local concentration of Ca2+ caused by hydroxyapatite dissolution. It is thought that activation by Ca2+ of a surface membrane Ca2+ receptor mediates these effects, hence providing a feedback control. Second, a number of molecules produced locally by the endothelial cell, with which the osteoclast is in intimate contact, have been found to affect bone resorption profoundly. For instance, the autocoid nitric oxide strongly inhibits bone resorption. Finally, reactive oxygen species have been found to aid bone resorption and enhance osteoclastic activity directly. Here, we will attempt to integrate these control mechanisms into a unified hypothesis for the local control of bone resorption.

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Feng, Shi, Zhiyong Zhang, Lei Shi, Xiaojun Tang, Wei Liu, Lin Yin, and Bin Yang. "Temporal Bone Resorption." Journal of Craniofacial Surgery 26, no. 2 (March 2015): e185-e187. http://dx.doi.org/10.1097/scs.0000000000001452.

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Taguchi, Takafumi, and Yoshio Terada. "Subperiosteal Bone Resorption." New England Journal of Medicine 370, no. 21 (May 22, 2014): e32. http://dx.doi.org/10.1056/nejmicm1308814.

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Aspenberg, P., and P. Herbertsson. "PERIPROSTHETIC BONE RESORPTION." Journal of Bone and Joint Surgery. British volume 78-B, no. 4 (July 1996): 641–46. http://dx.doi.org/10.1302/0301-620x.78b4.0780641.

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Fuller, Karen, Barrie Kirstein, and Timothy J. Chambers. "Regulation and enzymatic basis of bone resorption by human osteoclasts." Clinical Science 112, no. 11 (May 1, 2007): 567–75. http://dx.doi.org/10.1042/cs20060274.

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Although much has been learned recently of the mechanisms that regulate osteoclastic differentiation, much less is known of the means through which their resorptive activity is controlled. This is especially so for human osteoclasts. We have recently developed an assay that allows us to measure resorptive activity while minimizing confounding effects on differentiation by optimizing osteoclastogenesis, so that measurable resorption occurs over a short period, and by relating resorption in each culture during the test period to the resorption that had occurred in the same culture in a prior control period. In the present study, we found that RANKL (receptor activator of nuclear factor κB ligand) strongly stimulated the release of CTX-I (C-terminal telopeptide degradation product of type I collagen) by osteoclasts over a similar range to that over which it induces osteoclastic differentiation, consistent with a distinct action on osteoclastic function. CT (calcitonin) dose-dependently inhibited bone resorption, whereas PTH (parathyroid hormone), IL (interleukin)-1, TNF-α (tumour necrosis factor-α), IL-6, IL-8, VEGF (vascular endothelial growth factor), MCP-1 (monocyte chemoattractant protein-1), MIP-1γ (macrophage inflammatory protein-1γ), IFN (interferon)-γ and dibutyryl cGMP had no significant effect. Ca2+, cyclosporin A, IFN-β and dibutyryl cAMP all strongly suppressed resorption. Bone resorption was also strongly suppressed by alendronate, the cysteine protease inhibitor E64 and the cathepsin K inhibitor MV061194. Inhibitors of MMPs (matrix metalloproteinases) had no effect on CTX-I release. Moreover, the release of the MMP-derived collagen fragment ICTP (C-terminal cross-linked telopeptide of type I collagen) represented less that 0.01% of the quantity of CTX-I released in our cultures. This suggests that MMPs make, at most, a very small contribution to the bone-resorptive activity of osteoclasts.

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Borggaard, Xenia G., Dinisha C. Pirapaharan, Jean-Marie Delaissé, and Kent Søe. "Osteoclasts’ Ability to Generate Trenches Rather Than Pits Depends on High Levels of Active Cathepsin K and Efficient Clearance of Resorption Products." International Journal of Molecular Sciences 21, no. 16 (August 18, 2020): 5924. http://dx.doi.org/10.3390/ijms21165924.

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Until recently, it was well-accepted that osteoclasts resorb bone according to the resorption cycle model. This model is based on the assumption that osteoclasts are immobile during bone erosion, allowing the actin ring to be firmly attached and thereby provide an effective seal encircling the resorptive compartment. However, through time-lapse, it was recently documented that osteoclasts making elongated resorption cavities and trenches move across the bone surface while efficiently resorbing bone. However, it was also shown that osteoclasts making rounded cavities and pits indeed resorb bone while they are immobile. Only little is known about what distinguishes these two different resorption modes. This is of both basic and clinical interest because these resorption modes are differently sensitive to drugs and are affected by the gender as well as age of the donor. In the present manuscript we show that: 1. levels of active cathepsin K determine the switch from pit to trench mode; 2. pit and trench mode depend on clathrin-mediated endocytosis; and 3. a mechanism integrating release of resorption products and membrane/integrin recycling is required for prolongation of trench mode. Our study therefore contributes to an improved understanding of the molecular and cellular determinants for the two osteoclastic bone resorption modes.

11

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.

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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.

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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).

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Ransjö, Maria, and Ulf H. Lerner. "Calcitonin causes a sustained inhibition of protein kinase C-stimulated bone resorption in contrast to the transient inhibition of parathyroid hormone-induced bone resorption." Acta Endocrinologica 123, no. 3 (September 1990): 251–56. http://dx.doi.org/10.1530/acta.0.1230251.

