Interleukin-6 and tumor necrosis factor α levels after bisphosphonates treatment in vitro and in patients with malignancy

Sauty, Alain; Pecherstorfer, Martin; Zimmer-Roth, I; Fioroni, P.; Juillerat, Lucienne; Markert, Michèle; Ludwig, Heinz; Leuenberger, P; Burckhardt, P.; Thiébaudi, D.

doi:10.1016/8756-3282(95)00448-3

Cited by 163 publications

(101 citation statements)

References 33 publications

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“…Clodronate was demonstrated to downregulate the production of IL-6 and TNF-a (Monkkonen et al 1994), as well as NF-kB activation (Makkonen et al 1999) in mouse macrophage-like RAW264 cells stimulated with lipopolysaccharides; inhibition of IL-6 production by osteosarcoma MG-63 cells was also documented (Giuliani et al 1998). Cancer patients receiving clodronate treatment showed reduction in serum IL-6 levels, which was not associated with cytotoxic effects (Sauty et al 1996). These results suggest that clodronate may possess therapeutic potential for cancer cachexia.…”

Section: Introductionmentioning

confidence: 54%

Clodronate alleviates cachexia and prolongs survival in nude mice xenografted with an anaplastic thyroid carcinoma cell line

Wang

Shen

Hsieh

et al. 2006

Journal of Endocrinology

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Cancer cachexia is one of the most common manifestations of advanced malignant disease and is frequently associated with decreased survival. Previously, we reported the establishment of a new anaplastic thyroid carcinoma cell line, Thena, and its mouse xenograft, Thena-Nu, which induced cachexia in athymic nude mice. Subsequent studies showed that the addition of clodronate to Thena-Nu cultures reduced cell proliferation as well as cytokine production in a dose-and timedependent manner. Weekly administration of clodronate induced tumor cytostasis, attenuation of cachexia, as well as prolongation of survival in Thena-Nu-bearing mice. Reduced serum interleukin 6, tumor necrosis factor-a, and granulocyte colony stimulating factor levels were detected, whereas, serum leukemia inhibitory factor levels were not reduced. Liver necrosis, observed in tumor-bearing mice, was also improved following clodronate treatment. Discontinuation of clodronate treatment, however, resulted in progressive tumor growth and weight loss. Our results demonstrated that clodronate could exert therapeutic efficacy on amelioration of cancer cachexia in the hosts. Nevertheless, this study also points out that a longer period of treatment is required to maintain these effects.

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Section: Introductionmentioning

confidence: 54%

Clodronate alleviates cachexia and prolongs survival in nude mice xenografted with an anaplastic thyroid carcinoma cell line

Wang

Shen

Hsieh

et al. 2006

Journal of Endocrinology

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“…Nitrogen-containing bisphosphonates (such as alendronate) induce various inflammatory reactions via interleukin dependent mechanisms. [27][28][29][30] Bisphosphonate-induced inflammation exacerbates pathologic conditions such as arthritis 31 and atherosclerosis. 32 Blockage of matrix metalloproteinases improves anterior cruciate graft healing in the bone tunnels.…”

Section: Discussionmentioning

confidence: 99%

Alendronate prevents bone loss and improves tendon‐to‐bone repair strength in a canine model

