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Journal articles on the topic 'Resorption (Physiology)'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

Liesegang, A., M. L. Sassi, J. Risteli, R. Eicher, M. Wanner, and J. L. Riond. "Physiology of bone resorption during hypocalcemia in dairy cows." Journal of Animal Physiology and Animal Nutrition 80, no. 1-5 (September 12, 1998): 82–85. http://dx.doi.org/10.1111/j.1439-0396.1998.tb00507.x.

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2

Chattopadhyay, Naibedya. "Adiponectin Signaling Regulates Skeletal Physiology." INDIAN JOURNAL OF PHYSIOLOGY AND ALLIED SCIENCES 74, no. 02 (June 15, 2022): 39–40. http://dx.doi.org/10.55184/ijpas.v74i02.57.

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Bone remodelling is important to maintain the skeletal physiology. Bone loss with aging and hormonal pathologies may be result ofaltered bone remodelling leading to osteoporosis. Even in presence of existing therapies, there is an unmet clinical need to look forideal alternatives that would stimulate bone formation and keep resorption in check. Adiponectin and its derivatives could be a possiblecandidate for such therapy. Orally active small molecule AdipoR agonists may be a proposed solution for this.
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3

Ancajima Ramírez, Charton Dick, Frederik Maximiliano Parra Peña, Grace Teresa Panta Juárez, Luis Jaramillo Liviapoma, Ruth Marianella Huertas Coronado, and Marisel Roxana Valenzuela Ramosa. "Pregnancy, orthodontics and bone resorption." World Health Journal 2, no. 1 (April 23, 2021): 12–15. http://dx.doi.org/10.47422/whj.v2i1.10.

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Pregnant women present different changes in the skeletal system, such as the increase in calcium throughout this period, there are also small reductions in bone density. Orthodontic tooth movement is based on the principles of tissue resorption and formation at the level of the surrounding bone and periodontal ligament. It should be noted that there are multiple factors that affect the speed of this type of movement. During pregnancy and lactation, certain alterations in orthodontic dental movement may be perceived, caused by changes in bone homeostasis, alterations in tooth resorption and observed bone deposition. In this article we will cover topics such as the physiology and history of pregnancy, as well as the analysis of various articles related to orthodontic dental movement in pregnant women.
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4

Lees, Rita L., and Johan N. M. Heersche. "Differences in regulation of pHi in large (≥10 nuclei) and small (≤5 nuclei) osteoclasts." American Journal of Physiology-Cell Physiology 279, no. 3 (September 1, 2000): C751—C761. http://dx.doi.org/10.1152/ajpcell.2000.279.3.c751.

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Osteoclasts are multinucleated cells that resorb bone by extrusion of protons and proteolytic enzymes. They display marked heterogeneity in cell size, shape, and resorptive activity. Because high resorptive activity in vivo is associated with an increase in the average size of osteoclasts in areas of greater resorption and because of the importance of proton extrusion in resorption, we investigated whether the activity of the bafilomycin A1-sensitive vacuolar-type H+-ATPase (V-ATPase) and amiloride-sensitive Na+/H+ exchanger differed between large and small osteoclasts. Osteoclasts were obtained from newborn rabbit bones, cultured on glass coverslips, and loaded with the pH-sensitive indicator 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF). Intracellular pH (pHi) was recorded in single osteoclasts by monitoring fluorescence. Large (≥10 nuclei) and small (≤5 nuclei) osteoclasts differed in that large osteoclasts had a higher basal pHi, their pHi was decreased by bafilomycin A1 addition or removal of extracellular Na+, and the realkalinization upon readdition of Na+ was bafilomycin A1 sensitive. After acid loading, a subpopulation of large osteoclasts (40%) recovered by V-ATPase activity alone, whereas all small osteoclasts recovered by Na+/H+ exchanger activity. Interestingly, in 60% of the large osteoclasts, pHi recovery was mediated by both the Na+/H+ exchanger and V-ATPase activity. Our results show a striking difference between pHi regulatory mechanisms of large and small osteoclasts that we hypothesize may be associated with differences in the potential resorptive activity of these cells.
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5

Turner, R. T., L. S. Kidder, M. Zhang, S. A. Harris, K. C. Westerlind, A. Maran, and T. J. Wronski. "Estrogen has rapid tissue-specific effects on rat bone." Journal of Applied Physiology 86, no. 6 (June 1, 1999): 1950–58. http://dx.doi.org/10.1152/jappl.1999.86.6.1950.

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The decrease in cancellous bone formation after estrogen treatment is generally thought to be coupled with a prior decrease in bone resorption. To test the possibility that estrogen has rapid tissue-specific actions on bone metabolism, we determined the time course (1–32 h) effects of diethylstilbestrol on steady-state mRNA levels for immediate-response genes, extracellular matrix proteins, and signaling peptides in the proximal tibial metaphysis and uterus by using Northern blot and RNase protection assays. The regulation of signaling peptides by estrogen, although tissue specific, followed a similar time course in bone and uterus. The observed rapid decreases in expression of insulin-like growth factor I, a growth factor associated with bone formation; decreases in mRNA levels for bone matrix proteins; evidence for reduced bone matrix synthesis; failure to detect rapid increases in mRNA levels for signaling peptides implicated in mediating the inhibitory effects of estrogen on bone resorption (interleukin-1 and -6) as well as other cytokines that can increase bone resorption; and the comparatively long duration of the bone remodeling cycle in rats indicate that estrogen can decrease bone formation by a mechanism that does not require a prior reduction in bone resorption.
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6

Geng, W., and G. L. Wright. "Skeletal sensitivity to dietary calcium deficiency is increased in the female compared with the male rat." Canadian Journal of Physiology and Pharmacology 79, no. 5 (May 1, 2001): 379–85. http://dx.doi.org/10.1139/y01-005.

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We investigated potential sex differences in bone resorption and the conservation of whole body bone mass in 24-week-old Sprague-Dawley rats maintained on a 1.0% calcium diet and then fed diets containing 0.02, 0.5, 1.0, or 1.75% calcium for 31 days. Lowering dietary calcium from 1.00% to 0.02% doubled whole skeleton bone resorption (urinary 3H-tetracycline loss). Female rats were more sensitive to calcium stress, exhibiting the maximal resorptive response when fed the 0.5% calcium diet, whereas the 0.02% calcium diet was required to elicit this response in males. Despite the evidence of increased bone resorption, whole skeleton mass was unchanged in females and was significantly increased in males, indicating that switching to even the 0.02% calcium diet did not result in an overt loss of total body bone mass. Compared with controls, the skeleton mass of females (97 ± 1.4%) maintained on the 0.02% calcium diet was significantly lower than males (107 ± 2.4%), again suggesting a greater impact of calcium deficiency in females. The calculation of the average percentage growth of selected individual bones in male rats indicated a proportional increase in bone mass between the axial and appendicular skeleton of approximately +4% and +18% in animals maintained on 0.02 and 1.75% diets, respectively. By comparison, female rats consuming the 0.02% calcium diet showed an average 14% loss in axial bone and 7.5% gain in appendicular bone mass. The results indicate increased sensitivity to dietary calcium deficiency in female rats which involves a significant loss in axial bone mass not observed in male rats maintained under similar dietary conditions.Key words: skeleton bone mass, calcium diet, 3H-tetracycline, axial, appendicular, gender, sex.
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7

Xie, Jingbo, Jian Guo, Zaeema Kanwal, Mingzheng Wu, Xiangyang Lv, Nihal Abdalla Ibrahim, Ping Li, Manal Ali Buabeid, El-Shaimaa A. Arafa, and Qingshan Sun. "Calcitonin and Bone Physiology: In Vitro, In Vivo, and Clinical Investigations." International Journal of Endocrinology 2020 (September 10, 2020): 1–20. http://dx.doi.org/10.1155/2020/3236828.

