title: Cell populations involved in pigmented villonodular synovitis of the knee.
abstract: OBJECTIVE
  Pigmented villonodular synovitis (PVNS) of the knee is a tumor-like process of uncertain nature. We analyzed the involved cell populations, iron deposition, and cell proliferation in PVNS to propose a pathogenetic concept of this still elusive disease entity.
  
  
  METHODS
  The study was performed on a series of 14 cases of localized PVNS of the knee. Histology and histochemistry were used to evaluate basic morphology and iron deposit distribution. Immunohistochemistry was performed to characterize the inflammatory cell infiltrate and to identify the proliferating cell compartments. In situ hybridization analysis using a cDNA probe against type I collagen was utilized to further characterize the mononuclear cell infiltrate.
  
  
  RESULTS
  In addition to the classic features (mononuclear cell infiltrate, multinuclear giant cells, iron deposits, and stromal fibrosis) we observed a chronic inflammatory cell infiltrate in all PVNS samples, in which CD8 positive T cells were conspicuous. A high portion of non-phagocytotic cells resorbed iron and became CD68 positive. A proportion of mononuclear cells expressed type I collagen, thus resembling B synoviocytes.
  
  
  CONCLUSIONS
  Our results suggest that preexisting chronic inflammation plays an important pathogenetic role in the PVNS disease process. Chronic inflammation increases the risk of articular bleeding and probably deranges the iron processing capacity of local synovial macrophages. The resulting iron overload could lead to a shift of iron storing cells from synovial macrophages to B synoviocytes and fibroblasts. A perpetuated proliferation and activation of these cells can explain why PVNS behaves like a neoplastic process.
authors.affiliation: Department of Pathology, University of Erlangen-Nürnberg, Erlangen, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Oehler
authors.forename: H G
authors.initials: HG
authors.lastname: Fassbender
authors.forename: D
authors.initials: D
authors.lastname: Neureiter
authors.forename: C
authors.initials: C
authors.lastname: Meyer-Scholten
authors.forename: T
authors.initials: T
authors.lastname: Kirchner
authors.forename: T
authors.initials: T
authors.lastname: Aigner
mesh_terms: D000328:Adult; D000368:Aged; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018414:CD8-Positive T-Lymphocytes / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000378:metabolism / Q000473:pathology*; D007501:Iron / Q000378:metabolism; D007717:Knee / Q000473:pathology; D008297:Male; D008875:Middle Aged; D013586:Synovitis, Pigmented Villonodular / Q000378:metabolism / Q000473:pathology*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D007501:Iron; C067980:CD68 antigen, human; D000097382:CD68 Molecule