Villonodular synovitis in the spinal canal

1980 ◽  
Vol 52 (6) ◽  
pp. 846-848 ◽  
Author(s):  
George M. Kleinman ◽  
T. Forcht Dagi ◽  
Charles E. Poletti

✓ Villonodular synovitis is believed to be an inflammatory, proliferative reaction of synovial tissues. The case of a 65-year-old woman with a cervical epidural mass is presented in which histological examination showed that the lesion was villonodular synovitis, an extremely rare occurrence. Because of its cellularity and occasional multinucleated giant cells, villonodular synovitis may be confused with metastatic malignancies or giant-cell tumor of bone.

1994 ◽  
Vol 80 (1) ◽  
pp. 148-151 ◽  
Author(s):  
Lee Reed ◽  
Crystl D. Willison ◽  
Sydney S. Schochet ◽  
Joseph L. Voelker

✓ A giant cell tumor involving the vertex of the skull is described in a 3-year-old child with no history of head trauma. The mass was present approximately 4 months prior to resection. Microscopically, the lesion consisted of highly cellular tissue composed of oval to spindle-shaped stromal cells admixed with numerous multinucleated giant cells. Giant cell tumor of the skull is a rare lesion, usually involving the sphenoid or temporal bone in adults. The differential diagnosis is discussed with reference to the literature regarding giant cell lesions, especially of the cranium. The authors are unaware of previous reports of a similar lesion in this location in such a young child.


2019 ◽  
Vol 72 (12) ◽  
Author(s):  
Olena O Dyadyk ◽  
Anastasiia Hryhorovska

Introduction: Tenosynovial giant cell tumor (TSGCT) (synonym – pigmented villonodular synovitis) – is a rare benign proliferative lesion of the synovial sheath, localized in the joint capsule, bursa or tendon sheath and characterized by locally destructive growth. Depending on the prevalence within the joint elements, the presence of a capsule around the tumor, histophotographic features of cell structure and clinical behavior TSGCT can be divided to localized or diffuse type. The aim of the study was researching of histopathological properties of diffuse-type TSGCT, determine the parameters its morphological indicators and to find out the correlation between these morphological and clinical parameters. Materials and methods: The research material was used biopsy (resect) of pathological lesions from 50 patients who were diagnosed and histologically verified diffuse-type TSGCT. Microscopic examinations of the stained sections and their photo archiving were carried out with use of a Olympus-CX 41 light optical microscope. Group measurable parameters (mean values and Pearson tetrachoric index (association coefficient) were calculated in groups of comparison for morphological and clinical indices of TSGCT. The mean values were compared by Student’s test, P value of ≤0.1 was considered statistically significant. Results:Correlation analysis of indicators that accounted for the pairs of cases «clinic – morphology» revealed the relationships, that had the highest parameters of the association coefficient between such indicators: «presence of villous growths» - «severity of hemosiderosis» (if hypertrophied synovial villi available, with vascular injection and pronounced proliferation of synovial cells, there is also a significant accumulation of hemosiderin pigment); «presence of villous growths» - «type of predominant cellular proliferates» (if cells of TSGCT diffuse type consists of monotonous sheets of stromal cells, with uniform, oval to reniform nuclei, the proliferation of villi in synovial layer is non-distinctive); «presence of nodes» - «kind of stroma» (if nodes predominate, their histological structure is mainly represented by polymorphic clusters of synovitis cells in the form of cells, strands, chains, solid formations, among immature connective tissue with low hyalinosis); «cell size (area, cm²)» - «severity of haemosiderosis» and «cell size (area, cm²)» - «the number of multinucleated giant cells» (there is a pronounced deposition of pigment and accumulation of osteoclast-like multinucleated giant cells type, although usually their number is relatively small compared to the localized type of TSGCT). Conclusions: Morphological parameters, that we have identified, characterize pathological changes in the tissues of TSGCT; careful analysis of the frequency of their occurrence in the different comparison groups made it possible to establish intergroup differences and correlations between individual indicators, which were previously unknown or not obvious. Our study was determine to analyze of incidence rates and correlation relationships, revealed some previously unknown differences and dependencies that are important for understanding the pathogenesis, improvement of diagnosis and prognosis of diffuse-type TSGCT.


1992 ◽  
Vol 77 (6) ◽  
pp. 952-955 ◽  
Author(s):  
Asim Mahmood ◽  
Dario V. Caccamo ◽  
Jay K. Morgan

✓ A case of tenosynovial giant-cell tumor affecting the cervical spine is reported. The lesion is seen primarily in the fingers, knee, or ankle, and there are no previous reports of it occurring in the spine. The histological and radiological features of this tumor are discussed along with a brief description of the disease entity.


1987 ◽  
Vol 66 (6) ◽  
pp. 924-928 ◽  
Author(s):  
J. Max Findlay ◽  
David Chiasson ◽  
Alan R. Hudson ◽  
Mario Chui

✓ The authors report the case of a 23-year-old man with a giant-cell tumor of the right middle cranial fossa floor. His presentation and management are described, and some aspects of this rare neoplasm of the skull base are reviewed. The role of adjuvant radiotherapy is discussed.


2003 ◽  
Vol 98 (4) ◽  
pp. 854-859 ◽  
Author(s):  
Kenkou Maeda ◽  
Masaaki Mizuno ◽  
Toshihiko Wakabayashi ◽  
Syuntarou Takasu ◽  
Tetsurou Nagasaka ◽  
...  