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Calcitonin was discovered as a peptide hormone that was known to reduce the calcium levels in the systemic circulation. This hypocalcemic effect is produced due to multiple reasons such as inhibition of bone resorption or suppression of calcium release from the bone. Thus, calcitonin was said as a primary regulator of the bone resorption process. This is the reason why calcitonin has been used widely in clinics for the treatment of bone disorders such as osteoporosis, hypercalcemia, and Paget’s disease. However, presently calcitonin usage is declined due to the development of efficacious formulations of new drugs. Calcitonin gene-related peptides and several other peptides such as intermedin, amylin, and adrenomedullin (ADM) are categorized in calcitonin family. These peptides are known for the structural similarity with calcitonin. Aside from having a similar structure, these peptides have few overlapping biological activities and signal transduction action through related receptors. However, several other activities are also present that are peptide specific. In vitro and in vivo studies documented the posttreatment effects of calcitonin peptides, i.e., positive effect on bone osteoblasts and their formation and negative effect on osteoclasts and their resorption. The recent research studies carried out on genetically modified mice showed the inhibition of osteoclast activity by amylin, while astonishingly calcitonin plays its role by suppressing osteoblast and bone turnover. This article describes the review of the bone, the activity of the calcitonin family of peptides, and the link between them.
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8

Sims, Natalie A., and T. John Martin. "Osteoclasts Provide Coupling Signals to Osteoblast Lineage Cells Through Multiple Mechanisms." Annual Review of Physiology 82, no. 1 (February 10, 2020): 507–29. http://dx.doi.org/10.1146/annurev-physiol-021119-034425.

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Bone remodeling is essential for the repair and replacement of damaged and old bone. The major principle underlying this process is that osteoclast-mediated resorption of a quantum of bone is followed by osteoblast precursor recruitment; these cells differentiate to matrix-producing osteoblasts, which form new bone to replace what was resorbed. Evidence from osteopetrotic syndromes indicate that osteoclasts not only resorb bone, but also provide signals to promote bone formation. Osteoclasts act upon osteoblast lineage cells throughout their differentiation by facilitating growth factor release from resorbed matrix, producing secreted proteins and microvesicles, and expressing membrane-bound factors. These multiple mechanisms mediate the coupling of bone formation to resorption in remodeling. Additional interactions of osteoclasts with osteoblast lineage cells, including interactions with canopy and reversal cells, are required to achieve coordination between bone formation and resorption during bone remodeling.
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9

Kullama, L. K., C. L. Agnew, L. Day, M. G. Ervin, and M. G. Ross. "Ovine fetal swallowing and renal responses to oligohydramnios." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 3 (March 1, 1994): R972—R978. http://dx.doi.org/10.1152/ajpregu.1994.266.3.r972.

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Amniotic fluid (AF) volume regulation is dependent on a balance between fluid production and fluid resorption. We examined the effects of reduced AF volume on AF production by fetal urine and resorption by fetal swallowing and the response of these parameters to AF volume replacement. Eight time-dated pregnant ewes (125 +/- 1 days gestation) were studied before (day 1) and after (day 3) AF and fetal urine drainage. Drainage resulted in a significant decrease in AF volume (415 +/- 89 to 157 +/- 36 ml). Fetal urine osmolality increased (139 +/- 10 to 286 +/- 33 mosmol/kgH2O), while urine flow did not change significantly (0.31 +/- 0.04 to 0.23 +/- 0.06 ml/min), resulting in nonsignificant increases in osmolar, sodium, and chloride excretions. Fetal electromyographic swallowing activity decreased 30% (1.0 +/- 0.1 to 0.7 +/- 0.1 swallows/min; P < 0.05), while net esophageal flow decreased 74% (0.31 +/- 0.12 to 0.07 +/- 0.04 ml/min; P < 0.05). On day 4, 0.15 M NaCl (500 ml; 37 degrees C) was administered into the AF over 30 min. During the 2 h after reinfusion, urine flow (0.29 +/- 0.07 to 0.40 +/- 0.09 ml/min) and osmolar sodium and chloride excretion significantly increased, though fetal swallowing activity and esophageal flow did not change. Thus the ovine fetus responded to reduced AF volume by maintaining AF production and decreasing AF resorption. In response to AF replacement, urine flow increased while fetal swallowing activity did not change, consistent with an intramembranous pathway for fetal AF resorption.
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10

Carano, A., P. H. Schlesinger, N. A. Athanasou, S. L. Teitelbaum, and H. C. Blair. "Acid and base effects on avian osteoclast activity." American Journal of Physiology-Cell Physiology 264, no. 3 (March 1, 1993): C694—C701. http://dx.doi.org/10.1152/ajpcell.1993.264.3.c694.

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Osteoclasts generate a massive acid flux to mobilize bone calcium. Local extracellular acidification by polarized vacuolar-type H(+)-ATPase, balanced by contralateral HCO3-(-)Cl- exchange to maintain physiological intracellular pH, is theorized to drive this process. It follows that extracellular pH, PCO2, or HCO3- concentration ([HCO3-]) should impact bone matrix dissolution. However, the effects on bone resorption of the concentrations of these ions or their transmembrane gradients are unknown. Furthermore, because bone management is a vital process, regulatory feedback may minimize such effects. Thus a complex relationship between bone resorption and pH, PCO2, and [HCO3-] is expected but requires experimental determination. We measured bone resorption by isolated avian osteoclasts while varying these parameters across the physiological range. Bone degradation increased 50% from pH 7.3 to 6.7, whether achieved by changing [HCO3-] (2.3-38 mM) at constant HCO3- or PCO2 (15-190 mmHg) at constant [HCO3-]. However, at constant pH, changing PCO2 and [HCO3-] within physiological limits did not affect bone resorption. In contrast, total HCO3- removal at pH 7.4 reduced bone degradation by rat or avian osteoclasts substantially, confirming that normal acid secretion requires HCO3-. These observations support a model coupling osteoclastic bone resorption to proton and HCO3- transport but indicate that [HCO3-] is not rate limiting under physiological conditions. Extracellular pH changes affect osteoclastic bone resorption measurably, but not dramatically, at physiological [HCO3-].
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11

Krieger, Nancy S., and David A. Bushinsky. "Metabolic acidosis regulates RGS16 and G protein signaling in osteoblasts." American Journal of Physiology-Renal Physiology 321, no. 4 (October 1, 2021): F424—F430. http://dx.doi.org/10.1152/ajprenal.00166.2021.