Thomopoulos

Matsuzaki

Zaegel

et al. 2007

Journal Orthopaedic Research

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Previously we showed a loss of bone and a concomitant decrease in mechanical properties in the first 21 days after flexor tendon insertion site injury and repair in a canine model. The goal of this short-term study was to suppress bone loss after insertion site repair using alendronate in an attempt to prevent the reduction in biomechanical properties. Flexor tendons of the second and fifth digits of the right forelimbs of canines were injured and repaired. Dogs received a daily oral dose of alendronate (2 mg/kg). One digit in each dog also received a local dose of alendronate in the bone tunnel at the time of surgery. The repair was evaluated for bone mineral density (BMD) and biomechanical properties and compared to data from a previous study in which no alendronate was used. Alendronate was effective in protecting the distal phalanx from resorption during tendonto-bone healing (BMD was 94 and 104% of control for systemic alendronate and for systemic plus local alendronate, respectively). Alendronate treatment prevented much of the decrease in ultimate load that occurs in the first 21 days. Without treatment, ultimate load was 42% of control. With systemic alendronate treatment and systemic plus local alendronate treatment, ultimate load was 78 and 69% of control, respectively. Failure mode was significantly different when comparing alendronate treatment to repair alone. A lower incidence of suture pull through was found in alendronate treated dogs, suggesting less tendon degeneration. Ultimate load can be improved in association with preventing the bone loss that normally occurs during the early period following tendon-to-bone repair. These initial short-term data demonstrate the potential for a clinical treatment that could enhance tendon-to-bone healing. ß

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“…In contrast, another study has demonstrated that zoledronate did not reduce the population of osteoclast precursor after 18 months of treatment in osteopenic women, (27) There are also conflicting in vitro data regarding the effect of bisphosphonates on osteoclastogenic cytokines such as IL-1, TNF and circulating levels of RANKL and osteoprotegerin (OPG) (28)(29)(30)(31)). RANKL is produced by the osteoblasts and binds to the receptor RANK which is located on the osteoclast precursor cells as well as the mature osteoclast (32).…”

Section: Introductionmentioning

confidence: 97%

The effect of bisphosphonate treatment on osteoclast precursor cells in postmenopausal osteoporosis: The TRIO study

Gossiel

Hoyle

McCloskey

et al. 2016

Bone

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Bisphosphonates are used to treat bone disease characterised by increased bone resorption by inhibiting the activity of mature osteoclasts, resulting in decreased bone turnover.Bisphosphonates may also reduce the population of osteoclast precursor cells. Our aims were to investigate the effect of bisphosphonates on i) osteoclast precursor cells and ii) circulating cytokine and cytokine receptor in postmenopausal women with osteoporosis compared with healthy premenopausal women. Participants were 62 postmenopausal women (mean age 66) from a 48-week parallel group trial of bisphosphonates. They received ibandronate 150mg/month (n=22), alendronate 70mg/week (n=19) or risedronate 35mg/week (n=21). Fasting blood was collected at baseline, weeks 1 and 48. At baseline, blood was also collected from 25 healthy premenopausal women (mean age 37) to constitute a control group. Peripheral blood mononuclear cells were extracted and stained for CD14, M-CSFR, CD11b and TNFRII receptors. Flow cytometry was used to identify cells expressing CD14+ and M-CSF+ or CD11b+ or TNFRII+. RANKL and OPG were measured to evaluate potential mediation of the bisphosphonate effect. After 48 weeks of treatment, there was a decrease in the percentage of cells expressing M-CSFR and CD11b receptors by 53% and 49% respectively (p<0.01). Cells expressing M-CSFR and CD11b were decreased with ibandronate and risedronate after 48 weeks to the lower part of the premenopausal reference interval. These effects were not significantly different between each of the treatment groups. There was no significant effect on RANKL and OPG throughout the study period. Bisphosphonates inhibit bone resorption in the short-term by direct action on mature osteoclasts. There is also a later effect mediated in part by a reduction in the population of circulating osteoclast precursors.

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Interleukin-6 and tumor necrosis factor α levels after bisphosphonates treatment in vitro and in patients with malignancy

Cited by 163 publications

References 33 publications

Clodronate alleviates cachexia and prolongs survival in nude mice xenografted with an anaplastic thyroid carcinoma cell line

Clodronate alleviates cachexia and prolongs survival in nude mice xenografted with an anaplastic thyroid carcinoma cell line

Alendronate prevents bone loss and improves tendon‐to‐bone repair strength in a canine model

The effect of bisphosphonate treatment on osteoclast precursor cells in postmenopausal osteoporosis: The TRIO study

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