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          Fibroma of Tendon Sheath 3

                    

 

Nodular fasciitis

Proliferative fasciitis

Proliferative myositis

Ischaemic fasciitis

Elastofibroma

Fibrous Hamartoma of Infancy

Infantile Myofibromatosis/ Myofibroma

Juvenile hyaline fibromatosis

Inclusion  Body Fibromatosis

Calcifying aponeurotic fibroma

Fibromatosis colli

Fibroma of tendon sheath

Desmoplastic fibroblastoma (collagenous fibroma)

Storiform Collagenoma (sclerotic fibroma)

Giant Cell Collagenoma

Pleomorphic Fibroma

Angiomyofibroblastoma

Dermatomyofibroma

Cellular Angiofibroma

Giant Cell Angiofibroma

Fibromatosis

Lipofibromatosis

Solitary fibrous tumour

[Hemangiopericytoma  including Lipomatous Hemangiopericytoma]

Inflammatory myofibroblastic tumour

Low grade myofibroblastic sarcoma

Myxoinflammatory fibroblastic sarcoma

Infantile fibrosarcoma

Adult fibrosarcoma

Myxofibrosarcoma

 Low grade fibromyxoid sarcoma

Hyalinizing Spindle Cell Tumour with Giant Rosettes

Sclerosing epithelioid fibrosarcoma

Fibroma of tendon sheath

Visit: Soft Tissue Pathology

Fibroma and giant cell tumor of tendon sheath: a comparative histological and immunohistological study. Mod Pathol. 1995 Feb;8(2):155-9.

Giant cell tumor of tendon sheath (GCTTS; "nodular tenosynovitis") and fibroma of tendon sheath (FTS) have traditionally been considered to be two points in a single neoplastic continuum. However, no systematic studies have addressed this concept directly to date. To more clearly define their relationship to one another, we studied five FTSs and seven typical GCTTSs by light microscopy and paraffin section immunohistochemistry. Tissue samples were stained for vimentin, desmin, smooth muscle actin (SMA), S100 protein, leukocyte common antigen (CD45), CD68 antigen (KP1), HAM56 antigen, alpha-1-antichymotrypsin (AACT), and MAC387 antigen. These reagents were chosen to address proposed "fibrohistiocytic" and myofibroblastic lineages for the two lesions. All tumors had a lobular appearance. GCTTS was more cellular than FTS; it contained conspicuous numbers of osteoclast-like cells, and the stroma was not extensively hyalinized. In contrast, FTS was matrix-rich, often with extensive stromal sclerosis, and contained only rare giant cells. Immunophenotyping of GCTTS showed that both the spindle cell and giant cell components were positive for vimentin, LCA, CD68, HAM56, AACT, and MAC387, suggesting monocyte-macrophage-like features. Limited reactivity for desmin and SMA also implied conjoint myofibroblastic differentiation. On the other hand, FTS showed focal staining with HAM56 (all cases) and for CD68 (one case); staining for vimentin and SMA was uniformly intense and diffuse. Based on these results, we conclude that GCTTS and FTS both exhibit varying degrees of monocyte-macrophage-like and myofibroblastic differentiation. The predominance of macrophage-related determinants in GCTTS and myofibroblastic markers in FTS supports the premise that these lesions represent phenotypic extremes of a single clinicopathologic entity.

 

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