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The results presented in this study indicate that regulation of regulator of G protein signaling 16 and G protein signaling in the osteoblast plays an important role in modulating the response of osteoblastic ovarian cancer G protein-coupled receptor 1 (OGR1) to metabolic acidosis and the subsequent stimulation of osteoclastic bone resorption. Further characterization of the regulation of OGR1 in metabolic acidosis-induced bone resorption will help in understanding bone loss in acidotic patients with chronic kidney disease.
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12

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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13

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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14

Lasnier, Joseph M., O. Douglas Wangensteen, Laura S. Schmitz, Cynthia R. Gross, and David H. Ingbar. "Terbutaline stimulates alveolar fluid resorption in hyperoxic lung injury." Journal of Applied Physiology 81, no. 4 (October 1, 1996): 1723–29. http://dx.doi.org/10.1152/jappl.1996.81.4.1723.

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Lasnier, Joseph M., O. Douglas Wangensteen, Laura S. Schmitz, Cynthia R. Gross, and David H. Ingbar. Terbutaline stimulates alveolar fluid resorption in hyperoxic lung injury. J. Appl. Physiol. 81(4): 1723–1729, 1996.—Alveolar fluid resorption occurs by active epithelial sodium transport and is accelerated by terbutaline in healthy lungs. We investigated the effect of terbutaline on the rate of alveolar fluid resorption from rat lungs injured by hyperoxia. Rats exposed to >95% O2 for 60 h, sufficient to increase wet-to-dry lung weight and cause alveolar edema, were compared with air-breathing control rats. After anesthesia, the animals breathed 100% O2 for 10 min through a tracheostomy. Ringer solution was instilled into the alveoli, and the steady-state rate of volume resorbed at 6 cmH2O pressure was measured via a pipette attached to the tracheostomy tubing. Ringer solution in some animals contained terbutaline (10−3 M), ouabain (10−3 M), or both. Normoxic animals resorbed 49 ± 6 μl ⋅ kg−1 ⋅ min−1; ouabain reduced this by 39%, whereas terbutaline increased the rate by 75%. The effect of terbutaline was blocked by ouabain. Hyperoxic animals absorbed 78 ± 9 μl ⋅ kg−1 ⋅ min−1; ouabain reduced this by 44%. Terbutaline increased the rate by a mean of 39 μl ⋅ kg−1 ⋅ min−1, similar to the absolute effect seen in the normoxic group, and this was blocked by ouabain. Terbutaline accelerates fluid resorption from both normal and injured rat lungs via its effects on active sodium transport.
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15

Krieger, Nancy S., and David A. Bushinsky. "Pharmacological inhibition of intracellular calcium release blocks acid-induced bone resorption." American Journal of Physiology-Renal Physiology 300, no. 1 (January 2011): F91—F97. http://dx.doi.org/10.1152/ajprenal.00276.2010.

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In vivo chronic metabolic acidosis induces net Ca2+ efflux from bone, and incubation of neonatal mouse calvariae in medium simulating physiological metabolic acidosis induces bone resorption. It appears that activation of the proton (H+) receptor OGR1 in the osteoblast leads to an increase in intracellular Ca2+, which is associated with an increase in cyclooxygenase 2 (COX2) and PGE2-induced receptor activator of NF-κB ligand (RANKL) and H+-induced osteoclastic bone resorption. To support this hypothesis, we tested whether intracellular Ca2+ signaling was integral to H+-induced bone resorption by determining whether 8-( N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) and 2-aminoethoxydiphenyl borate (2-APB), inhibitors of inositol trisphosphate-mediated Ca2+ signaling, would block H+-induced bone resorption in cultured neonatal calvariae and, if so, would do so by inhibiting H+-induced stimulation of COX2 and RANKL in osteoblastic cells. We found that H+-induced bone resorption is significantly inhibited by TMB-8 and 2-APB. Both compounds also inhibit H+-induced stimulation of COX2 protein in calvariae and COX2 mRNA and protein levels in primary osteoblasts. H+-induced stimulation of RANKL in calvarial cultures, as well as primary cells, is also completely inhibited by TMB-8 and 2-APB. These results support the hypothesis that H+ stimulation of net Ca2+ efflux from bone, mediated by COX2- and subsequent PGE2-induced RANKL production, is initiated in the osteoblast via activation of Ca2+ signaling.
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16

Ngarmukos, Chardpraorn, and Roger J. Grekin. "Nontraditional aspects of aldosterone physiology." American Journal of Physiology-Endocrinology and Metabolism 281, no. 6 (December 1, 2001): E1122—E1127. http://dx.doi.org/10.1152/ajpendo.2001.281.6.e1122.

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Aldosterone is the most important circulating mineralocorticoid. It is secreted by the zona glomerulosa of the adrenal gland and plays a major role in sodium and potassium metabolism by binding to epithelial mineralocorticoid receptors (MR) in the renal collecting duct, promoting sodium resorption and potassium excretion. The action of aldosterone on its classic target epithelia has been extensively studied, and many of the signaling events that mediate its effects have been described. Recently, there has been increased interest in aldosterone actions on the cardiovascular system, which are mediated through nonclassical actions. These include local tissue production, nongenomic actions, and effects on nonepithelial targets. In this review article, we focus on the effects of aldosterone in nonepithelial tissues that are mediated through MR, especially cardiovascular effects.
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17

Pavlos, Nathan J., Jiake Xu, Dietmar Riedel, Joyce S. G. Yeoh, Steven L. Teitelbaum, John M. Papadimitriou, Reinhard Jahn, F. Patrick Ross, and Ming H. Zheng. "Rab3D Regulates a Novel Vesicular Trafficking Pathway That Is Required for Osteoclastic Bone Resorption." Molecular and Cellular Biology 25, no. 12 (June 15, 2005): 5253–69. http://dx.doi.org/10.1128/mcb.25.12.5253-5269.2005.

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ABSTRACT Rab3 proteins are a subfamily of GTPases, known to mediate membrane transport in eukaryotic cells and play a role in exocytosis. Our data indicate that Rab3D is the major Rab3 species expressed in osteoclasts. To investigate the role of Rab3D in osteoclast physiology we examined the skeletal architecture of Rab3D-deficient mice and found an osteosclerotic phenotype. Although basal osteoclast number in null animals is normal the total eroded surface is significantly reduced, suggesting that the resorptive defect is due to attenuated osteoclast activity. Consistent with this hypothesis, ultrastructural analysis reveals that Rab3D−/− osteoclasts exhibit irregular ruffled borders. Furthermore, while overexpression of wild-type, constitutively active, or prenylation-deficient Rab3D has no significant effects, overexpression of GTP-binding-deficient Rab3D impairs bone resorption in vitro. Finally, subcellular localization studies reveal that, unlike wild-type or constitutively active Rab3D, which associate with a nonendosomal/lysosomal subset of post-trans-Golgi network (TGN) vesicles, inactive Rab3D localizes to the TGN and inhibits biogenesis of Rab3D-bearing vesicles. Collectively, our data suggest that Rab3D modulates a post-TGN trafficking step that is required for osteoclastic bone resorption.
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18

Okamoto, Fujio, Hiroshi Kajiya, Kazuko Toh, Shinichi Uchida, Momono Yoshikawa, Sei Sasaki, Mizuho A. Kido, Teruo Tanaka, and Koji Okabe. "Intracellular ClC-3 chloride channels promote bone resorption in vitro through organelle acidification in mouse osteoclasts." American Journal of Physiology-Cell Physiology 294, no. 3 (March 2008): C693—C701. http://dx.doi.org/10.1152/ajpcell.00251.2007.