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Abstract. Calcitonin is a well known inhibitor of osteoclastic bone resorption, both in vivo and in vitro. However, it is also known that calcitonin has only a transient inhibitory effect on bone resorption. The mechanism for this so-called "escape from inhibition" phenomenon is not clear. In the present study, the inhibitory effect of calcitonin on phorbol ester-induced bone resorption was examined in cultured neonatal mouse calvaria. Bone resorption was assessed as the release of radioactivity from bones prelabelled in vivo with 45Ca. Two protein kinase C-activating phorbol esters, phorbol-12-myristate-13-acetate and phorbol-12,13-dibutyrate, both stimulated 45Ca release in 120-h cultures at a concentration of 10 nmol/l. Calcitonin (30 nmol/l) inhibited phorbol esterstimulated bone resorption without any "escape from inhibition". This was in contrast to the transient inhibitory effect of calcitonin on bone resorption stimulated by parathyroid hormone (10 nmol/l), prostaglandin E2 (2 μmol/l), and bradykinin (1 μmol/l). Our results suggest that activation of protein kinase C produces a sustained inhibitory effect of calcitonin on bone resorption.

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Datta, Harish K., Iain MacIntyre, and Mone Zaidi. "The effect of extracellular calcium elevation on morphology and function of isolated rat osteoclasts." Bioscience Reports 9, no. 6 (December 1, 1989): 747–51. http://dx.doi.org/10.1007/bf01114813.

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Osteoclasts are large multinucleate cells unique in their capacity to resorb bone. These cells are exposed locally to high levels of ionised calcium during the process of resorption. We have therefore examined the effect of elevated extracellular calcium on the morphology and function of freshly disaggregated rat osteoclasts. Cell size and motility were quantitated by time-lapse video recording together with digitisation and computer-centred image analysis. In order to assess the resorptive capacity of isolated osteoclasts, we measured the total area of resorption of devitalised cortical bone by means of scanning electron microscopy and computer-based morphometry. The results show that elevation of the extracellular calcium concentration causes a dramatic reduction of cell size, accompanied by a marked diminution of enzyme release and abolition of bone resorption. We propose that ionised calcium might play an important role in the local regulation of osteoclastic bone resorption.

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Gross, Ted S., Ariff A. Damji, Stefan Judex, Robert C. Bray, and Ronald F. Zernicke. "Bone hyperemia precedes disuse-induced intracortical bone resorption." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 230–35. http://dx.doi.org/10.1152/jappl.1999.86.1.230.

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An in vivo model was used to determine whether bone hyperemia precedes increased intracortical porosity induced by disuse. Twenty-four adult male roosters (age 1 yr) were randomly assigned to intact-control, 7-days-sham-surgery, 7-days-disuse, and 14-days-disuse groups. Disuse was achieved by isolating the left ulna diaphysis from physical loading via parallel metaphyseal osteotomies. The right ulna served as an intact contralateral control. Colored microspheres were used to assess middiaphyseal bone blood flow. Bone blood flow was symmetric between the left and right ulnae of the intact-control and sham-surgery groups. After 7 days of disuse, median (±95% confidence interval) standardized blood flow was significantly elevated compared with the contralateral bone (6.5 ± 5.2 vs. 1.0 ± 0.8 ml ⋅ min−1 ⋅ 100 g−1; P = 0.03). After 14 days of disuse, blood flow was also elevated but to a lesser extent. Intracortical porosity in the sham-surgery and 7-days-disuse bones was not elevated compared with intact-control bones. At 14 days of disuse, the area of intracortical porosity was significantly elevated compared with intact control bones (0.015 ± 0.02 vs. 0.002 ± 0.002 mm2; P = 0.03). We conclude that disuse induces bone hyperemia before an increase in intracortical porosity. The potential interaction between bone vasoregulation and bone cell dynamics remains to be studied.

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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.

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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.

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Klein, Gordon L. "The Role of Bone in Muscle Wasting." International Journal of Molecular Sciences 22, no. 1 (December 31, 2020): 392. http://dx.doi.org/10.3390/ijms22010392.

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This review describes the role of bone resorption in muscle atrophy as well as in muscle protein anabolism. Both catabolic and anabolic pathways involve components of the proinflammatory cytokine families and release of factors stored in bone during resorption. The juxtaposition of the catabolic and anabolic resorption-dependent pathways raises new questions about control of release of factors from bone, quantity of release in a variety of conditions, and relation of factors released from bone. The catabolic responses involve release of calcium from bone into the circulation resulting in increased inflammatory response in intensity and/or duration. The release of transforming growth factor beta (TGF-β) from bone suppresses phosphorylation of the AKT/mTOR pathway and stimulates ubiquitin-mediated breakdown of muscle protein. In contrast, muscle IL-6 production is stimulated by undercarboxylated osteocalcin, which signals osteoblasts to produce more RANK ligand, stimulating resorptive release of undercarboxylated osteocalcin, which in turn stimulates muscle fiber nutrient uptake and an increase in muscle mass.

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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.

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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.

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Mathis, Katlynn M., Kathleen M. Sturgeon, Renate M. Winkels, Joachim Wiskemann, Mary Jane De Souza, and Katherine H. Schmitz. "Bone resorption and bone metastasis risk." Medical Hypotheses 118 (September 2018): 36–41. http://dx.doi.org/10.1016/j.mehy.2018.06.013.

