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PubMed1996

Giant cell myocarditis: an entity distinct from sarcoidosis characterized by multiphasic myocyte destruction by cytotoxic T cells and histiocytic giant cells.

Giant cell myocarditis (GCM) is a rare, rapidly fatal myocarditis with histologic features that have some similarities to cardiac sarcoidosis (CS). The natures of the inflammatory infiltrates of GCM and CS have not been systematically compared. We retrospectively compared the immunohistochemical and light microscopic findings at autopsy in eight hearts with GCM and seven hearts with CS. The patients with GCM were six women and two men (mean age, 50 +/- 13 yr) who presented with congestive heart failure with a mean duration of 46 days until death (range, 1-180 d). We observed three histologic phases, often within a single heart. The acute phase (seven cases of eight) demonstrated an extensive infiltrate of lymphocytes and eosinophils with plentiful macrophages and macrophage-derived KP-1 positive giant cells (GCs) associated with myocytic necrosis. No granulomas were identified. A healing phase (three cases of eight) showed granulation tissue, moderate macrophagic GCs, and scattered KP-1-negative myogenic GCs. A healed phase (three cases of eight) showed dense scar with no GCs. Macrophagic GCs were present preferentially in areas of myocytic damage and were never present in epicardial fat. The majority of lymphocytes were T cells, with a predominance of CD8 cells. The seven patients with CS were men (mean age, 44 +/- 18 yr). Six patients presented with sudden cardiac death and one with congestive heart failure. The histologic patterns were similar in all seven, with scattered interstitial and epicardial (five cases of seven) granulomas composed of KP-1 positive macrophages and macrophagic GCs and T lymphocytes, which were predominantly CD4 cells. Necrosis, myogenic GCs, and significant numbers of eosinophils were absent. Dense scarring was present in five cases of seven. GCM is characterized by myocytic destruction mediated by cytotoxic T cells, macrophagic GCs, and eosinophils. In contrast, CS is an interstitial granulomatous disease without myocytic necrosis.

Adult↗
PubMed2003

Hepatocellular carcinoma with osteoclast-like giant cells: possibility of osteoclastogenesis by hepatocyte-derived cells.

Giant cell tumor (GCT) of bone is a primary osteolytic tumor that is characterized by the formation of osteoclast-like giant cells. In addition to GCT of bone, extraskeletal GCT are known to be formed in several soft tissues. Giant cells in GCT of bone were suggested to be identical to osteoclasts, but the characterization of giant cells in extraskeletal GCT remains incomplete. In this study, a case of sarcomatoid hepatocellular carcinoma with osteoclast-like giant cells was analyzed. Immunohistochemistry revealed the expression of almost all markers of osteoclasts: tartrate-resistant acid phosphatase, CD68, CD51, CD54 and matrix metalloprotease-9, in osteoclast-like giant cells in the tumor. In situ hybridization revealed the expression of receptor activator of nuclear factor-kappa B (RANK) in the giant cells and receptor activator of nuclear factor-kappa B ligand (RANKL) in the tumor cells. The hepatic origin of the sarcomatoid hepatocellular carcinoma cells was confirmed by the expression of albumin. This is the first report suggesting that hepatocyte-derived cells possess the potential for osteoclastogenesis. In addition, these findings suggest that osteoclast-like cells in the hepatocellular carcinoma were formed by the same mechanism as osteoclastogenesis in bone.

Aged↗
PubMed1982

Inflammatory giant cells.

Giant cells are commonly seen in granulomas produced by a wide variety of known and unknown agents. It is widely accepted that giant cell formation results from fusion of mononuclear phagocytes. Both experimental and circumstantial evidence suggests that fusion takes place following the attachment of more than one macrophage to the same endocytic material. This view is in keeping with the consistent observation of giant cell formation in granulomas, where macrophages are actively ingesting material in close apposition to other macrophages. The experimental evidence for this view derives from the finding that if more than one macrophage is attached simultaneously to the same endocytic material in vitro, fusion results. Study of the phagocytic capacity of giant cells formed in vivo suggests that the same mechanism of fusion operates in granulomatous inflammation. Giant cell formation in granulomas thus appears to be the incidental result of macrophages ingesting material in close apposition to other macrophages. The material responsible for fusion may either be the visible particulate cause of granuloma formation or the denatured macromolecules formed by the inflammatory process.