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ClC-7 Cl− channels expressed in osteoclasts are important for bone resorption since it has been shown that disruption of the ClCN7 gene in mice leads to severe osteopetrosis. We have previously reported that Cl− currents recorded from mouse osteoclasts resemble those of ClC-3 Cl− channels. The aim of the present study was to determine the expression of ClC-3 channels in mouse osteoclasts and their functional role during bone resorption. We detected transcripts for both ClC-7 and ClC-3 channels in mouse osteoclasts by RT-PCR. The expression of ClC-3 was confirmed by immunocytochemical staining. Mouse osteoclasts lacking ClC-3 Cl− channels (ClC-3−/− osteoclasts) derived from ClCN3 gene-deficient mice (ClC-3−/−) showed lower bone resorption activity compared with ClC-3+/+ osteoclasts derived from wild-type mice (ClC-3+/+). Treatment of ClC-3+/+ osteoclasts with small interfering RNA (siRNA) against ClC-3 also significantly reduced bone resorption activity. Electrophysiological properties of basal and hypotonicity-induced Cl− currents in ClC-3−/− osteoclasts did not differ significantly from those in ClC-3+/+ osteoclasts. Using immunocytochemistry, ClC-3 was colocalized with lysosome-associated membrane protein 2. Using pH-sensitive dyes, organelle acidification activity in ClC-3−/− osteoclasts was weaker than in ClC-3+/+ osteoclasts. Treatment of ClC-3+/+ osteoclasts with siRNA against ClC-3 also reduced the organelle acidification activity. In conclusion, ClC-3 Cl− channels are expressed in intracellular organelles of mouse osteoclasts and contribute to osteoclastic bone resorption in vitro through organelle acidification.
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19

Li, Qingsong, Xueshun Tao, and Yubing Zhang. "Rosmarinic acid alleviates diabetic osteoporosis by suppressing the activation of NLRP3 inflammasome in rats." Physiology International 109, no. 1 (March 10, 2022): 46–57. http://dx.doi.org/10.1556/2060.2022.00154.

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Abstract Background Diabetic osteoporosis is a common metabolic bone disorder characterized by bone loss in diabetic patients, which causes an enormous social burden due to the unsatisfactory outcome of current therapeutic strategy. Methods Based on the importance of inflammasome activation in diabetic osteoporosis, we evaluated the protective effect of an antioxidant, rosmarinic acid (RA) in diabetic osteoporosis. Bone marrow-derived monocytes isolated from rats were treated with receptor activator of nuclear factor kappa-Β ligand (RANKL) and macrophage colony stimulating factor to differentiate into mature osteoclasts (OCs). Next OCs were stimulated with RA under high glucose condition to evaluate bone resorption. Next, streptozotocin (STZ)-injected rats were orally treated with 50 mg kg−1 RA to analyze its effect on diabetic osteoporosis. Results RA inhibited high glucose-stimulated inflammation and inflammasome activation in OCs. Bone resorption was also reduced after RA treatment as shown by the resorption pits assay. Moreover, RA significantly reduced bone resorption, alleviated bone weight loss and increased bone mineral density by inhibiting the activation of NACHT-LRR-PYD domains–containing protein 3 (NLRP3) inflammasome in STZ-induced diabetic rats, leading to the improvement of diabetic osteoporosis. Conclusion RA effectively ameliorates diabetic osteoporosis in STZ-induced rats by inhibiting the activation of NLRP3 inflammasome in OCs, which suggests that RA might serve as a potential candidate drug for treating diabetic osteoporosis.
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Mundy, GR. "28. Cytokines and bone resorption." Bone 9, no. 4 (1988): 260. http://dx.doi.org/10.1016/8756-3282(88)90066-x.

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21

Martin, T. "Uncoupling anabolism from bone resorption." Bone 44 (June 2009): S203. http://dx.doi.org/10.1016/j.bone.2009.03.016.

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22

Hodkin, V., RGG Russell, and JA Gallagher. "P68. The effect of tenidap on bone resorption in an avian osteoclast resorption assay." Bone 15, no. 2 (March 1994): 246. http://dx.doi.org/10.1016/8756-3282(94)90801-x.

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23

Orcel, P., M. Feuga, J. Bielakoff, and M. C. De Vernejoul. "Local bone injections of LPS and M-CSF increase bone resorption by different pathways in vivo in rats." American Journal of Physiology-Endocrinology and Metabolism 264, no. 3 (March 1, 1993): E391—E397. http://dx.doi.org/10.1152/ajpendo.1993.264.3.e391.

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We investigated the local in vivo action of lipopolysaccharide (LPS), a potent monocyte activator, and of macrophage colony-stimulating factor (M-CSF), a hemopoietic growth factor influencing monocyte differentiation, on bone resorption in normal female 8-wk-old rats. LPS (2 injections of 0.5 microgram), M-CSF (2 injections of either 12.5, 25, 100, or 500 ng), or vehicle was injected into bone marrow space through a thin catheter implanted, under hydrochloride anesthesia, in the distal end of the right femur. Histomorphometry was performed after staining of the tartrate-resistant acid phosphatase (TRAP). The number of osteoclasts and of TRAP-positive marrow cells (considered as osteoclast precursors) were counted in the secondary spongiosa. LPS caused a 3-fold increase in osteoclast surface, a 4.5-fold increase in the number of osteoclasts, but no change in the number of TRAP-positive marrow cells. M-CSF induced a striking dose-dependent biphasic effect on the number of TRAP-positive marrow cells and on bone resorption (no change with the lowest or with the highest concentrations, although the two intermediate doses significantly increased resorption surfaces and the number of osteoclasts). Our results demonstrate a local in vivo effect of LPS and of M-CSF on bone resorption and suggest that these substances act at different stages of osteoclast development and function.
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24

Lloyd, Shane A. J., Neil D. Travis, Teng Lu, and Ted A. Bateman. "Development of a low-dose anti-resorptive drug regimen reveals synergistic suppression of bone formation when coupled with disuse." Journal of Applied Physiology 104, no. 3 (March 2008): 729–38. http://dx.doi.org/10.1152/japplphysiol.00632.2007.

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Safe and effective countermeasures to spaceflight-induced osteoporosis are required to mitigate the potential for mission-critical fractures and ensure long-term bone health in astronauts. Two anti-resorptive drugs, the bisphosphonate zoledronic acid (ZOL) and the anti-receptor activator of NF-κB ligand protein osteoprotegerin (OPG), were investigated to find the minimum, comparable doses that yield a maximal increase in bone quality, while minimizing deleterious effects on turnover and mineralization. Through a series of five trials in normally loaded female mice ( n = 56/trial), analysis of trabecular volume fraction and connectivity using microcomputed tomography, along with biomechanical testing, quantitative histomorphometry, and compositional analysis, was used to select 45 μg/kg ZOL and 500 μg/kg OPG as doses that satisfy these criteria. These doses were then examined for their ability to mitigate bone loss following short-term unloading through hindlimb suspension (HLS). Seventy-two mice were prophylactically administered ZOL, OPG, or PBS and assigned to loaded control or 2-wk HLS groups ( n = 12 for each of 6 groups). Both anti-resorptives were able to preserve trabecular microarchitecture and femoral elastic and maximum force in HLS mice (+30–40% ZOL/OPG vs. PBS). In HLS mice, anti-resorptive dosing reduced resorption perimeter at the femoral endocortical surface by 30% vs. PBS. In loaded control mice, anti-resorptives produced no change in bone formation rate; however, reductions in bone formation rate brought about by HLS were exacerbated by anti-resorptive treatment, suggesting synergistic inhibition of osteoblasts during disuse. Refined anti-resorptive dosing will tend to target countermeasures to the period of disuse, resulting in faster recovery and less adverse effects for astronauts.
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25

Meir, Tomer, Ronen Levi, Liesbet Lieben, Steven Libutti, Geert Carmeliet, Roger Bouillon, Justin Silver, and Tally Naveh-Many. "Deletion of the vitamin D receptor specifically in the parathyroid demonstrates a limited role for the receptor in parathyroid physiology." American Journal of Physiology-Renal Physiology 297, no. 5 (November 2009): F1192—F1198. http://dx.doi.org/10.1152/ajprenal.00360.2009.