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Toledo, Sílvia Regina Caminada, Indhira Dias Oliveira, Oswaldo Keith Okamoto, Marco Antonio Zago, Maria Teresa de Seixas Alves, Reynaldo Jesus Garcia Filho, Carla Renata Pacheco Donado Macedo, and Antonio Sergio Petrilli. "Bone deposition, bone resorption, and osteosarcoma." Journal of Orthopaedic Research 28, no. 9 (March 11, 2010): 1142–48. http://dx.doi.org/10.1002/jor.21120.

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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.

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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.

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Al Batran, Rami, Fouad H. Al-Bayaty, and Mazen M. Jamil Al-Obaidi. "In-VivoEffect of Andrographolide on Alveolar Bone Resorption Induced byPorphyromonas gingivalisand Its Relation with Antioxidant Enzymes." BioMed Research International 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/276329.

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Alveolar bone resorption is one of the most important facts in denture construction.Porphyromonas gingivalis(Pg) causes alveolar bone resorption, and morphologic measurements are the most frequent methods to identify bone resorption in periodontal studies. This study has aimed at evaluating the effect of Andrographolide (AND) on alveolar bone resorption in rats induced byPg. 24 healthy maleSprague Dawleyrats were divided into four groups as follows: normal control group and three experimental groups challenged orally withPgATCC 33277 five times a week supplemented with 20 mg/kg and 10 mg/kg of AND for twelve weeks. Alveolar bones of the left and right sides of the mandible were assessed by a morphometric method. The bone level, that is, the distance from the alveolar bone crest to cementumenamel junction (CEJ), was measured using 6.1 : 1 zoom stereomicroscope and software. AND reduced the effect ofPgon alveolar bone resorption and decreased the serum levels of Hexanoyl-Lysine (HEL); furthermore the reduced glutathione/oxidised glutathione (GSH/GSSG) ratio in AND treated groups (10 and 20 mg/kg) significantly increased when compared with thePggroup(P<0.05). We can conclude that AND suppresses alveolar bone resorption caused byPgin rats.

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Duka, Milos, Zoran Lazic, and Marija Bubalo. "Effect of local administration of platelet-rich plasma and guided tissue regeneration on the level of bone resorption in early dental implant insertion." Vojnosanitetski pregled 65, no. 6 (2008): 462–68. http://dx.doi.org/10.2298/vsp0806462d.

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Background/Aim. Osseointegration is a result of cellular migration, differentiation, bone formation, and bone remodeling on the surface of an implant. Each of these processes depends on platelets and blood coagulum. Platelet-rich plasma (PRP) is used to improve osseointegration and stability of implants. The aim of the research was to test the influence that PRP and guided tissue regeneration in bone defects have on bone defect filling and the level of bone resorption in early implant insertion. Methods. This experimental study included 10 dogs. A total of 40 BCT implants were inserted, 4 in each dog (two on the left side and two on the right side), with guided tissue regeneration. Radiologic analyses were done immediately after the insertion and 10 weeks after the insertion. Bone defect filling was measured by a graduated probe 10 weeks after the implant insertion. The following protocols were tested: I - PRP in combination with bovine deproteinized bone (BDB) and resorptive membrane of bovine origin (RBDM), II - BDB + RBDM, III - PRP + RBDM and IV - RBDM. Results. The applied protocols affected differently the bone defect filling and the level of bone resorption. Significantly better results (the lowest bone resorption) were achieved with protocol I (PRP + BDB + RBDM) in comparison with protocols III (PRP + RBDM) and IV (RBDM), but not with protocol II (BDB + RBDM). On the other hand, no significant difference was found among protocols II (BDB + RBDM), III (PRP + RBDM) and IV (RBDM) in the level of bone tissue resorption. Conslusion. The bone defect filling was largest and the level of bone resorption was lowest in the protocol with PRP applied in combination with BDB and RBDM.

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Iqbal, Jameel, and Mone Zaidi. "Bone resorption goes green." Cell 184, no. 5 (March 2021): 1137–39. http://dx.doi.org/10.1016/j.cell.2021.02.023.

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Buckland, Jenny. "BCLXL blocks bone resorption." Nature Reviews Rheumatology 5, no. 12 (December 2009): 656. http://dx.doi.org/10.1038/nrrheum.2009.220.

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MORIYAMA, HIROSHI, YOSHIO HONDA, CHENG CHUN HUANG, and MAXWELL ABRAMSON. "BONE RESORPTION IN CHOLESTEATOMA." Laryngoscope 97, no. 7 (July 1987): 854???859. http://dx.doi.org/10.1288/00005537-198707000-00016.

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Key Jr., L. L., W. C. Wolf, C. M. Gundberg, and W. L. Ries. "Superoxide and bone resorption." Bone 15, no. 4 (July 1994): 431–36. http://dx.doi.org/10.1016/8756-3282(94)90821-4.

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Pertot, Wilhelm-Joseph, and Jacques De´jou. "Bone and root resorption." Oral Surgery, Oral Medicine, Oral Pathology 74, no. 3 (September 1992): 357–65. http://dx.doi.org/10.1016/0030-4220(92)90076-3.

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van Niekerk, Gustav, Megan Mitchell, and Anna-Mart Engelbrecht. "Bone resorption: supporting immunometabolism." Biology Letters 14, no. 2 (February 2018): 20170783. http://dx.doi.org/10.1098/rsbl.2017.0783.

