Resorption of bone by isolated rabbit osteoclasts

Chambers, T.J.; Revell, Peter A.; Fuller, K.; Athanasou, N A

doi:10.1016/0221-8747(84)90057-2

Cited by 114 publications

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“…Bone resorption was quantified using the disaggregated osteoclast resorption assay originated by Boyde et al (1984) and Chambers et al (1984) and performed as described by Dempster et al (1987). Briefly, osteoclasts were isolated from the long bones of neonatal rats onto devitalized 4.4 × 4.4 mm bovine cortical bone slices prewetted with medium 199 + Hanks' salts.…”

Section: Bone Resorption Assaymentioning

confidence: 99%

Endothelin-1 from prostate cancer cells is enhanced by bone contact which blocks osteoclastic bone resorption

et al. 2000

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The causes for the propensity of metastasized prostate cancer cells to grow in bone and to induce osteoblastic lesions remain unresolved. Co-culture of human prostate cancer cell lines with bone slices was determined to increase the level of endothelin-1 (ET-1) mRNA and its production. ET-1 is an ejaculate protein that also stimulates osteoblasts. Osteoclastic bone resorption was significantly blocked by the presence of androgen-independent prostate cancer cells in a dose-dependent manner as that of synthetic ET-1. The inhibition could be neutralized by specific ET-1 antibody, indicating the association of prostate cancer-derived ET-1 with inhibition of bone resorption. The combined ET-1 activity on osteoclasts and osteoblasts disrupts bone remodelling. ET-1 production is also elevated in the presence of prostate-specific antigen (PSA). ET-1 in turn enhances DNA synthesis of prostate cancer cells. Interactions among cancer cells, bone, ET-1 and PSA may be critical in cancer growth and lesions in bone. © 2000 Cancer Research Campaign

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Section: Bone Resorption Assaymentioning

confidence: 99%

Endothelin-1 from prostate cancer cells is enhanced by bone contact which blocks osteoclastic bone resorption

et al. 2000

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“…[5][6][7] Osteoclastic bone resorption consists of multiple steps: proliferation of osteoclast progenitors, differentiation of progenitors into mononuclear prefusion osteoclasts (pOCs), fusion of pOCs into multinucleated osteoclasts, activation of osteoclasts to resorb bone and apoptosis.…”

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confidence: 99%

Oral squamous cell carcinoma cells induce osteoclast differentiation by suppression of osteoprotegerin expression in osteoblasts

Tada

Jimi

Okamoto

et al. 2005

Intl Journal of Cancer

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The invasion of oral squamous cell carcinoma (SCC) cells into the mandibular bone is a common clinical problem. It has been reported that BHY cells, a human oral SCC cell line, are capable of invading mandibular bone of nude mice. These results led us to examine possible mechanisms of osteoclastogenesis induced by BHY cells using in vitro culture systems. When BHY cells were cocultured with mouse bone marrow cells (BMCs), only few osteoclasts were formed, even though BHY cells express the receptor activator of NF-jB ligand (RANKL). However, adding BHY cells to a coculture of mouse primary osteoblasts (POBs) and BMCs markedly induced osteoclastogenesis in the absence of osteotropic factors. Furthermore, another oral SCC cell line, HSC-2, which does not express RANKL, also induced osteoclastogenesis in our cocultures. These effects were significantly, but not completely, inhibited by adding osteoprotegerin (OPG). In addition, we also found that TNFa released from these cells partially contributes to osteoclastogenesis via a RANKL-independent mechanism. Adding BHY or HSC-2 cells suppressed mouse OPG mRNA expression and protein production by POBs in cocultures of POBs and human oral SCC cells. This finding is consistent with the result that BHY cells and HSC-2 cells did not enhance osteoclastogenesis in cocultures of BMCs and POBs from OPG-deficient mice. Immunohistochemical analysis showed a reduction of OPG expression in osteolytic lesions as compared to normal lesions from oral SCC patients. Therefore, oral SCC-induced suppression of OPG expression in POBs appears critical for osteoclastogenesis, rather than expression of RANKL in SCC cells. ' 2005 Wiley-Liss, Inc.Key words: squamous cell carcinoma; RANKL; OPG; osteoclastogenesis Oral cancer most commonly involves the tissue of the tongue and the lips, and it can also occur on the floor of the mouth, gingiva or plate.1,2 The vast majority of oral cancers are squamous cell carcinomas (SCCs) 1,2 and oral SCCs frequently invade the mandibular bone. Advanced oral SCC has a high mortality and treatment is complicated by the disruption of speech and swallowing after surgical resection. It is generally agreed that patients with mandibular invasion should be treated surgically, but the extent of mandibular resection required remains controversial. Resection of the mandibular bone leads to physical damage as well as frequent psychological problems for the patients.It is well known that oral SCC invades the mandibular bone by direct extension and not by metastasis.3,4 Previous studies have suggested that the bone destruction associated with carcinoma invasion is mediated by osteoclasts rather than directly by the carcinoma.3,4 Invasion of the mandible by oral SCC is currently established only by radiological inspection. The cellular and molecular mechanisms regulating bone invasion and osteoclastic bone resorption by oral SCC are poorly understood.Osteoclasts are multinucleated cells that are responsible for bone resorption. [5][6][7] Osteoclastic bone resorption consists...