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1,25(OH)2D3 decreases parathyroid hormone (PTH) gene transcription through the vitamin D receptor (VDR). Total body VDR−/− mice have high PTH levels, hypocalcemia, hypophosphatemia, and bone malformations. To investigate PTH regulation by the VDR specifically in the parathyroid, we generated parathyroid-specific VDR knockout mice ( PT-VDR−/−). In both strains, there was a decrease in parathyroid calcium receptor (CaR) levels. The number of proliferating parathyroid cells was increased in the VDR−/− mice but not in the PT-VDR−/− mice. Serum PTH levels were moderately but significantly increased in the PT-VDR−/− mice with normal serum calcium levels. The sensitivity of the parathyroid glands of the PT-VDR−/− mice to calcium was intact as measured by serum PTH levels after changes in serum calcium. This indicates that the reduced CaR in the PT-VDR−/− mice enables a physiologic response to serum calcium. Serum C-terminal collagen crosslinks, a marker of bone resorption, were increased in the PT-VDR−/− mice with no change in the bone formation marker, serum osteocalcin, consistent with a resorptive effect due to the increased serum PTH levels in the PT-VDR−/− mice. Therefore, deletion of the VDR specifically in the parathyroid decreases parathyroid CaR expression and only moderately increases basal PTH levels, suggesting that the VDR has a limited role in parathyroid physiology.
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26

Teti, A., P. C. Marchisio, and A. Z. Zallone. "Clear zone in osteoclast function: role of podosomes in regulation of bone-resorbing activity." American Journal of Physiology-Cell Physiology 261, no. 1 (July 1, 1991): C1—C7. http://dx.doi.org/10.1152/ajpcell.1991.261.1.c1.

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The adhesion of osteoclasts to the bone matrix is mandatory for bone resorption. Contact of the osteoclast with bone surface induces, in fact, cell polarization and organization of the resorbing apparatus, the so-called “ruffled border.” Cell-matrix interaction in osteoclasts is a complex phenomenon resulting from formation of the “clear zone,” a cytoplasmic area presenting the adhering plasma membrane, or “sealing membrane.” The sealing membrane surrounds the ruffled border and seals the resorbing compartment, namely the extracellular space in which bone resorption takes place. Adhesion at this level occurs via specialized discrete structures, the “podosomes.” Podosomes present most of the protein commonly found in focal adhesions, but with a peculiar organization. They are dynamic elements suitable for regulation, according with the functional demand of the cell. Their assembly increases during bone resorption and is regulated by the cytosolic free calcium concentration and the activity of protein kinase C.
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27

Frick, Kevin K., John R. Asplin, Christopher D. Culbertson, Ignacio Granja, Nancy S. Krieger, and David A. Bushinsky. "Persistence of 1,25D-induced hypercalciuria in alendronate-treated genetic hypercalciuric stone-forming rats fed a low-calcium diet." American Journal of Physiology-Renal Physiology 306, no. 9 (May 1, 2014): F1081—F1087. http://dx.doi.org/10.1152/ajprenal.00680.2013.

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Genetic hypercalciuric stone-forming (GHS) rats demonstrate increased intestinal Ca absorption, increased bone resorption, and reduced renal tubular Ca reabsorption leading to hypercalciuria and all form kidney stones. GHS have increased vitamin D receptors (VDR) at these sites of Ca transport. Injection of 1,25(OH)2D3 (1,25D) leads to a greater increase in urine (u)Ca in GHS than in control Sprague-Dawley (SD), possibly due to the additional VDR. In GHS the increased uCa persists on a low-Ca diet (LCD) suggesting enhanced bone resorption. We tested the hypothesis that LCD, coupled to inhibition of bone resorption by alendronate (alen), would eliminate the enhanced 1,25D-induced hypercalciuria in GHS. SD and GHS were fed LCD and half were injected daily with 1,25D. After 8 days all were also given alen until euthanasia at day 16. At 8 days, 1,25D increased uCa in SD and to a greater extent in GHS. At 16 days, alen eliminated the 1,25D-induced increase in uCa in SD. However, in GHS alen decreased, but did not eliminate, the 1,25D-induced hypercalciuria, suggesting maximal alen cannot completely prevent the 1,25D-induced bone resorption in GHS, perhaps due to increased VDR. There was no consistent effect on mRNA expression of renal transcellular or paracellular Ca transporters. Urine CaP and CaOx supersaturation (SS) increased with 1,25D alone in both SD and GHS. Alen eliminated the increase in CaP SS in SD but not in GHS. If these results are confirmed in humans with IH, the use of bisphosphonates, such as alen, may not prevent the decreased bone density observed in these patients.
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28

LERNER, U. H., L. JOHANSSON, M. RANSJÖ, J. B. ROSENQUIST, F. P. REINHOLT, and A. GRUBB. "Cystatin C, an inhibitor of bone resorption produced by osteoblasts." Acta Physiologica Scandinavica 161, no. 1 (August 1997): 81–92. http://dx.doi.org/10.1046/j.1365-201x.1997.d01-1933.x.

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29

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.

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30

Rousselle, A. V., and D. Heymann. "Osteoclastic acidification pathways during bone resorption." Bone 30, no. 4 (April 2002): 533–40. http://dx.doi.org/10.1016/s8756-3282(02)00672-5.

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31

Manolagas, S. C. "Role of cytokines in bone resorption." Bone 17, no. 2 (August 1995): S63—S67. http://dx.doi.org/10.1016/8756-3282(95)00180-l.

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32

Sissons, H. A., G. J. Kelman, and G. Marotti. "Bone resorption in calcium-deficient rats." Bone 6, no. 5 (1985): 345–47. http://dx.doi.org/10.1016/8756-3282(85)90328-x.

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33

Camerino, Claudia, Adriana Di Benedetto, Graziana Colaianni, Roberto Tamma, Giovanni Greco, Maurizio Strippoli, Rosaria Vergari, Antonella Grano, Lucia Mancini, and Alberta Zallone. "In vitro bone resorption during spaceflight." Bone 42 (March 2008): S35. http://dx.doi.org/10.1016/j.bone.2007.12.052.

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34

Zeng, Canjun, Helen Goodluck, Xuezhong Qin, Bo Liu, Subburaman Mohan, and Weirong Xing. "Leucine-rich repeat kinase-1 regulates osteoclast function by modulating RAC1/Cdc42 Small GTPase phosphorylation and activation." American Journal of Physiology-Endocrinology and Metabolism 311, no. 4 (October 1, 2016): E772—E780. http://dx.doi.org/10.1152/ajpendo.00189.2016.