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Activation of the immune system is associated with an increase in the breakdown of various peripheral tissues, including bone. Despite the widely appreciated role of inflammatory mediators in promoting bone resorption, the functional value behind this process is not completely understood. Recent advances in the field of immunometabolism have highlighted the metabolic reprogramming that takes place in activated immune cells. It is now believed that the breakdown of peripheral tissue provides metabolic substrates to fuel metabolic anabolism in activated immune cells. We argue that phosphate, liberated by bone resorption, plays an indispensable role in sustaining immune cell metabolism. The liberated phosphate is then incorporated into macromolecules such as nucleotides and phospholipids, and is also used for the phosphorylation of metabolites (e.g. glycolytic intermediates). In addition, magnesium, also liberated during the breakdown of bone, is an essential cofactor required by various metabolic enzymes which are upregulated in activated immune cells. Finally, calcium activates various additional molecules involved in immune cell migration. Taken together, these factors suggest a key role for bone resorption during infection.

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Teitelbaum, S. L. "Bone Resorption by Osteoclasts." Science 289, no. 5484 (September 1, 2000): 1504–8. http://dx.doi.org/10.1126/science.289.5484.1504.

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Bonartsev, A. P., A. A. Muraev, R. V. Deyev, and A. V. Volkov. "Material-Associated Bone Resorption." Sovremennye tehnologii v medicine 10, no. 4 (December 2018): 26. http://dx.doi.org/10.17691/stm2018.10.4.03.

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Petrovic, M., and G. Cournot. "Barbiturate and bone resorption." Calcified Tissue International 56, no. 5 (May 1995): 408–9. http://dx.doi.org/10.1007/bf00301611.

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Chambers, T. J. "Prostaglandins and bone resorption." Clinical Materials 3, no. 4 (January 1988): 317. http://dx.doi.org/10.1016/0267-6605(88)90007-8.

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Klein, Gordon L. "Transforming Growth Factor-Beta in Skeletal Muscle Wasting." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1167. http://dx.doi.org/10.3390/ijms23031167.

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Transforming growth factor-beta (TGF-β) is part of a family of molecules that is present in many body tissues and performs many different functions. Evidence has been obtained from mice and human cancer patients with bony metastases and non-metastatic disease, as well as pediatric burn patients, that inflammation leads to bone resorption and release of TGF-β from the bone matrix with paracrine effects on muscle protein balance, possibly mediated by the generation of reactive oxygen species. Whether immobilization, which confounds the etiology of bone resorption in burn injury, also leads to the release of TGF-β from bone contributing to muscle wasting in other conditions is unclear. The use of anti-resorptive therapy in both metastatic cancer patients and pediatric burn patients has been successful in the prevention of muscle wasting, thereby creating an additional therapeutic niche for this class of drugs. The liberation of TGF-β may be one way in which bone helps to control muscle mass, but further investigation will be necessary to assess whether the rate of bone resorption is the determining factor for the release of TGF-β. Moreover, whether different resorptive conditions, such as immobilization and hyperparathyroidism, also involve TGF-β release in the pathogenesis of muscle wasting needs to be investigated.

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Calle, Yolanda, Gareth E. Jones, Chris Jagger, Karen Fuller, Mike P. Blundell, Jade Chow, Tim Chambers, and Adrian J. Thrasher. "WASp deficiency in mice results in failure to form osteoclast sealing zones and defects in bone resorption." Blood 103, no. 9 (May 1, 2004): 3552–61. http://dx.doi.org/10.1182/blood-2003-04-1259.

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Abstract No defects related to deficiency of the Wiskott-Aldrich Syndrome protein (WASp) have been described in osteoclasts. Here we show that there are significant morphologic and functional abnormalities. WASp-null cells spread over a much larger surface area and are highly polykaryotic. In their migratory phase, normal cells assemble clusters of podosomes behind their leading edges, whereas during the bone resorptive phase multiple podosomes are densely aggregated in well-defined actin rings forming the sealing zone. In comparison, WASp-null osteoclasts in either phase are markedly depleted of podosomes. On bone surfaces, this results in a failure to form actin rings at sealing zones. Complementation of WASp-null osteoclasts with an enhanced green fluorescent protein (eGFP)-WASp fusion protein restores normal cytoarchitecture. These structural disturbances translate into abnormal patterns of bone resorption both in vitro on bone slices and in vivo. Although physiologic steady-state levels of bone resorption are maintained, a major impairment is observed when WASp-null animals are exposed to a resorptive challenge. Our results provide clear evidence that WASp is a critical component of podosomes in osteoclasts and indicate a nonredundant role for WASp in the dynamic organization of these actin structures during bone resorption. (Blood. 2004;103:3552-3561)

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Miyahara, Tatsuro, Masakazu Takata, Sayuri Mori-Uchi, Masaki Miyata, Miyuki Nagai, Akemi Segure, Mari Matsusista, Hiroshi Kozuka, and Shougo Kuze. "Stimulative effects of cadmium on bone resorption in neonatal pariental bone resorption." Toxicology 73, no. 1 (January 1992): 93–99. http://dx.doi.org/10.1016/0300-483x(92)90173-c.

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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.

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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.

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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.

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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.

