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PubMed1986

The in vitro effect of gold complexes on bone resorption.

Mouse calvaria were maintained in organ culture without serum additives. The effects of three gold complexes--aurothioglucose, aurothiomalate, and auranofin--on active bone resorption (45Ca release) and hydroxyproline synthesis were determined. The influence of these compounds on DNA and protein synthesis and lysosomal enzyme release from calvaria was also assessed. All gold complexes reduced bone resorption to some extent, with auranofin being the most potent within a narrow concentration range (10(-6) M). This concentration of auranofin also significantly inhibited collagen synthesis, although DNA and protein synthesis were unaffected. None of the compounds tested appeared to mediate their action via significant inhibition of lysosomal enzyme release.

Animals↗
PubMed1984

Inhibition of parathormone-stimulated bone resorption by type I interferon.

The effect of Type I interferon on bone resorption was studied by measuring its effect on parathormone-stimulated calcium release from neonatal murine calvaria in vitro. A pure human recombinant leukocyte interferon hybrid of the A and D subtypes was used, which has high antiviral activity on mouse cells. Calcium release was inhibited in a dose dependent fashion with 50% inhibition at about 10(-10) M or 600 U/ml, and the inhibition was reversible. The presence of interferon was required before or during the activation phase of the resorptive response, when the formation of osteoclasts from precursor cells would occur. When added to actively resorbing bone it had no effect. The data suggest that Type I interferon can inhibit the parathormone-regulated development of active osteoclasts, possibly by inhibiting osteoclast precursor differentiation.

Animals↗
PubMed1996

Regulation of avian osteoclastic H+ -ATPase and bone resorption by tamoxifen and calmodulin antagonists. Effects independent of steroid receptors.

We used highly purified avian osteoclasts and isolated membranes from osteoclasts to study effects of tamoxifen, 4-hydroxytamoxifen, calmodulin antagonists, estrogen, diethylstilbestrol, and the anti-estrogen ICI 182780 on cellular degradation of 3H-labeled bone in vitro and on membrane HCl transport. Bone resorption was reversibly inhibited by tamoxifen, 4-hydroxytamoxifen, and trifluoperazine with IC50 values of approximately 1 microM. Diethylstilbestrol and 17-beta-stradiol had no effects on bone resorption at receptor-saturating concentrations, while ICI 182780 inhibited bone resorption at concentrations greater than 1 microM. At these concentrations ICI 182780, like tamoxifen, inhibits calmodulin-stimulated cyclic nucleotide phosphodiesterase activity. Membrane HCl transport, assessed by ATP-dependent acridine orange uptake, was unaffected by 17-beta-estradiol and diethylstilbestrol at concentrations up to 10 microM, while ICI greater than 1 microM. In contrast HCl transport was inhibited by tamoxifen, 4-hydroxytamoxifen, and the calmodulin antagonists, trifluoperazine and the calmidazolium, with IC50 values of 0.25-1.5 microM. These results suggested the presence of a membrane-associated non-steroid receptor for tamoxifen in osteoclasts. Tamoxifen binding studies demonstrated saturable binding in the osteoclast particulate fraction, but not in the nuclear or cytosolic fractions. Membranes enriched in ruffled border by differential centrifugation following nitrogen cavitation showed binding consistent with one site, Kd approximately microM. Our findings indicate that tamoxifen inhibits osteoclastic HCl transport by binding membrane-associated target(s), probably similar or related to calmodulin antagonist targets. Further, effects of estrogens or highly specific anti-estrogens on bone turnover do not support the hypothesis of a direct effect on osteoclasts by these compounds in this species.

Animals↗
PubMed2005

Effects of thickened beverages fortified with inulin on beverage acceptance, gastrointestinal function, and bone resorption in institutionalized adults.

OBJECTIVES: We wanted to develop thickened beverages that contain soluble fiber (inulin) with acceptable consistency, taste, and texture and to determine the effects of these beverages on bone resorption markers (to determine calcium retention), bowel frequency, and indicators of gastrointestinal function in institutionalized adults bound to wheelchairs. METHODS: A double-blind, 3-wk, cross-over study testing 13-g/d inulin-fortified versus isocaloric standard modified starch-thickened beverages was conducted in institutionalized adults who were bound to wheelchairs and had dysphagia or did not have dysphagia. Beverage acceptability, as assessed by discriminative and descriptive sensory testing, bowel frequency, fecal output, and laxative use, were determined by direct testing or by nursing charts. Bone resorption was measured by using the urinary excretion of fasting calcium and of cross-linked N-telopeptides of collagen. RESULTS: Sensory panelists were unable to detect a difference between beverages thickened with modified starch and those fortified with inulin. Few differences were found between the control and inulin-fortified beverages for sensory descriptors. No significant difference was found in frequency of bowel movements between treatments; however, weighted bowel movement frequency increased by 13% with inulin (P < 0.01), whereas enema and laxative administration decreased by 13% (P < 0.05). Bone resorption, as an indicator of calcium retention, remained unchanged. CONCLUSIONS: Inulin was incorporated into thickened beverages, with no decrease in acceptability; when consumed, perceived stool output increased in residents of long-term care facilities.

