Bone Resorption

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M. Schaueblin - One of the best experts on this subject based on the ideXlab platform.

  • TAXOL INHIBITS OSTEOCLASTIC Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin
    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1–0.001 μM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 μM. Osteoclast survival on Bone slices was unaffected by 0.01–1 μM taxol, but 10 μ M was cytotoxic. Taxol (1 μM) also ihibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliterative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by intertering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hyperealcemia and Bone metastases.

  • Taxol inhibits osteoclastic Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin
    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1-0.001 microM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 microM. Osteoclast survival on Bone slices was unaffected by 0.01-1 microM taxol, but 10 microM was cytotoxic. Taxol (1 microM) also inhibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliferative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by interfering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hypercalcemia and Bone metastases.

T.j. Hall - One of the best experts on this subject based on the ideXlab platform.

  • TAXOL INHIBITS OSTEOCLASTIC Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin
    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1–0.001 μM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 μM. Osteoclast survival on Bone slices was unaffected by 0.01–1 μM taxol, but 10 μ M was cytotoxic. Taxol (1 μM) also ihibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliterative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by intertering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hyperealcemia and Bone metastases.

  • The role of reactive oxygen intermediates in osteoclastic Bone Resorption.
    Biochemical and Biophysical Research Communications, 1995
    Co-Authors: T.j. Hall, H. Jeker, K. Fuller, M. Schaeublin, T J Chambers
    Abstract:

    Abstract Osteoclasts have been shown to produce reactive oxygen intermediates (ROI) and it has been suggested that ROI are involved in the process of Bone Resorption. ROI have also been shown to play a central role in the activation of the multisubunit transcription factor NF-κB that enhances the transcription of genes encoding defence and signaling proteins. Therefore, we have assessed the effect of pyrrolidine dithiocarbamate (PDTC), an oxygen-radical scavenger and metal chelator that is a selective and potent inhibitor of NF-κB activation, on osteoclastic Bone Resorption in the Bone slice assay. PDTC (0.001 - 0.1 mM) dose-dependently and non-cytotoxically inhibited osteoclast activity with an IC 50 of 0.01 mM. PDTC (0.01 mM) caused no change in the ratio of Resorption pit area to Resorption pit depth as measured by Lasertec confocal microscopy, indicating that ROI are not involved in the resorptive process per se . This view is supported by time-course studies showing that addition of PDTC or N-acetyl cysteine (NAG; an ROI scavenger, but not metal chelator), 6 hr after the start of the assay had no significant effect on subsequent Bone Resorption. Desferal (100 μM), a chelator of iron and other metal ions, had no significant effect on Bone Resorption, indicating (along with the results with NAG) that ROI-scavenging rather than metal chelation is responsible for inhibition of osteoclastic Bone Resorption by PDTC. Taken together these results indicate that ROI produced by osteoclasts in the Bone slice assay are not involved in the process of Bone Resorption, but are important during osteoclast activation for Bone Resorption, possibly being involved in activation of the transcription factor NF-κB.

  • Taxol inhibits osteoclastic Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin
    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1-0.001 microM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 microM. Osteoclast survival on Bone slices was unaffected by 0.01-1 microM taxol, but 10 microM was cytotoxic. Taxol (1 microM) also inhibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliferative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by interfering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hypercalcemia and Bone metastases.

  • Gallium inhibits Bone Resorption by a direct effect on osteoclasts
    Bone and Mineral, 1990
    Co-Authors: T.j. Hall, Timothy J. Chambers
    Abstract:

    Abstract Gallium nitrate has been used clinically to treat cancer-related hypercalcemia. It has been suggested that gallium may reduce calcium release from Bone by inhibiting Bone Resorption, but the mechanism(s) involved remain to be elucidated. Therefore, we have examined the effect of gallium on Bone Resorption in vitro using osteoclasts isolated from neonatal rat long Bones cultured on slices of cortical Bone. Gallium nitrate (0.01–100 μg/ml) produced a concentration-dependent inhibition of Bone Resorption. Morphological studies showed that even (100μg/ml) gallium nitrate induced no light microscopical change in osteoclast morphology and did not affect their survival on Bone slices. Pretreatment of Bone slices with gallium nitrate (100μg/ml for 18 h), followed by extensive washing also inhibited subsequent osteoclastic Bone Resorption. These results suggest that gallium can be adsorbed onto the calcified surface of Bone and inhibit osteoclastic Bone Resorption.

H. Jeker - One of the best experts on this subject based on the ideXlab platform.

  • TAXOL INHIBITS OSTEOCLASTIC Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin
    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1–0.001 μM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 μM. Osteoclast survival on Bone slices was unaffected by 0.01–1 μM taxol, but 10 μ M was cytotoxic. Taxol (1 μM) also ihibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliterative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by intertering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hyperealcemia and Bone metastases.