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Leucine-rich repeat kinase-1 (Lrrk1) consists of ankyrin repeats (ANK), leucine-rich repeats (LRR), a GTPase-like domain of Roc (ROC), a COR domain, a serine/threonine kinase domain (KD), and WD40 repeats (WD40). Previous studies have revealed that knockout (KO) of Lrrk1 in mice causes severe osteopetrosis, and a human mutation of Lrrk1 leads to osteosclerotic metaphysial dysplasia. The molecular mechanism by which Lrrk1 regulates osteoclast function is unknown. In this study, we generated a series of Lrrk1 mutants and evaluated their ability to rescue defective bone resorption in Lrrk1-deficient osteoclasts by use of pit formation assays. Overexpression of Lrrk1 or LRR-truncated Lrrk1, but not ANK-truncated Lrrk1, WD40-truncated Lrrk1, Lrrk1-KD, or K651A mutant Lrrk1, rescued bone resorption function of Lrrk1 KO osteoclasts. We next examined whether RAC1/Cdc42 small GTPases are direct substrates of Lrrk1 in osteoclasts. Western blot and pull-down assays revealed that Lrrk1 deficiency in osteoclasts resulted in reduced phosphorylation and activation of RAC1/Cdc42. In vitro kinase assays confirmed that recombinant Lrrk1 phosphorylated RAC1-GST protein, and immunoprecipitation showed that the interaction of Lrrk1 with RAC1 occurred within 10 min after RANKL treatment. Overexpression of constitutively active Q61L RAC1 partially rescued the resorptive function of Lrrk1-deficient osteoclasts. Furthermore, lack of Lrrk1 in osteoclasts led to reduced autophosphorylation of p21 protein-activated kinase-1 at Ser144, catalyzed by RAC1/Cdc42 binding and activation. Our data indicate that Lrrk1 regulates osteoclast function by directly modulating phosphorylation and activation of small GTPase RAC1/Cdc42 and that its function depends on ANK, ROC, WD40, and kinase domains.
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35

Wei, Cheng-Ming, Yi-Ji Su, Xiong Qin, Jia-Xin Ding, Qian Liu, Fang-Ming Song, Shao-Hui Zong, Jiake Xu, Bo Zhou, and Jin-Min Zhao. "Monocrotaline Suppresses RANKL-Induced Osteoclastogenesis In Vitro and Prevents LPS-Induced Bone Loss In Vivo." Cellular Physiology and Biochemistry 48, no. 2 (2018): 644–56. http://dx.doi.org/10.1159/000491892.

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Background/Aims: Extensive osteoclast formation plays a critical role in bone diseases, including rheumatoid arthritis, periodontitis and the aseptic loosening of orthopedic implants. Thus, identification of agents that can suppress osteoclast formation and bone resorption is important for the treatment of these diseases. Monocrotaline (Mon), the major bioactive component of crotalaria sessiliflora has been investigated for its anti-cancer activities. However, the effect of Mon on osteoclast formation and osteolysis is not known. Methods: The bone marrow macrophages (BMMs) were cultured with M-CSF and RANKL followed by Mon treatment. Then the effects of Mon on osteoclast differentiation were evaluated by counting TRAP (+) multinucleated cells. Moreover, effects of Mon on hydroxyapatite resorption activity of mature osteoclast were studied through resorption areas measurement. The involved potential signaling pathways were analyzed by performed Western blotting and quantitative real-time PCR examination. Further, we established a mouse calvarial osteolysis model to measure the osteolysis suppressing effect of Mon in vivo. Results: In this study, we show that Mon can inhibit RANKL-induced osteoclast formation and function in a dose-dependent manner. Mon inhibits the expression of osteoclast marker genes such as tartrate-resistant acid phosphatase (TRAP) and cathepsin K. Furthermore, Mon inhibits RANKL-induced the activation of p38 and JNK. Consistent with in vitro results, Mon exhibits protective effects in an in vivo mouse model of LPS-induced calvarial osteolysis. Conclusion: Taken together our data demonstrate that Mon may be a potential prophylactic anti-osteoclastic agent for the treatment of osteolytic diseases caused by excessive osteoclast formation and function.
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36

Bushinsky, D. A., K. Gavrilov, V. M. Stathopoulos, N. S. Krieger, J. M. Chabala, and R. Levi-Setti. "Effects of osteoclastic resorption on bone surface ion composition." American Journal of Physiology-Cell Physiology 271, no. 4 (October 1, 1996): C1025—C1031. http://dx.doi.org/10.1152/ajpcell.1996.271.4.c1025.

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Osteoclasts are responsible for resorption of bone mineral. To determine how osteoclasts alter bone surface ion composition, neonatal mouse bone cells were isolated and cultured in the presence of parathyroid hormone (PTH) on bovine cortical bone. Surface ion composition of the resulting osteoclastic resorption pits was compared with that of unresorbed bone, utilizing a high-resolution scanning ion microprobe. Cortical bone cultured with cells in the presence of PTH had numerous resorption pits. The unresorbed area adjacent to the pits had a ratio of surface 23Na/40Ca of 18.7 + 1.6 (mean counts per second of detected secondary ions +95% confidence interval) and 39K/40Ca of 2.3 + 2.2. At the base of the pits, the ratio of 23Na/40Ca was 1.0 + 2.0 and 39K/40Ca was 0.1 + 1.0 (each different from area adjacent to the pit, P < 0.001). The ratio of 23Na/39K in the unresorbed area was not different from that at the base of the pit. Thus osteoclasts induce a decrease in the ratio of surface ion composition of both 23Na/40Ca and 39K/40Ca but not 23Na/39K in bovine cortical bone. The elevated ratios of 23Na/40Ca and 39K/40Ca on the surface, but not at the base of the pits, indicate adsorption of medium ions onto the mineral. Because osteoclasts foster the release of bone Ca, these results indicate that osteoclastic resorption causes a greater, and approximately equal, release of both 23Na and 39K compared with 40Ca from bone mineral. Osteoclasts appear to remove nonselectively the surface mineral that had been exposed to the medium, uncovering underlying mineral.
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37

Chole, Richard A. "Osteoclasts in Chronic Otitis Media, Cholesteatoma, and Otosclerosis." Annals of Otology, Rhinology & Laryngology 97, no. 6 (November 1988): 661–66. http://dx.doi.org/10.1177/000348948809700615.

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Bone resorption and remodeling are characteristic of chronic otitis media with and without cholesteatoma and otosclerosis. The consequences of this remodeling process may be hearing loss, repeated infection, vestibular disturbance, or intracranial complications. Evidence of osteoclastic bone resorption was found in surgical specimens of 11 of 24 cases of cholesteatoma, two of three cases of chronic otitis media, and three of ten cases of otosclerotic stapes; all three spongiotic lesions had osteoclasts. With careful serial sectioning these cells are almost always multinucleate and have the typical appearance of osteoclasts with ruffled borders. Some specimens had evidence of bone erosion in the absence of osteoclasts; this finding represents an inactive phase of the remodeling process. Since the osteoclast plays an important role in the resorption and remodeling of bone in these middle ear diseases, the source, physiology, and local control of these cells are of prime importance in investigating the pathophysiology of these diseases. At the present time, the local control of activation and recruitment of osteoclasts, as well as their chemotactic responses, is poorly understood.
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38

Gross, Ted S., Nagako Akeno, Thomas L. Clemens, Svetlana Komarova, Sundar Srinivasan, David A. Weimer, and Sergey Mayorov. "Selected Contribution: Osteocytes upregulate HIF-1α in response to acute disuse and oxygen deprivation." Journal of Applied Physiology 90, no. 6 (June 1, 2001): 2514–19. http://dx.doi.org/10.1152/jappl.2001.90.6.2514.