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Fuller, K., J. M. Owens, and T. J. Chambers. "Macrophage inflammatory protein-1 alpha and IL-8 stimulate the motility but suppress the resorption of isolated rat osteoclasts." Journal of Immunology 154, no. 11 (June 1, 1995): 6065–72. http://dx.doi.org/10.4049/jimmunol.154.11.6065.

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Abstract Cells of the osteoblastic lineage play a major role in the regulation of osteoclastic bone resorption. Recent studies have demonstrated production of chemokines by osteoblastic cells. Although these phagocyte-stimulating and proinflammatory cytokines act as chemoattractants and activators for other members of the hemopoietic lineage, their actions on osteoclasts have not been characterized. We found that macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-8 inhibited bone resorption by rat osteoclasts, primarily through reduction in the proportion of osteoclasts resorbing bone, a pattern of inhibition previously observed in response to macrophage CSF (M-CSF). MIP-2, RANTES, MIP-1 beta, and monocyte chemotactic protein-1 were without effect on resorption. MIP-1 alpha and IL-8, but not the other chemokines, also stimulated osteoclastic motility and increased the osteoclast spread area in a dose-dependent manner, over the same concentration range as that which inhibited bone resorption. In addition, MIP-1 alpha induced osteoclast orientation in a gradient of the chemokine, and stimulated osteoclast migration. We detected no effect of chemokines on osteoclast formation or survival. Our data suggest that chemokines can promote osteoclast orientation and migration, processes that might be involved in chemotaxis; it seems appropriate that resorptive functions should be suppressed during migration. Because chemokines are proinflammatory, their actions on osteoclasts might represent mechanisms by which bone resorption is modulated by the inflammatory process when this occurs in bone. However, given that chemokines are increasingly recognized to be multifunctional and that they are produced by cells of the osteoblastic lineage, they may also be components of the physiologic regulation of bone resorption.

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Moonga, BS, OA Adebanjo, HJ Wang, S. Li, XB Wu, B. Troen, A. Inzerillo, et al. "Differential effects of interleukin-6 receptor activation on intracellular signaling and bone resorption by isolated rat osteoclasts." Journal of Endocrinology 173, no. 3 (June 1, 2002): 395–405. http://dx.doi.org/10.1677/joe.0.1730395.

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The effects of the related cytokines interleukin-6 (IL-6), leukemia inhibitory factor (LIF) and oncostatin-M on bone resorption and cytosolic Ca(2+) signaling were compared in isolated rat osteoclasts. In the traditional disaggregated osteoclast (pit) assay, IL-6 and LIF, but not oncostatin-M, conserved the bone resorption otherwise inhibited by high extracellular [Ca(2+)] (15 mM). It produced a paradoxical, concentration-dependent stimulation of resorption by elevated extracellular Ca(2+). In the micro-isolated single osteoclast resorption assay, IL-6, high [Ca(2+)] or IL-6 plus high [Ca(2+)] all increased pit formation. In contrast, the IL-6 receptor (IL-6R)-specific agonist antibody MT-18 inhibited bone resorption in a concentration-dependent manner (1:500 to 1:500 000). MT-18 triggered cytosolic Ca(2+) signals in fura 2-loaded osteoclasts within approximately 10 min of application. Each cytosolic Ca(2+) transient began with a peak deflection that persisted in Ca(2+)-free, EGTA-containing extracellular medium, consistent with a release of intracellularly stored Ca(2+). This was followed by a sustained elevation of cytosolic [Ca(2+)] that was abolished in Ca(2+)-free medium, as expected from an entry of extracellular Ca(2+), and by the Ca(2+) channel antagonist Ni(2+). The inclusion of either IL-6 or soluble human (sh) IL-6R specifically reversed both the above effects of MT-18, confirming that both effects were specific for the IL-6R. The findings suggest that IL-6R activation by IL-6 stimulates osteoclastic bone resorption either by reversing the inhibitory effect of high extracellular Ca(2+) in stromal-containing systems or itself stimulating bone resorption along with Ca(2+) by micro-isolated osteoclasts. In contrast, activation of the IL-6R by an agonist antibody produces an inhibition of bone resorption and an associated triggering of the cytosolic Ca(2+) signals previously associated with regulation of bone resorptive function in other situations.

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Lin, Xiaoping, Xiaozhe Han, Toshihisa Kawai, and Martin A. Taubman. "Antibody to Receptor Activator of NF-κB Ligand Ameliorates T Cell-Mediated Periodontal Bone Resorption." Infection and Immunity 79, no. 2 (November 15, 2010): 911–17. http://dx.doi.org/10.1128/iai.00944-10.