  • The role of reactive oxygen intermediates in osteoclastic Bone Resorption.
    Biochemical and Biophysical Research Communications, 1995
    Co-Authors: T.j. Hall, H. Jeker, K. Fuller, M. Schaeublin, T J Chambers
    Abstract:

    Abstract Osteoclasts have been shown to produce reactive oxygen intermediates (ROI) and it has been suggested that ROI are involved in the process of Bone Resorption. ROI have also been shown to play a central role in the activation of the multisubunit transcription factor NF-κB that enhances the transcription of genes encoding defence and signaling proteins. Therefore, we have assessed the effect of pyrrolidine dithiocarbamate (PDTC), an oxygen-radical scavenger and metal chelator that is a selective and potent inhibitor of NF-κB activation, on osteoclastic Bone Resorption in the Bone slice assay. PDTC (0.001 - 0.1 mM) dose-dependently and non-cytotoxically inhibited osteoclast activity with an IC 50 of 0.01 mM. PDTC (0.01 mM) caused no change in the ratio of Resorption pit area to Resorption pit depth as measured by Lasertec confocal microscopy, indicating that ROI are not involved in the resorptive process per se . This view is supported by time-course studies showing that addition of PDTC or N-acetyl cysteine (NAG; an ROI scavenger, but not metal chelator), 6 hr after the start of the assay had no significant effect on subsequent Bone Resorption. Desferal (100 μM), a chelator of iron and other metal ions, had no significant effect on Bone Resorption, indicating (along with the results with NAG) that ROI-scavenging rather than metal chelation is responsible for inhibition of osteoclastic Bone Resorption by PDTC. Taken together these results indicate that ROI produced by osteoclasts in the Bone slice assay are not involved in the process of Bone Resorption, but are important during osteoclast activation for Bone Resorption, possibly being involved in activation of the transcription factor NF-κB.

  • Taxol inhibits osteoclastic Bone Resorption
    Calcified Tissue International, 1995
    Co-Authors: T.j. Hall, H. Jeker, M. Schaueblin
    Abstract:

    We have examined the effect of the anti-tumor compound taxol, on osteoclastic Bone Resorption. In the Bone slice assay, taxol (0.1-0.001 microM) dose-dependently inhibited Bone Resorption with an IC50 of 0.08 microM. Osteoclast survival on Bone slices was unaffected by 0.01-1 microM taxol, but 10 microM was cytotoxic. Taxol (1 microM) also inhibited osteoclast spreading (45%) on fibronectin-coated slides. The antiproliferative effects of taxol are due to its unique ability to stabilize microtubules. Primary osteoclasts are nonproliferating end cells, so taxol probably inhibits Bone Resorption by interfering with other microtubule-dependent functions such as cell polarization, motility or vesicle exocytosis. Since these inhibitory effects on osteoclasts in vitro are seen with therapeutically relevant concentrations, taxol therapy may have beneficial side-effects e.g. inhibition of hypercalcemia and Bone metastases.

R. C. Mühlbauer - One of the best experts on this subject based on the ideXlab platform.

  • Ipriflavone inhibits Bone Resorption in intact and ovariectomized rats
    Calcified Tissue International, 1997
    Co-Authors: M. G. Cecchini, H. Fleisch, R. C. Mühlbauer
    Abstract:

    The aim of this study was to investigate the possible inhibitory effect of ipriflavone on Bone Resorption in rats. For this purpose, 10-week-old, intact and ovariectomized (OVX) rats, prelabeled from birth with [^3H]tetracycline, were used. Bone Resorption was monitored by measuring the urinary excretion of [^3H]. The animals were fed a purified diet devoid of naturally occurring flavonoids. In the intact rats, the daily meal was given either as a single portion or divided into four portions, a procedure known to lead by itself to a decrease in Bone Resorption. Ipriflavone, given 7 days after OVX at the dose of 400 mg/kg B.W. daily mixed with the food, led within 2–3 days to a significant decrease in Bone Resorption equivalent to that of 27.2 μg/kg S.C. of 17β-estradiol. The inhibition was sustained for the length of the experiment, up to 21 days. Ipriflavone given 7 days before OVX prevented the increase in Bone Resorption induced by castration, the effect being dose-dependent between 50 and 400 mg/kg B.W. In contrast to 17β-estradiol, a 5-week treatment with ipriflavone failed to prevent the OVX-induced uterine atrophy. Significant inhibition of Bone Resorption was also seen in intact animals, provided they rapidly ingested the daily meal. Actually, the decrease in Bone Resorption induced by portioning the daily food masked the inhibitory effect of ipriflavone in intact animals. In conclusion, ipriflavone can decrease Bone Resorption in both intact and OVX animals given a purified diet as a single daily meal. In the OVX model, ipriflavone mimics the osteoprotective effect of estrogen. However, the lack of a uterotropic effect suggests that the compound can discriminate between Bone and reproductive tissues.