Adult↗
PubMed2000

Levels of markers of bone resorption are moderately increased in patients with inactive rheumatoid arthritis.

OBJECTIVE: Clinical remission occurs in 10-20% of patients with rheumatoid arthritis (RA). However, it is questionable whether clinical remission corresponds to the complete absence of the inflammatory process. To answer this question we measured collagen degradation products (which are known to be increased in active disease) in patients with inactive RA and in healthy controls. PATIENTS AND METHODS: The urinary levels of bone resorption markers (pyridinoline, deoxypyridinoline, N-terminal telopeptide and C-terminal telopeptide) were measured in 184 patients with inactive RA, as defined by the preliminary criteria of clinical remission of the American College of Rheumatology, and in 118 healthy individuals. RESULTS: After adjusting for age, concentrations of all four bone resorption markers were found to be significantly higher in patients with inactive RA than in healthy controls. CONCLUSION: The urinary excretion of bone resorption markers is increased in patients classified as having inactive RA. These results suggest that the inflammatory process is not completely absent.

Adult↗
PubMedDate not supplied

Ultrastructural investigations of bone resorptive cells in two types of autosomal dominant osteopetrosis.

In order to investigate the ultrastructure of bone resorptive cells in the two types of adult benign human osteopetrosis, iliac crest biopsies were obtained from 11 patients and 10 normal males, who served as a control group. Six patients had the radiological type I (4 women, 2 men, aged 23-58 years, mean = 36.5 years), and 5 type II disease (5 men, aged 20-48 years, mean = 29.8 years). The normal controls (aged 23-48 years, mean 34.1 years) were recruited from the medical staff. The biopsies were immediately divided. From each patients, half was embedded in paraffin for histochemistry and light microscopy, and half in epon for transmission electron microscopy. The osteoclasts were markedly reduced in number and size in Type I disease (0.2 +/- .7 cells vs. 2.9 +/- 1.0 cells per 2.7 mm2 of bone area, p < 0.01) compared to controls, and stained only weakly for tartrate-resistant acid phosphatase (TRAP). At the ultrastructural level, no signs of active bone resorption were identified, whereas numerous mononuclear cells were observed at the bone surfaces. In type II disease, the osteoclasts were large and highly multi-nucleated, with an increased number (8.3 +/- 2.3 cells vs. 2.9 +/- 1.0. cells per 2.7 mm2 of bone area, p < 0.01) compared to controls. In all patients with this type, but never in type I or in the controls, a smooth, TRAP-positive substance was seen between the osteoclasts and the bone surface. Ultrastructurally, this substance was amorphous, with a condensation along the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1980

Parathyroid hormone stimulates bone resorption via a Na-Ca exchange mechanism.

Parathyroid hormone (PTH) stimulates the release of calcium from bone and is thought to initiate its action by a direct effect on the plasma membrane of bone cells. Although specific membrane receptors for PTH have not yet been identified in bone, they have been characterized in kidney, and PTH does stimulate production of cyclic AMP in bone. However, the mechanism by which PTH causes the release of Ca from bone is not understood. We have determined that several agents that alter ion transport across biological membranes inhibit PTH-stimulated bone resorption in vitro. These agents include ouabain, veratridine and certain monovalent cation ionophores, which transport monovalent cations selectively. The inhibition of bone resorption is dose dependent and reversible within the first 24 h of treatment. All these compounds would be expected to increase intracellular sodium concentration in bone cells. Also, we find that decreasing the extracellular Na+ concentration prevents PTH-stimulated resorption. Therefore, we propose that PTH acts on bone to stimulate Ca release by means of a Na-Ca exchange mechanism. Decreasing the Na gradient across the bone cell plasma membrane would prevent the Na-Ca exchange and thus inhibit the physiological response to PTH.