Animals↗
PubMed2005

Modulation of trophoblast stem cell and giant cell phenotypes: analyses using the Rcho-1 cell model.

Trophoblast giant cells are located at the maternal-embryonic interface and have fundamental roles in the invasive and endocrine phenotypes of the rodent placenta. In this report, we describe the experimental modulation of trophoblast stem cell and trophoblast giant cell phenotypes using the Rcho-1 trophoblast cell model. Rcho-1 trophoblast cells can be manipulated to proliferate or differentiate into trophoblast giant cells. Differentiated Rcho-1 trophoblast cells are invasive and possess an endocrine phenotype, including the production of members of the prolactin (PRL) family. Dimethyl sulfoxide (DMSO), a known differentiation-inducing agent, was found to possess profound effects on the in vitro development of trophoblast cells. Exposure to DMSO, at non-toxic concentrations, inhibited trophoblast giant cell differentiation in a dose-dependent manner. These concentrations of DMSO did not significantly affect trophoblast cell proliferation or survival. Trophoblast cells exposed to DMSO exhibited an altered morphology; they were clustered in tightly packed colonies. Trophoblast giant cell formation was disrupted, as was the expression of members of the PRL gene family. The effects of DMSO were reversible. Removal of DMSO resulted in the formation of trophoblast giant cells and expression of the PRL gene family. The phenotype of the DMSO-treated cells was further determined by examining the expression of a battery of genes characteristic of trophoblast stem cells and differentiated trophoblast cell lineages. DMSO treatment had a striking stimulatory effect on eomesodermin expression and a reciprocal inhibitory effect on Hand1 expression. In summary, DMSO reversibly inhibits trophoblast differentiation and induces a quiescent state, which mimics some but not all aspects of the trophoblast stem cell phenotype.

Animals↗
PubMed1992

Immunophenotype of multinucleated and mononuclear cells in giant cell lesions of bone and soft tissue.

AIMS: To compare the antigenic phenotype of giant cells in giant cell lesions of bone and soft tissue with that of osteoclasts and macrophage polykaryons. METHODS: Formalin fixed, paraffin wax embedded sections of 106 giant cell lesions, 19 granulomatous, and 14 osteoclast containing lesions were immuno-histochemically stained for leucocyte common antigen (LCA), CD68, and HLA-DR. RESULTS: Osteoclasts and giant cells of giant cell tumour of bone and giant cell reparative granuloma could be distinguished by their generalised absence of HLA-DR reaction from macrophage polykaryons and giant cells in other giant cell lesions of bone and soft tissue. Staining for LCA, CD68, and HLA-DR was useful in distinguishing reactive histiocytic giant cells and osteoclasts from tumour giant cells. CONCLUSIONS: A panel of macrophage associated antigens should be diagnostically useful in differentiating the histological nature of giant cells in various giant cell lesions of bone and soft tissue.

Bone Diseases↗
PubMed2003

[Purification and study of the characteristics of the multinucleated giant cells of the giant cell tumor].

OBJECTIVE: To harvest high purified osteoclast-like giant cells from the giant cell tumor by using trypsin and EDTA(ethylenediamineteraacetic acid) digestion. And explore the role and the origin of the multinucleated giant cells of the giant cell tumor. METHODS: Multinucleated giant cells were isolated and cultured from 8 cases of giant cell tumor of the long bone. After 20 hours of culture, 0.5 g.L-1 trypsin/0.2 g.L-1 EDTA was applied to detach the mononuclear stromal cells. The isolated multinucleated giant cells were inoculated on dentine slice to observe bone resorption ability in vitro. Immunohistochemistry study with V-ATPase, CA II (carbonic anhydrate II), cathepsin K, MMP-9 (matrix metalloproteinase-9), CD68 and TRAP(tartrate-resistant acid phosphatase) staining were carried out in the purified multinucleated giant cells. RESULTS: We obtained 85% purified multinucleated giant cells by trypsin/EDTA digestion. Multinucleated giant cells formed resorption lacunae on dentine slice in vitro and positively stained for V-ATPase, CA II, cathepsin K and MMP-9. The TRAP staining was also positive. CONCLUSION: Using 0.5 g.L-1 trypsin/0.2 g.L-1 EDTA digestion can get high purified multinucleated giant cells from the giant cell tumor. The multinucleated giant cells match all the character of the osteoclast and may originate from the fusion of the mononuclear stromal cells of the lesion.