  • EFFECT OF BISPHOSPHONATES ON THE INCREASE IN Bone Resorption INDUCED BY A LOW CALCIUM DIET
    Calcified Tissue International, 1996
    Co-Authors: V. N. Antic, Herbert Fleisch, R. C. Mühlbauer
    Abstract:

    This study investigates whether bisphosphonate-treated rats are still able to adapt to low calcium supply through an increase in Bone Resorption assessed by measuring the urinary excretion of [3H]-tetracycline from chronically prelabeled rats. First it was shown that in this model, parathyroid hormone was responsible for the increase in Bone Resorption on the low calcium diet. In the second part, animals were treated with the three bisphosphonates—clodronate, alendronate, and ibandronate—given in two doses. Animals receiving a dose that already strongly inhibits Bone Resorption were still able to respond to a low calcium diet by increasing Bone Resorption, showing the potency of the latter as a stimulator of Bone Resorption. Higher doses were, however, able to blunt this response. As soon as the treatment was discontinued, this increase in Bone Resorption resumed with clodronate but not with alendronate or ibandronate.

M. G. Cecchini - One of the best experts on this subject based on the ideXlab platform.

  • Ipriflavone inhibits Bone Resorption in intact and ovariectomized rats.
    Calcified tissue international, 1997
    Co-Authors: M. G. Cecchini, H. Fleisch, R C Mühibauer
    Abstract:

    The aim of this study was to investigate the possible inhibitory effect of ipriflavone on Bone Resorption in rats. For this purpose, 10-week-old, intact and ovariectomized (OVX) rats, prelabeled from birth with [3H]-tetracycline, were used. Bone Resorption was monitored by measuring the urinary excretion of [3H]. The animals were fed a purified diet devoid of naturally occurring flavonoids. In the intact rats, the daily meal was given either as a single portion or divided into four portions, a procedure known to lead by itself to a decrease in Bone Resorption. Ipriflavone, given 7 days after OVX at the dose of 400 mg/kg B.W. daily mixed with the food, led within 2-3 days to a significant decrease in Bone Resorption equivalent to that of 27.2 micrograms/kg s.c. of 17 beta-estradiol. The inhibition was sustained for the length of the experiment, up to 21 days. Ipriflavone given 7 days before OVX prevented the increase in Bone Resorption induced by castration, the effect being dose-dependent between 50 and 400 mg/kg B.W. In contrast to 17 beta-estradiol, a 5-week treatment with ipriflavone failed to prevent the OVX-induced uterine atrophy. Significant inhibition of Bone Resorption was also seen in intact animals, provided they rapidly ingested the daily meal. Actually, the decrease in Bone Resorption induced by portioning the daily food masked the inhibitory effect of ipriflavone in intact animals. In conclusion, ipriflavone can decrease Bone Resorption in both intact and OVX animals given a purified diet as a single daily meal. In the OVX model, ipriflavone mimics the osteoprotective effect of estrogen. However, the lack of a uterotropic effect suggests that the compound can discriminate between Bone and reproductive tissues.

  • Ipriflavone inhibits Bone Resorption in intact and ovariectomized rats
    Calcified Tissue International, 1997
    Co-Authors: M. G. Cecchini, H. Fleisch, R. C. Mühlbauer
    Abstract:

    The aim of this study was to investigate the possible inhibitory effect of ipriflavone on Bone Resorption in rats. For this purpose, 10-week-old, intact and ovariectomized (OVX) rats, prelabeled from birth with [^3H]tetracycline, were used. Bone Resorption was monitored by measuring the urinary excretion of [^3H]. The animals were fed a purified diet devoid of naturally occurring flavonoids. In the intact rats, the daily meal was given either as a single portion or divided into four portions, a procedure known to lead by itself to a decrease in Bone Resorption. Ipriflavone, given 7 days after OVX at the dose of 400 mg/kg B.W. daily mixed with the food, led within 2–3 days to a significant decrease in Bone Resorption equivalent to that of 27.2 μg/kg S.C. of 17β-estradiol. The inhibition was sustained for the length of the experiment, up to 21 days. Ipriflavone given 7 days before OVX prevented the increase in Bone Resorption induced by castration, the effect being dose-dependent between 50 and 400 mg/kg B.W. In contrast to 17β-estradiol, a 5-week treatment with ipriflavone failed to prevent the OVX-induced uterine atrophy. Significant inhibition of Bone Resorption was also seen in intact animals, provided they rapidly ingested the daily meal. Actually, the decrease in Bone Resorption induced by portioning the daily food masked the inhibitory effect of ipriflavone in intact animals. In conclusion, ipriflavone can decrease Bone Resorption in both intact and OVX animals given a purified diet as a single daily meal. In the OVX model, ipriflavone mimics the osteoprotective effect of estrogen. However, the lack of a uterotropic effect suggests that the compound can discriminate between Bone and reproductive tissues.