Object. The nature and origin of multinucleated giant cells in glioma have not been made clear. To investigate the phosphorylation of intermediate filaments, the authors studied multinucleated giant cells in vitro and in vivo by using mitosis-specific phosphorylated antibodies. Methods. Cultured human glioma cells were immunostained with monoclonal antibodies (mAbs) 4A4, KT13, and TM71, which recognized the phosphorylation of vimentin at Ser55, glial fibrillary acidic protein at Ser13, and vimentin at Ser71, respectively. Subsequently, the nature of multinucleated giant cells was investigated using laser scanning confocal microscopy. In addition, paraffin-embedded tissue sections obtained in three patients with giant cell glioblastoma were also investigated. Multinucleated giant cells were immunoreacted with the mAb 4A4 and not with KT13 and TM71 in vitro and in vivo. In addition, the authors obtained these results in multinucleated giant cells under natural conditions, without drug treatments. Conclusions. Findings in this investigation indicated that multinucleated giant cells are those remaining in mitosis between metaphase and telophase, undergoing neither fusion nor degeneration.


2004 ◽  
Vol 101 (6) ◽  
pp. 1012-1017 ◽  
Author(s):  
Mitsugu Fujita ◽  
Masaaki Mizuno ◽  
Tetsuro Nagasaka ◽  
Toshihiko Wakabayashi ◽  
Kenkou Maeda ◽  
...  

Object. The origin of multinucleated giant cells in glioma has not been made clear. In a previous paper the authors studied multinucleated giant tumor cells by using mitosis-specific phosphorylated antibodies to determine the phosphorylation of intermediate filaments and demonstrated that these cells stay in the early mitotic stage, undergoing neither fusion nor degeneration. In the current study the authors investigated the possible genetic causes of multinucleated giant tumor cells. Methods. Cultured mono- or multinucleated human glioma cells were immunostained with monoclonal antibodies (mAbs) 4A4, YT33, TM71, HTA28, YG72, and αAIM-1. The three former antibodies revealed a particular mitotic cell cycle through site-specific phosphorylation of vimentin; that is, the early phase, mid phase, and late phase, respectively. The three later antibodies demonstrated phosphorylation of H3 at Ser28, phosphorylation of vimentin at Ser72, and aurora-B, respectively, making it possible to identify aurora-B distribution and function during mitosis. In addition, paraffin-embedded tissue sections obtained in three patients with giant cell glioblastoma were also examined. Multinucleated giant tumor cells immunoreacted with the mAb 4A4 and αAIM-1 but not with YT33, TM71, HTA28, and YG72 in vitro and in vivo. Conclusions. Findings in this study indicated that multinucleated giant tumor cells remain in the early mitotic phase because of aurora-B dysfunction, effecting aberrations in cytoplasmic cleavage without affecting nuclear division.


1981 ◽  
Vol 18 (6) ◽  
pp. 738-744 ◽  
Author(s):  
A. W. Confer ◽  
F. M. Enright ◽  
G. B. Beard

A subcutaneous extraskeletal giant cell tumor (malignant fibrous histiocytoma) was excised repeatedly from a 9-year-old Domestic Shorthair cat. Ultrastructurally, the mass was composed of fibroblast-like, histiocyte-like, and multinucleated giant cells, and some undifferentiated cells and mononuclear cells intermediate between the fibroblast-like and histiocyte-like cells. Fibroblast-like cells were characterized by abundant well-developed rough endoplasmic reticulum, relatively smooth cytoplasmic membranes, few lysosomal structures, and finely granular chromatin. Histiocyte-like cells resembled immature macrophages. The cell membranes had many villous projections. Rough endoplasmic reticulum varied in quantity. Lysosomes were numerous. Multinucleated giant cells had characteristics of both the fibroblast-like and histiocyte-like cells. No viral particles were seen.


2021 ◽  
Vol 27 ◽  
Author(s):  
Mate E. Maros ◽  
Peter Balla ◽  
Tamas Micsik ◽  
Zoltan Sapi ◽  
Miklos Szendroi ◽  
...  

Cells of the monocyte macrophage lineage form multinucleated giant cells (GCs) by fusion, which may express some cell cycle markers. By using a comprehensive marker set, here we looked for potential replication activities in GCs, and investigated whether these have diagnostic or clinical relevance in giant cell tumor of bone (GCTB). GC rich regions of 10 primary and 10 first recurrence GCTB cases were tested using immunohistochemistry in tissue microarrays. The nuclear positivity rate of the general proliferation marker, replication licensing, G1/S-phase, S/G2/M-phase, mitosis promoter, and cyclin dependent kinase (CDK) inhibitor reactions was analyzed in GCs. Concerning Ki67, moderate SP6 reaction was seen in many GC nuclei, while B56 and Mib1 positivity was rare, but the latter could be linked to more aggressive (p = 0.012) phenotype. Regular MCM6 reaction, as opposed to uncommon MCM2, suggested an initial DNA unwinding. Early replication course in GCs was also supported by widely detecting CDK4 and cyclin E, for the first time, and confirming cyclin D1 upregulation. However, post-G1-phase markers CDK2, cyclin A, geminin, topoisomerase-2a, aurora kinase A, and phospho-histone H3 were rare or missing. These were likely silenced by upregulated CDK inhibitors p15INK4b, p16INK4a, p27KIP1, p53 through its effector p21WAF1 and possibly cyclin G1, consistent with the prevention of DNA replication. In conclusion, the upregulation of known and several novel cell cycle progression markers detected here clearly verify early replication activities in GCs, which are controlled by cell cycle arresting CDK inhibitors at G1 phase, and support the functional maturation of GCs in GCTB.


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