Bone Neoplasms↗
PubMed1988

The multinucleate cells in giant cell granulomas of the jaw are osteoclasts.

The giant cell granuloma of jaw is a well-vascularised lesion comprising a mononuclear cell infiltrate with a large number of giant cells. It has been suggested that the lesion is reparative in nature, rather than neoplastic, and that the giant cells are phagocytes accumulating in chronic reparative granulation tissue. However, the nature of the multinucleate giant cells never has been established. One possibility is that the constituent giant cells are osteoclasts. The authors assessed expression by the giant cells of several osteoclast-specific characteristics: excavation of bone; motility inhibition by calcitonin (CT); and binding of osteoclast specific monoclonal antibodies. Two tumors were disaggregated and incubated on slices of cortical bone in the presence and absence of CT. Both tumors were found to excavate bone, a function unique to osteoclasts. The giant cells also were responsive to CT, resulting in cytoplasmic quiescence and inhibition of bone resorption. Two osteoclast-specific monoclonal antibodies bound all the giant cells in one central and six peripheral tumors examined immunohistochemically. These results provide strong evidence for the osteoclastic nature of the giant cells. The presence of alkaline phosphatase-positive cells forming woven bone in giant cell granulomas suggests that osteoblasts are present in the lesion. As cells of osteoblastic lineage are known to regulate osteoclastic function, it may be that osteoblasts account for the characteristic infiltration of osteoclasts into giant cell granulomas of jaws, either as part of a reparative response by reactive osteoblasts or as an infiltrate induced by osteoblasts of aberrant function, as suggested for giant cell tumors of bone.

Antibodies, Monoclonal↗
PubMed1974

A histological comparison of the giant cells in the central giant cell granuloma of the jaws and the giant cell tumor of long bone.

A histological comparison has been made of the giant cells in 10 cases which had been diagnosed as central giant cell granuloma of the jaws and 10 cases diagnosed as giant cell tumor of long bone. The numbers of nuclei in each of 50 giant cells were counted in the 20 lesions. The giant cells were measured in order to compare their sizes in the respective lesions. It was found that the giant cells of the jaw lesions contained significantly fewer nuclei than those of the lesions in other bones. Secondly it was found that cells in the lesions of long bone have significantly larger dimensions than those in the jaw lesions. There was, however, an area of overlap. It was concluded that these data supported the view that giant cell tumor and giant cell granuloma are distinct entities. Some giant cell lesions of long bones are, however, morphologically indistinguishable from lesions of the jaws; and conversely giant cell lesions of the jaws are indistinguishable from some giant cell lesions of the long bones. It seems possible, therefore, that some jaw lesions are giant cell tumors and that some giant cell lesions outside the jaws are giant cell granulomas.

Bone Neoplasms↗
PubMed1975

Quantitative immunofluorescence studies of the tumor antigen-bearing cell in giant cell tumor of bone and osteogenic sarcoma.