Animals↗
PubMed2006

Changes in bone resorption and vascular endothelial growth factor after a single zoledronic acid infusion in cancer patients with bone metastases from solid tumours.

Zoledronic acid (Zometa, ZOL) is increasingly used to treat tumour-induced bone disease, and is also reported to have antiangiogenic properties in vivo. In this study, we have investigated the correlations between changes in the proangiogenic cytokine, vascular endothelial growth factor (VEGF), and markers of bone resorption in a cohort of patients with metastatic bone disease, following a single infusion of ZOL. Twenty-four consecutive selected cancer patients with scintigraphic and radiographic evidence of bone metastases were treated for the first time with a single infusion of 4 mg ZOL. Patients were considered ineligible if they had received any steroid therapy, radiotherapy, chemotherapy, immunotherapy or haemopoietic growth factors in the 4 weeks before or during the study period. Circulating levels of VEGF and beta crosslinked type I collagen C-telopeptide (betaCTX) were measured at base-line and at 1, 2, 7 and 21 days following ZOL infusion. The majority of our patients (23/24) developed a significant reduction in circulating levels of betaCTX at just 1 day after the single zoledronic acid infusion, median percentage decrease 67.05% (95% CI, 52.39%; 76.27%). This reduction persisted at all following time points in almost all subjects in our patient population (day 2, 95.8%; day 7, 100%; day 21, 91.7%). The median decrease at day 2 was 85.67% (95% CI, 78.23%; 90.16%); at day 7, 67.38% (95% CI, 67.38%; 86.98); and at day 21, 76.89% (95% CI, 35.00%; 83.16%). Moreover, a linear regression model with variance analysis demonstrated a statistically significant correlation between median VEGF and betaCTX circulating levels at each of the time points (1, 2, 7 and 21 days after ZOL infusion). The present work demonstrates that a single infusion of ZOL was able to induce a rapid and long lasting decrease of betaCTX plasma levels in the majority (23/24) of the included cancer patients. Furthermore, we found that there is a correlation between the levels of VEGF and betaCTX following ZOL treatment. Future clinical trials should be designed to prospectively evaluate the prognostic role of reduction of betaCTX and VEGF in response to ZOL to predict clinical and skeletal outcome.

Adult↗
PubMed2005

Pyridinium-1-yl bisphosphonates are potent inhibitors of farnesyl diphosphate synthase and bone resorption.

We report the design, synthesis and testing of a series of novel bisphosphonates, pyridinium-1-yl-hydroxy-bisphosphonates, based on the results of comparative molecular similarity indices analysis and pharmacophore modeling studies of farnesyl diphosphate synthase (FPPS) inhibition, human Vgamma2Vdelta2 T cell activation and bone resorption inhibition. The most potent molecules have high activity against an expressed FPPS from Leishmania major, in Dictyostelium discoideum growth inhibition, in gammadelta T cell activation and in an in vitro bone resorption assay. As such, they represent useful new leads for the discovery of new bone resorption, antiinfective and anticancer drugs.

Alkyl and Aryl Transferases↗
PubMedDate not supplied

Formulation and evaluation of Alendronate Sodium gel for the treatment of bone resorptive lesions in Periodontitis.

Alendronate sodium is formulated into gels and evaluated for the treatment of bone resorptive lesions in periodontitis. Carbopol 934P was used for the preparation of gels in three different concentrations. The prepared gel was evaluated for various properties such as preformulation, content uniformity, viscosity, compatibility, sterility, in vitro diffusion, and in vivo studies. The drug and the polymer were found to be compatible and confirmed by Fourier transform infrared spectroscopy. Viscosity of the gels increased with the increase in the polymer concentration. The formulations were found to be sterile. In vitro release study revealed that drug released from the gel follows non-Fickian diffusion followed by first-order release. In vivo studies were carried out for 6 months in patients. The results revealed a significant improvement in the clinical parameters such as gingival index, probing pocket depth, clinical attachment level, and potent inhibitory effect on bone resorption by inhibition of osteoclasts. In addition, there was increase in the new bone formation.

Administration, Buccal↗
PubMed1998

Histopathological study of the role of CD4- and CD8-positive T cells on bone resorption induced by Escherichia coli endotoxin.

