title: An assessment of mast cells and myofibroblasts in denture-induced fibrous hyperplasia.
abstract: OBJECTIVE
  The pathogenesis of denture-induced fibrous hyperplasias has not been examined in detail to explain how tissue injury results in fibrous hyperplasia of the oral mucosa.
  
  
  METHODS
  We examined the presence of mast cells and myofibroblasts in 33 denture-induced fibrous hyperplasias (DIFH) compared with 10 healthy gingival tissues. The parameters examined included mast cell numbers, tissue distribution, degranulation, and cell subtypes using immunohistochemistry. The presence of myofibroblasts and their likely origin was also examined by double immunofluorescense staining. Furthermore, we investigated the synthesis of osteopontin and TGF-β, considered to be involved in the transformation of a fibroblast to a myofibroblast.
  
  
  RESULTS
  The results demonstrated that the mast cell numbers are significantly increased in the DIFH compared with non-disease controls. The mast cell localization in lesions was higher in the superficial areas with inflammatory cell infiltration compared with the deep fibrotic area (P < 0.01). The number of tryptase-positive mast cells was significantly higher compared with chymase-positive ones. The TGF-β- or osteopontin-positive cell infiltration into the lesion was found in high numbers. The presence of myofibroblasts was identified in 14 of 33 cases (42%), and some of these cells showed apoptosis when assessed by the TUNEL assay. On the survey of the origin of myofibroblasts, results showed αSMA and vimentin positivity indicating these transformed from fibroblasts.
  
  
  CONCLUSIONS
  These results are the first to show that mast cells and myofibroblasts can be detected in DIFH, indicating important roles of these cells in the pathogenesis of this lesion.
authors.affiliation: Department of Partial Denture Prosthodontics, Nihon University School of Dentistry, Tokyo, Japan.
authors.forename: Misa
authors.initials: M
authors.lastname: Kiuchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Yamamura
authors.forename: Michisato
authors.initials: M
authors.lastname: Okudera
authors.forename: Vongsa
authors.initials: V
authors.lastname: Souksavanh
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Ishigami
authors.forename: Takashi
authors.initials: T
authors.lastname: Iwase
authors.forename: Saman
authors.initials: S
authors.lastname: Warnakulasuriya
authors.forename: Kazuo
authors.initials: K
authors.lastname: Komiyama
mesh_terms: D000199:Actins / Q000032:analysis; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000502:physiology; D002452:Cell Count; D015550:Cell Degranulation / Q000502:physiology; D054338:Cell Transdifferentiation / Q000502:physiology; D053818:Chymases / Q000032:analysis; D003778:Dentures / Q000009:adverse effects*; D005260:Female; D005347:Fibroblasts / Q000473:pathology; D005355:Fibrosis; D005881:Gingiva / Q000473:pathology; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008407:Mast Cells / Q000473:pathology* / Q000502:physiology; D008875:Middle Aged; D009061:Mouth Mucosa / Q000473:pathology*; D058628:Myofibroblasts / Q000473:pathology*; D053495:Osteopontin / Q000032:analysis; D016212:Transforming Growth Factor beta / Q000032:analysis; D053802:Tryptases / Q000032:analysis; D014746:Vimentin / Q000032:analysis
chemical_list: C541116:ACTA2 protein, human; D000199:Actins; D016212:Transforming Growth Factor beta; D014746:Vimentin; D053495:Osteopontin; D053818:Chymases; D053802:Tryptases
keywords: apoptosis; chymase; denture-induced fibrous hyperplasia; mast cells; myofibroblasts; tryptase