title: Jaw bone remodeling at the invasion front of gingival squamous cell carcinomas.
abstract: BACKGROUND
  It is still unknown how jaw bone remodeling occurs at actual invasion sites of oral squamous cell carcinomas. Since there is no other human carcinomas which make a direct invasion of the bone, gingival carcinomas are valuable examples.
  
  
  METHODS
  Twelve surgical specimens of gingival squamous cell carcinoma were examined histopathologically and immunohistochemically for remodeling of bone and its surrounding tissue.
  
  
  RESULTS
  Three types of bone interfaces with carcinomatous invasion were distinguished. These included areas with bone resorption, smooth bone surface and new bone formation. In the bone-resorption area, numerous osteoclasts were located along the bone surface, which was surrounded by myxoid stroma. The myxoid stroma was characterized by immunopositivity for heparan sulfate proteoglycan (HSPG), abundant vascularity and macrophagic infiltration. In the bone-formation area, rows of osteoblasts were aligned on the bone surface. The stroma around osteoblasts was also HSPG-immunopositive, poor in vascularity but rich in activated fibroblasts. In the smooth-bone area, the stroma showed an organizing phase of granulation tissue with slender fibroblasts and mature collagen fibers but with less vascularity and inflammatory infiltrates.
  
  
  CONCLUSIONS
  The results indicate that the stromal architecture, especially in terms of its inflammatory cellular, vascular and matrix compositions, is strictly regulated in the timing and site of jaw bone remodeling which is causes by carcinomatous invasion.
authors.affiliation: Division of Reconstructive Surgery for Oral and Maxillofacial Region, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: Masahiro
authors.initials: M
authors.lastname: Ito
authors.forename: Naoya
authors.initials: N
authors.lastname: Izumi
authors.forename: Jun
authors.initials: J
authors.lastname: Cheng
authors.forename: Hideaki
authors.initials: H
authors.lastname: Sakai
authors.forename: Susumu
authors.initials: S
authors.lastname: Shingaki
authors.forename: Tamio
authors.initials: T
authors.lastname: Nakajima
authors.forename: Kimimitsu
authors.initials: K
authors.lastname: Oda
authors.forename: Takashi
authors.initials: T
authors.lastname: Saku
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D015214:Antigens, Differentiation, Myelomonocytic / Q000032:analysis; D016723:Bone Remodeling; D001862:Bone Resorption; D002294:Carcinoma, Squamous Cell / Q000503:physiopathology*; D056657:Cathepsin K; D002403:Cathepsins / Q000032:analysis; D005887:Gingival Neoplasms / Q000503:physiopathology*; D006497:Heparan Sulfate / Q000032:analysis; D006801:Humans; D007124:Immunoenzyme Techniques; D007568:Jaw / Q000098:blood supply / Q000737:chemistry / Q000473:pathology*; D009361:Neoplasm Invasiveness / Q000503:physiopathology*; D009389:Neovascularization, Pathologic; D010010:Osteoclasts / Q000502:physiology; D019063:Tenascin / Q000032:analysis; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D056657:Cathepsin K; D002403:Cathepsins; D006497:Heparan Sulfate; D019063:Tenascin; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C534130:CTSK protein, human