The purpose of this study was to clarify the involvement of CD4+ and CD8+ T cells on bone resorption induced by Escherichia coli endotoxin. Two kinds of monoclonal antibodies, anti-CD4 and/or anti-CD8, were employed for the depletion of each or both T cell subsets. E. coli endotoxin was injected into mouse mesial gingiva of the first molar of the left mandible every 48 hours for up to 14 days (7 injections). The mice were divided into four groups: CD4-depleted, CD8-depleted, T cell-depleted, and normal. The mice were sacrificed on the day after the 1st, 3rd, 4th, 5th, and 7th injection and alveolar bone was examined histopathologically and histomorphometrically. Bone surface in contact with osteoclasts was defined as the site of active resorption and the ratios of active resorption were compared among the four groups. In addition, sections obtained after the 1st, 4th, and 7th injection were immunohistologically stained in order to confirm the presence or absence of CD4+ or CD8+ T cells. Alveolar bone resorption gradually increased in normal mice as the number of injections increased. In contrast, alveolar bone resorption was significantly weaker in each or both subset-depleted mice. For the duration of the experimental period, the number of CD4+ T cells in CD8-depleted and normal mice significantly increased with increasing bone resorption. Considering the function of CD4+ and CD8+ T cells, these results suggest that each subset preferentially acts as a macrophage activator in the early period of bone resorption induced by E. coli endotoxin.

Animals↗
PubMed2005

Ovariectomy fails to augment bone resorption and marrow B lymphopoiesis in granulocyte colony-stimulating factor transgenic mice.

The mechanism of pathological bone loss induced by estrogen deficiency has not been fully elucidated. It has been shown in recent animal studies that increased B lymphopoiesis induced by estrogen deficiency is involved in the mechanism of stimulated bone resorption. Mice transgenic for granulocyte colony-stimulating factor (G-CSF) (G-Tg) exhibit generalized osteopenia with an increase in osteoclast number and enhancement of bone resorption, which coexists with enhanced hematopoiesis. When ovariectomy was performed on G-Tg, it did not further reduce bone mass as revealed by radiography, dual-energy X-ray absorptiometry, and peripheral quantitative computed tomography. Ovariectomy increased the amount of colony-forming units of interleukin 7 (CFU-IL-7) by threefold in the marrow of normal mice in association with an increase in the number of B220-positive cells expressing the receptor activator of nuclear factor-kappaB ligand (RANKL). In contrast, the number of B220-positive cells expressing RANKL and CFU-IL-7 remarkably decreased in the marrow of G-Tg. Ovariectomy induced neither CFU-IL-7 nor B220-positive cells expressing RANKL in the marrow of G-Tg. Strong inhibition of B lymphopoiesis by G-CSF resulted in depletion of B cells expressing RANKL from the marrow, which may lead to resistance to bone loss due to ovariectomy. This observation suggests that B lymphopoiesis plays a possible role in bone loss in a condition of acute estrogen deficiency.

Analysis of Variance↗
PubMed2000

The effect of high salt and high protein intake on calcium metabolism, bone composition and bone resorption in the rat.

The effects of salt (NaCl) supplementation of rat diets (50 g/kg diet), with normal (200 g/kg) or high (500 g/kg) dietary casein content, were studied in 3-week-old male rats over a 3-week period. Weight gain was reduced by dietary salt but was unaffected by dietary casein. Salt-supplemented rats exhibited a two- and three-fold increase in urinary Mg and Ca excretion respectively, irrespective of dietary casein content. Dietary casein had no effect on urinary Ca or Mg. Salt reduced femoral mass but not femoral mass expressed relative to body weight, but neither variable was affected by dietary casein. Femoral Mg and P contents and concentrations were unaffected by dietary salt or casein. While femoral Ca concentration was unaffected by dietary salt, the Ca content was reduced by salt supplementation, irrespective of dietary casein content. Neither the content nor concentration of Ca in femora was affected by dietary casein. Urinary pyridinoline and deoxypyridinoline levels were increased by salt supplementation, irrespective of dietary casein content, but were unaffected by casein. Net Ca absorption was unaffected by dietary salt or casein. In conclusion, these results show that salt supplementation over the short-term increased the rate of bone resorption in rats. This was as a consequence of Na-induced calciuria. On the other hand, a high dietary protein intake had no effect on Ca metabolism, bone composition or bone resorption, nor did it augment the Na-induced calciuria or increased rate of bone resorption.

Amino Acids↗
PubMed1999

The effect of kampo formulae on bone resorption in vitro and in vivo. II. Detailed study of berberine.