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ABSTRACTActivated T and B lymphocytes in periodontal disease lesions express receptor activator of NF-κB ligand (RANKL), which induces osteoclastic bone resorption. The objective of this study was to evaluate the effects of anti-RANKL antibody on periodontal bone resorptionin vitroandin vivo. Aggregatibacter actinomycetemcomitansouter membrane protein 29 (Omp29) andA. actinomycetemcomitanslipopolysaccharide (LPS) were injected into 3 palatal gingival sites, and Omp29-specific T clone cells were transferred into the tail veins of rats. Rabbit anti-RANKL IgG antibody or F(ab′)2antibody fragments thereof were injected into the palatal sites in each rat (days −1, 1, and 3). Anti-RANKL IgG antibody significantly inhibited soluble RANKL (sRANKL)-induced osteoclastogenesisin vitro, in a dose-dependent manner, but also gave rise to a rat antibody response to rabbit IgGin vivo, with no significant inhibition of periodontal bone resorption detected. Lower doses (1.5 and 0.15 μg/3 sites) of F(ab′)2antibody were not immunogenic in the context of the experimental model. Periodontal bone resorption was inhibited significantly by injection of the anti-RANKL F(ab′)2antibody into gingivae. The sRANKL concentrations for the antibody-treated groups were decreased significantly compared to those for the untreated group. Osteoclasts on the alveolar bone surface were also diminished significantly after antibody injection. Gingival sRANKL concentration and bone loss showed a significant correlation with one another in animals receiving anti-RANKL F(ab′)2antibody. These results suggest that antibody to RANKL can inhibitA. actinomycetemcomitans-specific T cell-induced periodontal bone resorption by blockade and reduction of tissue sRANKL, providing an immunological approach to ameliorate immune cell-mediated periodontal bone resorption.

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Zaidi, Mone. "Modularity of osteoclast behaviour and “mode-specific” inhibition of osteoclast function." Bioscience Reports 10, no. 6 (December 1, 1990): 547–56. http://dx.doi.org/10.1007/bf01116615.

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This study is part of an attempt to understand the role of specific cellular activities in the bone resorptive process. Experiments were performed whereby known pharmacological agents were used to inhibit individual modes of osteoclastic activity, such as motility and secretion. The effects of such treatments on bone resorption were assessed by quantitative scanning electron microscopy. The compounds included colchicine, which was used to inhibit osteoclast motility; molybdate ions which were used to selectively inhibit the catalytic activity of secreted acid phosphatase, and omeprazole which was employed to inhibit the secretion of hydrogen ions. All compounds inhibited osteoclastic bone resorption, but singularly affected defined modes of activity. These findings suggest that each mode of osteoclastic activity is essential for the bone resorptive process, and that “mode-specific” inhibition may provide a means whereby excessive activity of the osteoclast can be regulated in disease.

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Tobias, J. H., and T. J. Chambers. "The effect of sex hormones on bone resorption by rat osteoclasts." Acta Endocrinologica 124, no. 1 (January 1991): 121–27. http://dx.doi.org/10.1530/acta.0.1240121.

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Abstract. Although sex hormones are important in the attainment and maintenance of bone mass, the mechanism by which they exert their effect is unknown. We therefore tested the effects of estradiol-17β, dihydrotestosterone, and progesterone on osteoclasts, the cells that resorb bone. Osteoclasts were disaggregated from neonatal rat long bones, and incubated with or without the addition of osteoblastic cells or osteoblast-like cell lines. Bone resorption was assessed by scanning electron microscopy as the extent of excavation of the bone surface after incubation. We found dihydrotestosterone (1-100 nmol/l) and progesterone (10-1000 nmol/l) to have no significant effect on bone resorption. By contrast, E2 (1 nmol/l) reduced bone resorption in osteoclast cultures to which osteoblasts had been added, by approximately 25%, although consistent inhibition with other concentrations (0.01, 0.1, 10 nmol/l) was not observed. To our surprise, E2 was also associated with a delayed, dose-responsive, stimulation of bone resorption, in the range 0.1-10 nmol/l, in osteoclast cultures free from added osteoblastic cells. Tamoxifen, which itself had no effect on bone resorption, appeared to antagonise these E2 effects. Although the physiological significance of the stimulatory effect is unclear, we hypothesize that its presence prevented us, and previous workers, from observing doseresponsive inhibition of bone resorption by E2 in vitro.

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Zhang, Jian, Fei Peng, Zhuang Liu, Jinli Luan, Xingming Liu, Chang Fei, and Xueyuan Heng. "Cranioplasty with autogenous bone flaps cryopreserved in povidone iodine: a long-term follow-up study." Journal of Neurosurgery 127, no. 6 (December 2017): 1449–56. http://dx.doi.org/10.3171/2016.8.jns16204.

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OBJECTIVEThe aim of this study was to investigate the long-term therapeutic efficacy of cranioplasty with autogenous bone flaps cryopreserved in povidone iodine and explore the risk factors for bone resorption.METHODSClinical data and follow-up results of 188 patients (with 211 bone flaps) who underwent cranioplasty with autogenous bone flaps cryopreserved in povidone-iodine were retrospectively analyzed. Bone flap resorption was classified into 3 types according to CT features, including bone flap thinning (Type I), reduced bone density (Type II), and osteolysis within the flaps (Type III). The extent of bone flap resorption was graded as mild, moderate, or severe.RESULTSShort-term postoperative complications included subcutaneous or extradural seroma collection in 19 flaps (9.0%), epidural hematoma in 16 flaps (7.6%), and infection in 8 flaps (3.8%). Eight patients whose flaps became infected and had to be removed and 2 patients who died within 2 years were excluded from the follow-up analysis. For the remaining 178 patients and 201 flaps, the follow-up duration was 24–122 months (mean 63.1 months). In 93 (46.3%) of these 201 flaps, CT demonstrated bone resorption, which was classified as Type I in 55 flaps (59.1%), Type II in 11 (11.8%), and Type III in 27 (29.0%). The severity of bone resorption was graded as follows: no bone resorption in 108 (53.7%) of 201 flaps, mild resorption in 66 (32.8%), moderate resorption in 15 (7.5%), and severe resorption in 12 (6.0%). The incidence of moderate or severe resorption was higher in Type III than in Type I (p = 0.0008). The grading of bone flap resorption was associated with the locations of bone flaps (p = 0.0210) and fragmentation (flaps broken into 2 or 3 fragments) (p = 0.0009). The incidence of bone flap collapse due to bone resorption was higher in patients who underwent ventriculoperitoneal (VP) shunt implantation than in those who did not (p = 0.0091).CONCLUSIONSBecause of the low incidence rates of infection and severe bone resorption, the authors conclude that cranioplasty with autogenous bone flaps cryopreserved in povidone-iodine solution is safe and effective. The changes characteristic of bone flap resorption became visible on CT scans about 2 months after cranioplasty and tended to stabilize at about 18 months postoperatively. The bone resorption of autogenous bone flap may be classified into 3 types. The rates of moderate and severe resorption were much higher in Type III than in Type I. The grade of bone flap resorption was associated with bone flap locations. Fragmented bone flaps or those implanted in patients treated with VP shunts may have a higher incidence of bone flap collapse due to bone resorption.