Tumor-associated antigen was found by reacting sera from two patients with giant cell tumor of bone with cells derived from their tumors, using autologous serum as intermediate reactant and fluorescein-conjugated goat anti-human IgG as final reactant. Approximately 40% of the plump, spindle-shaped cells that formed the background stroma of these tumors possessed the antigen; however, it was not present on giant cells. Fluorescence was much greater than that on similarly stained cells from 4 osteogenic sarcomas, suggesting that the antigenic density on cells from giant cell tumor was greater than that on cells from osteogenic sarcoma. Antibodies in sera from giant cell tumor patients and osteogenic sarcoma patients showed specific cross-reactivity. Stromal cells of giant cell tumors were established in culture and retained tumor-associated antigen, whereas giant cells failed to divide and detached from the flask within two weeks. Intensity of fluorescence (antigenic density) decreased with progressive passage levels, but a larger percentage of cells showed fluorescence. At the tenth passage, all cells bore tumor-associated antigen. Cultured cells that were injected s.c. into mice formed progressively growing nodules, the cells of which were morphologically indistinguishable from stromal cells of the original tumor; all cells retained tumor-associated antigen, but antigenic density had decreased to about one-seventh of the value found originally. No giant cells were present in the nodules.

Animals↗
PubMed1989

Intrathyroidal dendritic cells, epitheloid cells, and giant cells in iodine deficient goiter.

Immunohistochemistry and immunofluorescence were performed on thyroid sections of 44 consecutive patients undergoing thyroid surgery for goiter due to iodine deficiency. Sections were compared with specimens from ten individuals without goiters from the same endemic area, with specimens from ten sporadic nontoxic goiter patients, and with specimens from an area with sufficient iodine supply from nine healthy subjects. Cells were characterized using monoclonal antibodies to the CR3 receptor (CD11b) and the p150/95 antigen (CD11c) present on macrophages, to HLA-DR, to antigen presenting cells (RFD1), to T helper (CD4) and to T suppressor/cytotoxic cells (CD8), and with a polyclonal antibody to human cytokeratin. In iodine deficient goiters, focal aggregates were found of RFD1-positive dendritic cells. Furthermore, RFD1-positive epitheloid cells were seen. In 27% of cases, these epitheloid cells completely filled the thyroid follicles. Within the epitheloid cell clusters, multinucleated giant cells could be detected that carried the macrophage markers. Dendritic cells, epitheloid cells, and giant cells were strongly HLA-DR positive. In nongoitrous thyroids from the endemic area such aggregates could also be seen but they were more sparse and were RFD1 negative. Giant cells were absent there. In normal thyroids with sufficient iodine supply, only a few isolated dendritic cells were seen. All except RFD1, which was negative, showed the same marker pattern. In sporadic nontoxic goiters from an area with sufficient iodine supply, dendritic cells occurred in much higher numbers than in the normal thyroids from that area, and they were RFD1 positive. They never aggregated as in iodine deficiency, and giant cells were not observed. These observations on iodine deficient goiter strongly suggest involvement of active antigen-presenting cells in this disorder. However, the immunohistologic difference between this disease and sporadic goiter suggests different underlying mechanisms.

Adult↗
PubMed1999

Immunohistochemical expression of p53, MDM2, Ki-67 and PCNA in central giant cell granuloma and giant cell tumor.

Central giant cell granuloma (CGCG) is a reactive bone lesion that occurs mainly in the jaws. The giant cell tumour (GCT) is a benign locally aggressive neoplasm located near the articular end of tubular bones. Both lesions are characterised histologically by multinucleated giant cells in a background of ovoid to spindle-shaped mesenchymal cells. There is a basic question whether both lesions are separate entities or variants of the same disease. The study of cell cycle-associated proteins may give insights into clarifying such question. The expression of these proteins is also important to determine the cell cycle regulation in both tumours. The purpose of this study was to evaluate the immunohistochemical expression of p53, MDM2, Ki-67 and PCNA in CGCG and GCT. The results demonstrated that, despite the lack of p53 immunoreactivity, all the samples showed wide expression of MDM2. The percentage of Ki-67- and PCNA-positive cells in CGCG was statistically higher than that of GCT Our findings show that CGCG has a higher proliferative activity compared with that of the GCT. Our results also suggest that p53 inactivation by MDM2 expression may be involved in the pathogenesis of giant cell lesions of the jaws and long bones.

Adolescent↗
PubMed2002

Phenotypic characterization of mononuclear and multinucleated cells of giant cell reparative granuloma of small bones.