We previously isolated berberine from aqueous extracts of tsu-kan-gan, a Kampo formula used for the treatment of osteoporosis. Berberine caused an inhibitory effect on parathyroid hormone (PTH)-stimulated bone resorption in neonatal mouse bone. In this report we describe the inhibitory effect of berberine on the formation of osteoclast-like multinucleated cells (OCLs) in the co-culture of mouse osteoblastic cells and bone marrow cells in the presence of 1alpha,25-dihydroxyvitamin D3 [1alpha,25(OH)2D3], PTH and interleukin-1alpha (IL-1alpha). Berberine dose-dependently inhibited the formation of tartrate-resistant acid phosphatase (TRAP)-positive OCLs induced by 1alpha25(OH)2D3, PTH and IL-1alpha. We prepared OCLs in the co-culture of osteoblastic cells and bone marrow cells. The effect of berberine on pit formation by OCLs was examined using dentin slices. As OCLs are terminally differentiated multinucleated cells, the survival of OCLs affects the bone-resorbing activity of OCLs. This prompted us to count the number of TRAP-positive OCLs on the slices. Berberine dose-dependently inhibited pit formation and caused a decrease in the number of TRAP-positive OCLs. Calcitonin (CT) inhibited pit formation without affecting the number of OCLs. Berberine accelerated the cell death in OCLs cultivated on a culture plate, but CT did not affect the cell death of OCLs. This suggests that the decrease in the number of OCLs on dentin slices may be due to apoptotic cell death in OCLs. In fact, Hoechst 33258 staining revealed that the treatment of OCLs with berberine resulted in condensed nuclei and a decrease in cell size. Oral administration of the berberine (30 and 50 mg/kg/d) to ovariectomized rats prevented a decrease in bone mineral density (BMD) of the lumbar vertebra without affecting the weight of the uterus and plasma concentration of estradiol. These results suggested that berberine prevented a decrease in BMD in vivo by inhibiting osteoclastic bone resorption.

Animals↗
PubMed1998

TRK-530 inhibits accumulation of superoxide anions derived from human polymorphonuclear leukocytes and bone resorption induced by activated osteoclasts.

TRK-530, a newly synthesized bisphosphonate, was assessed for its effects on the accumulation of superoxide anions derived from human formyl-methionyl-leucyl-phenylalanine-stimulated polymorphonuclear leukocytes (PMN), and for its effects on bone resorption using a pit formation assay. TRK-530 concentration-dependently inhibited superoxide accumulation derived from PMN and osteoclast pit formation stimulated by 1,25-dihydroxyvitamin D3. Incadronate and risedronate had a strong inhibitory effect on pit formation, but no antioxidative activity. These data suggest that the anti-bone resorption activities of TRK-530 are possibly unrelated to its antioxidant properties. However, it is difficult to conclude at present which mechanisms play the most important role in the anti-bone resorption activities of TRK-530.

Animals↗
PubMed1992

Abnormalities in circadian patterns of bone resorption and renal calcium conservation in type I osteoporosis.

We compared changes over 24 h in 15 postmenopausal normal women (mean [+/- SD] age, 64 +/- 7 yr) with those in 15 postmenopausal women with type I osteoporosis and vertebral fractures (mean age, 64 +/- 5 yr). The serum osteocalcin concentration, a sensitive index of bone formation, increased by about 5% at night in both groups. Urinary deoxypyridinoline excretion, a sensitive index of bone resorption, increased by 48% at night (P less than 0.01) in the normal women, whereas in the osteoporotic women it was 62% higher overall (P less than 0.05), and the increase persisted into the morning. At night, urinary fractional excretion of calcium decreased by 20% (P less than 0.001) in the normal women, but was unchanged in the osteoporotic women; this circadian pattern differed between groups (P less than 0.05). The serum ionized calcium concentration did not change at night in either group. There was a trend (P = 0.07) for blunting of the nocturnal increase in the serum intact PTH level in osteoporotic women. Thus, the nocturnal serum ionized calcium level is maintained by decreased urinary calcium excretion and increased bone resorption in postmenopausal normal women, but almost entirely by increased resorption in postmenopausal osteoporotic women. This greater dependence on bone resorption during the nocturnal fast may account in part for the greater bone loss in osteoporotic women.

Amino Acids↗
PubMed1985

Carcinoma of the prostate: remission of paraparesis with inhibitors of bone resorption.

We describe a patient with metastatic carcinoma of the prostate associated with paraplegia. The patient also had Paget's disease of bone elsewhere. Because the neurological lesion was thought to be due to Paget's disease, the patient was treated with inhibitors of bone resorption. Treatment rapidly induced clinical remission and inhibition of bone resorption, and withdrawal was associated with relapse. This suggests that such agents may be of value in the treatment of bone disease of prostatic carcinoma.

Aged↗