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Ishii, Takenobu, Montserrat Ruiz-Torruella, Kenta Yamamoto, Tsuguno Yamaguchi, Alireza Heidari, Roodelyne Pierrelus, Elizabeth Leon, et al. "Locally Secreted Semaphorin 4D Is Engaged in Both Pathogenic Bone Resorption and Retarded Bone Regeneration in a Ligature-Induced Mouse Model of Periodontitis." International Journal of Molecular Sciences 23, no. 10 (May 18, 2022): 5630. http://dx.doi.org/10.3390/ijms23105630.

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It is well known that Semaphorin 4D (Sema4D) inhibits IGF-1-mediated osteogenesis by binding with PlexinB1 expressed on osteoblasts. However, its elevated level in the gingival crevice fluid of periodontitis patients and the broader scope of its activities in the context of potential upregulation of osteoclast-mediated periodontal bone-resorption suggest the need for further investigation of this multifaceted molecule. In short, the pathophysiological role of Sema4D in periodontitis requires further study. Accordingly, attachment of the ligature to the maxillary molar of mice for 7 days induced alveolar bone-resorption accompanied by locally elevated, soluble Sema4D (sSema4D), TNF-α and RANKL. Removal of the ligature induced spontaneous bone regeneration during the following 14 days, which was significantly promoted by anti-Sema4D-mAb administration. Anti-Sema4D-mAb was also suppressed in vitro osteoclastogenesis and pit formation by RANKL-stimulated BMMCs. While anti-Sema4D-mAb downmodulated the bone-resorption induced in mouse periodontitis, it neither affected local production of TNF-α and RANKL nor systemic skeletal bone remodeling. RANKL-induced osteoclastogenesis and resorptive activity were also suppressed by blocking of CD72, but not Plexin B2, suggesting that sSema4D released by osteoclasts promotes osteoclastogenesis via ligation to CD72 receptor. Overall, our data indicated that ssSema4D released by osteoclasts may play a dual function by decreasing bone formation, while upregulating bone-resorption.

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Koide, Masanori, Yasuhiro Kobayashi, Tadashi Ninomiya, Midori Nakamura, Hisataka Yasuda, Yoshinori Arai, Nobuo Okahashi, Nobuo Yoshinari, Naoyuki Takahashi, and Nobuyuki Udagawa. "Osteoprotegerin-Deficient Male Mice as a Model for Severe Alveolar Bone Loss: Comparison With RANKL-Overexpressing Transgenic Male Mice." Endocrinology 154, no. 2 (January 4, 2013): 773–82. http://dx.doi.org/10.1210/en.2012-1928.

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Periodontitis, an inflammatory disease of periodontal tissues, is characterized by excessive alveolar bone resorption. An increase in the receptor activator of nuclear factor-κB ligand (RANKL) to osteoprotegerin (OPG) ratio is thought to reflect the severity of periodontitis. Here, we examined alveolar bone loss in OPG-deficient (OPG−/−) mice and RANKL-overexpressing transgenic (RANKL-Tg) mice. Alveolar bone loss in OPG−/− mice at 12 weeks was significantly higher than that in RANKL-Tg mice. OPG−/− but not RANKL-Tg mice exhibited severe bone resorption especially in cortical areas of the alveolar bone. An increased number of osteoclasts was observed in the cortical areas in OPG−/− but not in RANKL-Tg mice. Immunohistochemical analyses showed many OPG-positive signals in osteocytes but not osteoblasts. OPG-positive osteocytes in the cortical area of alveolar bones and long bones were abundant in both wild-type and RANKL-Tg mice. This suggests the resorption in cortical bone areas to be prevented by OPG produced locally. To test the usefulness of OPG−/− mice as an animal model for screening drugs to prevent alveolar bone loss, we administered an antimouse RANKL antibody or risedronate, a bisphosphonate, to OPG−/− mice. They suppressed alveolar bone resorption effectively. OPG−/− mice are useful for screening therapeutic agents against alveolar bone loss.