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“…In the early phase, osteoclasts predominate and bone resorption proceeds rapidly with the establishment of an osteolytic metastasis. In the later phase, the metastasis grows more slowly and few or a (Chambers et al, 1984). no osteoclasts are evident.…”

Section: Discussionmentioning

confidence: 99%

“…Unlike osteoclasts which resorb all the components of bone unaided by other cell types and do so within the first 24 h in culture (Chambers et al, 1984) Furth, 1989). These proliferating mononuclear phagocytes are marrow derived and cannot be distinguished from resident macrophages.…”

Section: Discussionmentioning

confidence: 99%

“…Dexamethasone (Sigma, UK) (10-7 M) and 1,25 dihydroxy Vitamin D3 (Roche, UK) (10-8 M) were added at the beginning of co-cultures with ST2 cells and at each change of medium (every 3 days). Adherent cells on bone slices were cultured for 24 h, 3, 7 and 14 days after which evidence of bone resorption was sought by scanning electron microscopy (SEM) (Chambers et al, 1984). The effect of PTH (NIBSC, UK) (10 IU ml), PGE2 (Sigma, UK) (10-5 M) and conditioned medium (derived from culture of ST2 cells alone) on bone resorption by TAMs and AMs isolated from two of the above specimens was also examined.…”

Section: Methodsmentioning

confidence: 99%

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Human tumour-associated macrophages are capable of bone resorption

Athanasou

Quinn²

1992

Br J Cancer

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Summary Cellular mechanisms of bone resorption associated with skeletal metastasis are poorly understood. Human tumour-associated macrophages (TAMs) isolated from primary lung carcinomas were incubated on bone slices where they formed resorption lacunae after 14 days co-culture with a mouse marrow-derived stromal cell line (ST2) with added la, 25-dihydroxy Vitamin D3 and dexamethasone. These co-cultures were associated with the formation of increased numbers of tartrate resistant acid phosphatase positive mononuclear and multinucleated cells. (Galasko, 1976), but the contribution of other cells, principally tumour cells and tumour-associated macrophages (TAMs) within the tumour deposits in bone, is uncertain (Galasko, 1976;Galasko, 1982;Eilon & Mundy, 1978; Koeffier et al., 1978;Novak et al., 1984). This is largely because direct evidence of bone resorption by these cells has not clearly been demonstrated. However, there is now increasing evidence to show that mononuclear phagocytes derived from inflammatory and neoplastic lesions are capable of bone resorption (Athanasou et al., 1989;Athanasou et al., 1991;Athanasou et al., 1992), and that osteoclast-like cells can form directly from tissue macrophages (Udagawa et al., 1990). Materials and methodsTAMs were isolated from five pneumoonectomy specimens for lung carcinoma (three adenocarcinomas; two squamous carcinomas) by collagenase digestion and substrate adherence from 2 x 2 x 2 cm portion of tumour (McGee & Myrvik, 1981), and alveolar macrophages (AMs) from equal portions of lung uninvolved by tumour (Haskill, 1981). TAM or AM-containing cell suspensions in alpha minimal essential medium plus 10% foetal calf serum (Gibco) (MEM/FCS) were added to 6mm wells (500cells/well) containing either bone slices or glass coverslips, half of which had been seeded (1,000 cells/well) 24 h earlier with the mouse marrow stromal cell line ST2 (Riken cell bank, Japan) (Athanasou et al., 1989). Four bone slices (half previously seeded with ST2 cells) were studied for each variable, and cell cultures were incubated at 37°C (5% CO2). After settling for 1 h, these were washed vigorously in MEM/FCS and placed in 16 mm wells containing aMEM/FCS. Dexamethasone (Sigma, UK) (10-7 M) and 1,25 dihydroxy Vitamin D3 (Roche, UK) (10-8 M) were added at the beginning of co-cultures with ST2 cells and at each change of medium (every 3 days). Adherent cells on bone slices were cultured for 24 h, 3, 7 and 14 days after which evidence of bone resorption was sought by scanning electron microscopy (SEM) (Chambers et al., 1984). The effect of PTH (NIBSC, UK) (10 IU ml), PGE2 (Sigma, UK) (10-5 M) and conditioned medium (derived from culture of ST2 cells alone) on bone resorption by TAMs and AMs isolated from two of the above specimens was also examined. Cells cultured on glass coverslips for similar periods were assessed for several osteoclast characteristics viz. morphological response to salmon calcitonin (Rorer Pharmaceuticals, UK) 1 tg ml-' (Chambers & Magnus, 1982), acid phosphatase (AP) and tart...

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Resorption of bone by isolated rabbit osteoclasts

Cited by 114 publications

References 0 publications

Endothelin-1 from prostate cancer cells is enhanced by bone contact which blocks osteoclastic bone resorption

Endothelin-1 from prostate cancer cells is enhanced by bone contact which blocks osteoclastic bone resorption

Oral squamous cell carcinoma cells induce osteoclast differentiation by suppression of osteoprotegerin expression in osteoblasts

Human tumour-associated macrophages are capable of bone resorption

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