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Loss of mechanical loading, or disuse, rapidly precipitates locally mediated bone resorption. However, the pathway by which this process is initiated and mediated is poorly understood. In this study, we used a complementary in vivo and in vitro approach to determine whether disuse-induced osteocyte hypoxia resulted in upregulation of the hypoxia-dependent transcription factor HIF-1α. We found that acute disuse (1–5 days) resulted in a significant increase in the percentage of osteocytes staining positive for HIF-1α vs. normal bone (30.9 ± 6.1 vs. 14.1 ± 3.8%) and that this response was uniform around the cortex. In addition, we found that acute oxygen deprivation (4–12 h of 2% O2) resulted in a 2.1- to 3.7-fold upregulation of HIF-1α protein expression in MLO-Y4 osteocyte-like cells compared with cells cultured in parallel under normal oxygen conditions. Given known HIF-1α targets genes, we suggest that osteocyte hypoxia and subsequent upregulation of hypoxia-dependent pathways may serve to initiate and mediate disuse-induced bone resorption.
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39

Alexander, R. T., D. G. Fuster, and H. Dimke. "Mechanisms Underlying Calcium Nephrolithiasis." Annual Review of Physiology 84, no. 1 (February 10, 2022): 559–83. http://dx.doi.org/10.1146/annurev-physiol-052521-121822.

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Nephrolithiasis is a worldwide problem with increasing prevalence, enormous costs, and significant morbidity. Calcium-containing kidney stones are by far the most common kidney stones encountered in clinical practice, and thus, hypercalciuria is the greatest risk factor for kidney stone formation. Hypercalciuria can result from enhanced intestinal absorption, increased bone resorption, or altered renal tubular transport. Kidney stone formation is complex and driven by high concentrations of calcium-oxalate or calcium-phosphate in the urine. After discussing the mechanism mediating renal calcium salt precipitation, we review recent discoveries in renal tubular calcium transport from the proximal tubule, thick ascending limb, and distal convolution. Furthermore, we address how calcium is absorbed from the intestine and mobilized from bone. The effect of acidosis on bone calcium resorption and urinary calcium excretion is also considered. Although recent discoveries provide insight into these processes, much remains to be understood in order to provide improved therapies for hypercalciuria and prevent kidney stone formation.
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40

Bellinger, Robert G., and Robert L. Pienkowski. "NON-RANDOM RESORPTION OF OOCYTES IN GRASSHOPPERS (ORTHOPTERA: ACRIDIDAE)." Canadian Entomologist 117, no. 9 (September 1985): 1067–69. http://dx.doi.org/10.4039/ent1171067-9.

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AbstractResorption of terminal oocytes was investigated in 3 species of grasshoppers, Melanoplus femurrubrum femurrubrum (DeGeer), M. scudderi (Uhler), and Hippiscus ocelote (Saussure). Significant differences in percentage resorption were found between species. Anterior ovarioles resorbed terminal oocytes more frequently than ovarioles in the middle and posterior regions of the ovaries. Resorption of terminal oocytes due to differences in relative ovariole age does not appear to be a factor in percentage resorption based on the lengths of developing terminal oocytes. There was no difference in percentage resorption of terminal oocytes between ovaries.
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41

Frings-Meuthen, Petra, Judith Buehlmeier, Natalie Baecker, Peter Stehle, Rolf Fimmers, Francisca May, Goetz Kluge, and Martina Heer. "High sodium chloride intake exacerbates immobilization-induced bone resorption and protein losses." Journal of Applied Physiology 111, no. 2 (August 2011): 537–42. http://dx.doi.org/10.1152/japplphysiol.00454.2011.

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We examined, in immobilization, the effect of a diet high in sodium chloride (NaCl) on bone markers, nitrogen balance, and acid-base status. Eight healthy male test subjects participated in a 14-day head-down-tilt bed rest (HDBR) study. During the bed rest period they received, in a randomized crossover design, a high (7.7 meq Na+/kg body wt per day) and a low (0.7 meq Na+/kg body wt per day) NaCl diet. As expected, 24-h excretion of urinary calcium was significantly greater in the high-NaCl-intake HDBR phase than in the low-NaCl-intake HDBR phase ( P < 0.001). High NaCl intake caused a 43–50% greater excretion of the bone resorption markers COOH- (CTX) and NH2- (NTX) terminal telopeptide of type I collagen in HDBR than low NaCl in HDBR (CTX/NTX: P < 0.001). Serum concentrations of the bone formation markers bone-specific alkaline phosphatase (bAP) and NH2-terminal propeptide of type I procollagen (PINP) were identical in both NaCl intake phases. High NaCl intake led to a more negative nitrogen balance in HDBR ( P < 0.001). Changes were accompanied by increased serum chloride concentration ( P = 0.008), reduced blood bicarbonate ( P = 0.017), and base excess ( P = 0.009) whereas net acid excretion was lower during high than during low NaCl intake in immobilization ( P < 0.001). High NaCl intake during immobilization exacerbates disuse-induced bone and muscle loss by causing further protein wasting and an increase in bone resorption. Changes in the acid-base status, mainly caused by disturbances in electrolyte metabolism, seem to determine NaCl-induced degradation processes.
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42

Ryan, A. S., M. S. Treuth, M. A. Rubin, J. P. Miller, B. J. Nicklas, D. M. Landis, R. E. Pratley, C. R. Libanati, C. M. Gundberg, and B. F. Hurley. "Effects of strength training on bone mineral density: hormonal and bone turnover relationships." Journal of Applied Physiology 77, no. 4 (October 1, 1994): 1678–84. http://dx.doi.org/10.1152/jappl.1994.77.4.1678.

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The effects of a 16-wk strength-training program on bone mineral density (BMD) was assessed by dual-energy X-ray absorptiometry in 21 men [age 61 +/- 1 (SE) yr]. Sixteen men (age 59 +/- 2 yr) served as control subjects. To investigate the possible hormonal relationships underlying the effects on BMD, serum concentrations of growth hormone, insulin-like growth factor I, and testosterone were determined before and after training. In addition, osteocalcin and skeletal alkaline phosphatase (markers of bone formation) and tartrate-resistant acid phosphatase (a marker of bone resorption) were measured before and after training to assess bone turnover. The training program resulted in a 2.8 +/- 0.6% increase in femoral neck BMD (1.004 +/- 0.037 vs. 1.031 +/- 0.037 g/cm2; P < 0.001). However, there were no significant changes in total body, anterioposterior spine, lateral spine, Ward's triangle, or greater trochanter BMD. Moreover, there were no significant changes in growth hormone, insulin-like growth factor I, testosterone, osteocalcin, or skeletal alkaline phosphatase. There were no changes in the control group. Thus, strength training can increase femoral neck BMD, and this effect does not appear to be accompanied by changes in anabolic hormones or markers of bone formation and resorption.
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43

Chai, Lijuan, Kun Zhou, Shaoxia Wang, Han Zhang, Na Fan, Jie Li, Xiaofeng Tan, Limin Hu, and Xiang Fan. "Psoralen and Bakuchiol Ameliorate M-CSF Plus RANKL-Induced Osteoclast Differentiation and Bone Resorption Via Inhibition of AKT and AP-1 Pathways in Vitro." Cellular Physiology and Biochemistry 48, no. 5 (2018): 2123–33. http://dx.doi.org/10.1159/000492554.