Four cases of giant cell reparative granuloma (GCRG) of small bones were analysed in order to determine the pathogenesis of the lesion and the nature of the component mononuclear and multinucleated cells. In cell cultures, giant cells formed a non-proliferating homogeneous population which expressed features characteristic of the osteoclast phenotype, including leucocyte common antigen, CD68, vitronectin receptor, and tartrate-resistant acid phosphatase. The giant cells were capable of lacunar resorption and their activity was inhibited by calcitonin. In addition to numerous macrophage-like cells, some of which expressed osteoclast phenotypic characteristics, there were also mononuclear stromal cells which proliferated in culture and were alkaline phosphatase-positive; these cells expressed receptor activator of NF-kappaB ligand (RANKL) and were capable of supporting human osteoclast formation from circulating precursors in vitro. These findings suggest that the osteoclast-like giant cells in GCRG of small bones are formed from monocyte/macrophage-like osteoclast precursors which differentiate into osteoclasts under the influence of mononuclear osteoblast-like stromal cells.

Adult↗
PubMedDate not supplied

Similarities between giant cell tumor of bone, giant cell tumor of tendon sheath, and pigmented villonodular synovitis concerning ultrastructural cytochemical features of multinucleated giant cells and mononuclear stromal cells.

The authors investigated ultrastructural cytochemical features of multinucleated and mononuclear stromal cells in giant cell tumor of bone (GCTB), giant cell tumor of tendon sheath (GCTTS), and pigmented villonodular synovitis (PVNS). Specimens of each tumor, respectively numbering 4, 4, and 3, were stained for tartrate-resistant acid phosphatase (TRAP) reactions and examined with an electron microscope. In GCTB and GCTTS, multinucleated cells, including some relatively small giant cells, showed TRAP activity and cytoplasmic features characteristic of osteoclasts, and also sometimes abundant rough endoplasmic reticulum and siderosomes. A few giant cells with macrophage-like features and slight TRAP activity were demonstrated in GCCTS and PVNS. In each tumor type, mononuclear cells showing TRAP activity shared cytoplasmic features with osteoclast-like multinucleated giant cells, while some others had macrophage-like features, and still others were poorly differentiated; a few mononuclear cells showed cell-to-cell contact. Ultrastructural similarities of TRAP-positive mononuclear cells in the three tumor types, and those between TRAP-positive multinucleated cells in GCTB and GCTTS, suggest a common cell lineage capable of multinucleated giant cell formation in the 3 tumors, despite differing histogenesis.

Acid Phosphatase↗
PubMed1994

Interleukin-6 antisense deoxyoligonucleotides inhibit bone resorption by giant cells from human giant cell tumors of bone.

The effects of antisense constructs to IL-6 on the bone-resorbing capacity of purified giant cells from giant cell tumors of bone were examined to further define the role of IL-6 in human osteoclastic bone resorption. In addition, we wanted to determine the utility of antisense constructs to cytokines produced by osteoclasts as probes to identify the molecular events responsible for the bone-resorptive process. Giant cells were cultured on sperm whale dentin for 24 h in the presence of fluoresceinated antisense or scrambled antisense deoxyoligonucleotides complementary to IL-6 mRNA. The giant cells actively incorporated these oligonucleotides, as evidenced by their intense fluorescence. The number of resorptive lacunae formed and the area of the dentin resorbed were significantly decreased in cultures of giant cells treated with antisense IL-6 constructs compared with control cultures treated with scrambled antisense constructs to IL-6 (60 +/- 13 versus 12 +/- 6 lacunae and 1.2 +/- 0.3 versus 0.26 +/- 0.1 x 10(5) microns2). IL-6 levels in conditioned media from giant cell cultures treated with IL-6 antisense constructs were fourfold lower than those in control media obtained from giant cells treated with scrambled antisense constructs to IL-6. These data confirm the capacity of IL-6 antisense oligomers to block IL-6 production by these cells. These observations show that IL-6 plays an important role in the bone-resorptive process of human osteoclasts and suggest that antisense constructs to cytokines produced by bone cells may be useful for determining the molecular events occurring during bone resorption.

Animals↗