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Miyata, T., K. Notoya, K. Yoshida, K. Horie, K. Maeda, K. Kurokawa, and S. Taketomi. "Advanced glycation end products enhance osteoclast-induced bone resorption in cultured mouse unfractionated bone cells and in rats implanted subcutaneously with devitalized bone particles." Journal of the American Society of Nephrology 8, no. 2 (February 1997): 260–70. http://dx.doi.org/10.1681/asn.v82260.

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Advanced glycation end products (AGE) are formed in long-lived matrix proteins by a nonenzymatic reaction with sugar. The presence of AGE in beta 2-microglobulin-amyloid fibrils of dialysis-related amyloidosis, one of the characteristic features of which is an accelerated bone resorption around amyloid deposits, was recently demonstrated. This suggested a potential link of AGE in bone resorption and initiated this investigation of whether AGE enhance bone resorption. When mouse unfractionated bone cells containing osteoclasts were cultured on dentin slices, both AGE-modified beta 2-microglobulin and BSA increased the number of resorption pits formed by osteoclasts, whereas their normal counterparts of those modified with the early glycation products did not. AGE proteins, however, did not increase the number of newly formed osteoclasts, even in the coculture of mouse bone marrow cells with osteoblastic cells isolated from mouse calvaria. Enhanced bone resorption was also observed when unfractionated bone cells were cultured on AGE-modified dentin slices. AGE-enhanced bone resorption was effectively inhibited by calcitonin and ipriflavone, both of which are inhibitors of bone resorption. AGE-enhanced bone resorption was further supported by in vivo evidence that rat bone particles-upon incubation with glucose for 60 days (AGE-bone particles)-when implanted subcutaneously in rats, were resorbed to a much greater extent than control bone particles upon parallel incubation without glucose. These findings suggest that AGE enhance osteoclast-induced bone resorption. Although the mechanism remains unknown, AGE are unlikely to promote differentiation of osteoclast progenitors into osteoclasts, suggesting that AGE activate osteoclasts or alter microenvironments favorable for bone resorption by osteoclasts. The modification of bone matrices with AGE might play a role in the remodeling of senescent bone matrix tissues, further implicating a pathological significance of AGE in dialysis-related amyloidosis or osteoporosis associated with diabetes and aging.

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Hatton, R., M. Stimpel, and T. J. Chambers. "Angiotensin II is generated from angiotensin I by bone cells and stimulates osteoclastic bone resorption in vitro." Journal of Endocrinology 152, no. 1 (January 1997): 5–10. http://dx.doi.org/10.1677/joe.0.1520005.

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Abstract During bone resorption, osteoclasts are closely associated with endothelial cells. The latter are able to produce several agents that regulate bone resorption. In view of the increasing evidence that angiotensin II, which can be generated by endothelial cells, has actions outside the traditional renin-angiotensin system, we tested the effect of angiotensin II on bone resorption. Angiotensin II showed no effect either on osteoclast formation or on bone resorption by isolated osteoclasts. However, in co-cultures of osteoclasts with calvarial or MC3T3-E1 osteoblastic cells, and in osteoclastic cultures co-cultured with other bone cells obtained by prolonged sedimentation, angiotensin II stimulated bone resorption to a similar degree to that observed with 1,25(OH)2 vitamin D3. Stimulation of resorption was noted at concentrations of 10−7 m and above. We found that angiotensin I also stimulated bone resorption in co-cultures of osteoclasts with osteoblastic cells, and that this action was inhibited by inhibitors of angiotensin-converting enzyme. These results identify angiotensin I and II as potent stimulators of osteoclastic bone resorption, and raise the possibility that bone might contain a tissue-renin-angiotensin system that might play a role in the regulation of bone resorption. Journal of Endocrinology (1997) 152, 5–10

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

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

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Thomson, B. M., J. Saklatvala, and T. J. Chambers. "Osteoblasts mediate interleukin 1 stimulation of bone resorption by rat osteoclasts." Journal of Experimental Medicine 164, no. 1 (July 1, 1986): 104–12. http://dx.doi.org/10.1084/jem.164.1.104.

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A monocyte-derived factor with IL-1-like properties has recently been shown to cause resorption of bone in organ culture. We have investigated the action of IL-1 on disaggregated populations of osteoclasts, incubated alone or in the presence of osteoblastic cells, in an attempt to identify the target cell for IL-1 in bone, and to elucidate the mechanism by which IL-1 induces osteoclastic resorption. Osteoclasts were disaggregated from neonatal rat long bones and incubated on slices of human femoral cortical bone. Under these conditions, the majority of osteoclasts form distinctive excavations in the bone surface within 24 h, the volume of which can be quantified by computer-assisted morphometric and stereophotogrammetic techniques. IL-1 had no effect on bone resorption by osteoclasts alone, but when incubated in the presence of calvarial cells or cloned osteosarcoma cells, it induced a 3.8 (+/- 0.38)-fold increase in osteoclastic bone resorption, with significant enhancement at concentrations of greater than or equal to 30 pg/ml. The osteoblastic populations themselves did not resorb bone. The mechanism by which osteoblastic cells stimulate osteoclasts did not appear to depend upon PG synthesis; nor could we detect a diffusible substance in the medium of stimulated cocultures. These results indicate that IL-1 stimulates bone resorption through a primary action on osteoblasts, which are induced by IL-1 to transmit a short-range signal that stimulates osteoclastic bone resorption.

Journal articles on the topic 'Bone resorption'

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