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Background/Aims: Psoralen and bakuchiol are the main active compounds found in the traditional Chinese medicine Psoralea corylifolia L., and have been used to treat osteoporosis. This study aims to investigate the anti-osteoporosis effects of these two compounds using osteoclasts precursor differentiation and bone absorption assays in vitro. Methods: Primary mouse osteoclasts precursor cells were induced by M-CSF (macrophage colony stimulating factor) plus RANKL (receptor activator of nuclear factor kappa-B ligand) in vitro. TRACP (tartrate-resistant acid phosphatase) enzyme activity and toluidine blue staining were used to observe the effects of psoralen and bakuchiol on osteoclast differentiation and bone resorption, respectively. Gelatin zymography was used to assess MMP (matrix metalloproteinase) activity, and ELISA was performed to measure cathepsin K activity. Western blotting analysis for expression of phosphorylated AKT, ERK, NF-kB, and c-jun; and immunofluorescence analysis for c-jun and p65 nuclear translocation in induced osteoclasts were then used to determine the mechanism of anti-bone resorption of psoralen and bakuchiol. Results: Mature osteoclasts were induced by M-CSF plus RANKL from primary bone marrow macrophages in vitro. Both psoralen and bakuchiol significantly inhibited TRACP enzyme activity and slightly decreased the number of TRACP+ multinuclear osteoclasts induced by M-CSF plus RANKL. Bakuchiol significantly decreased bone lacunae area and attenuated MMP-2 activity induced by M-CSF plus RANKL in osteoclasts. Both psoralen and bakuchiol significantly decreased the expression and nuclear translocation of phosphorylated c-jun stimulated by M-CSF plus RANKL, but no significant effect on p65 translocation was observed in osteoclasts. Additionally, bakuchiol significantly attenuated the increased of M-CSF plus RANKL-induced phosphorylation of AKT in osteoclasts. Conclusions: Psoralen and bakuchiol ameliorated M-CSF plus RANKL-induced osteoclast differentiation and bone resorption via inhibition of AKT and AP-1 pathways activation in vitro.
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44

Deng, Jiezhong, Dong Sun, Fei Luo, Qiang Zhang, Feifan Chen, Jianzhong Xu, and Zehua Zhang. "Anti-IFN-γ Antibody Promotes Osteoclastogenesis in Human Bone Marrow Monocyte-Derived Macrophages Co-Cultured with Tuberculosis-Activated Th1 Cells." Cellular Physiology and Biochemistry 49, no. 4 (2018): 1512–22. http://dx.doi.org/10.1159/000493455.

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Background/Aims: Tuberculosis induces bone loss and activates Th1 cells that play an important role in the host defense of Bacille Calmette-Guérin tuberculosis vaccine. However, the role of tuberculosis-activated Th1 cells in differentiation of osteoclast precursors to osteoclasts is unclear. As secretion of IFN-γ in Th1 cells is induced by tuberculosis, we aimed to investigate the role of anti-IFN-γ antibody on the differentiation and activation of osteoclasts in bone marrow monocyte-derived macrophages (BMMs). Methods: BMMs were isolated and co-cultured with CD4+T helper 1 cells (Th1 cells), pretreated with anti-IFN-γ antibody. Then, cell proliferation, expression and release of cytokines, formation of actin ring, differentiation of osteoclasts and bone resorption function were measured by CCK8 assay, qRT-PCR/Western blot/flow cytometry, ELISA, immunofluorescence, tartrate-resistant acidic phosphatase (TRAP) staining and bone absorbance assay, respectively. Results: Anti-IFN-γ antibody inhibited the cell viability of BMMs, and induced the expressions of RANKL, TNF-α, NF-κB and TRAF6 in BMMs. In addition, it led to increased expression levels of RANK on cell surfaces, and increased production of RANKL, TNF-α, MCP-1 and SDF-1. Anti-IFN-γ antibody also induced the expression of osteoclast differentiation factor and actin ring formation, but inhibited the expression of osteoprotegerin. TRAP staining and bone resorption assays showed that anti-IFN-γ antibody induced an increase in osteoclast formation and bone resorption. Conclusion: The anti-IFN-γ antibody induced osteoclast formation, and is probably mediated by RANKL-induced activation of NF-κB, that induces TRAF6 in the RANKL-RANK signaling pathway. Our data suggest an inhibitory role for IFN-γ in osteoclast formation induced by tuberculosis.
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45

Naot, Dorit, David S. Musson, and Jillian Cornish. "The Activity of Peptides of the Calcitonin Family in Bone." Physiological Reviews 99, no. 1 (January 1, 2019): 781–805. http://dx.doi.org/10.1152/physrev.00066.2017.

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Calcitonin was discovered over 50 yr ago as a new hormone that rapidly lowers circulating calcium levels. This effect is caused by the inhibition of calcium efflux from bone, as calcitonin is a potent inhibitor of bone resorption. Calcitonin has been in clinical use for conditions of accelerated bone turnover, including Paget’s disease and osteoporosis; although in recent years, with the development of drugs that are more potent inhibitors of bone resorption, its use has declined. A number of peptides that are structurally similar to calcitonin form the calcitonin family, which currently includes calcitonin gene–related peptides (αCGRP and βCGRP), amylin, adrenomedullin, and intermedin. Apart from being structurally similar, the peptides signal through related receptors and have some overlapping biological activities, although other activities are peptide specific. In bone, in vitro studies and administration of the peptides to animals generally found inhibitory effects on osteoclasts and bone resorption and positive effects on osteoblasts and bone formation. Surprisingly, studies in genetically modified mice have demonstrated that the physiological role of calcitonin appears to be the inhibition of osteoblast activity and bone turnover, whereas amylin inhibits osteoclast activity. The review article focuses on the activities of peptides of the calcitonin family in bone and the challenges in understanding the relationship between the pharmacological effects and the physiological roles of these peptides.
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46

Hayashi, H., Y. Kuroki, K. Hirakawa, Y. Imazato, and M. Hirakawa. "Mechanism of bone resorption in hip prosthesis." Pathophysiology 1 (November 1994): 282. http://dx.doi.org/10.1016/0928-4680(94)90582-7.

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47

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.

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48

Dickson, G. R., and R. A. B. Mollan. "Mineralization and resorption in vanishing bone disease." Bone 6, no. 6 (January 1985): 482–83. http://dx.doi.org/10.1016/8756-3282(85)90284-4.

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49

Croucher, P. I., N. J. Garrahan, and J. E. Compston. "12. Resorption cavity characteristics in renal osteodystrophy." Bone 12, no. 4 (1991): 289. http://dx.doi.org/10.1016/8756-3282(91)90089-2.

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50

Bonucci, E., G. Silvestrini, P. Ballanti, M. L. Brandi, S. Benvenuti, and A. Martelli. "Effects of Ipriflavikashe on bone resorption and." Bone 13, no. 5 (July 1992): A4. http://dx.doi.org/10.1016/8756-3282(92)90472-9.

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