title: Mechanisms of giant papillary formation in vernal keratoconjunctivitis.
abstract: OBJECTIVE
  Tissue remodeling, known to accompany exacerbation of bronchial asthma (BA) and characterized by thickening of reticular basement membrane, increased fibrosis, and angiogenesis, is believed to be an important mechanism in giant papillary formation in vernal keratoconjunctivitis (VKC). This study was conducted to confirm the difference of tissue remodeling between BA and VKC and to determine the most relevant factor for VKC exacerbation.
  
  
  METHODS
  Histopathologic analysis of conjunctival specimens from 6 patients with VKC and 4 normal controls was performed. Immunohistochemistry tests for collagen types 1, 3, and 5, fibronectin, laminin (a marker of the basement membrane of the epithelium or vessels), fibroblast (prolyl 4-hydroxylase), and alpha-smooth muscle actin (alpha-SMA) were performed. Morphometric analysis evaluated immunoreactive areas for collagens and fibronectin and the number of cell nuclei in VKC papillae and normal control specimens.
  
  
  RESULTS
  In histopathologic sections of VKC papillae, mononuclear cells were mainly observed in the central region and granulocytes preferentially in the peripheral stroma. Immunohistochemistry showed increased vascularity and existence of fibroblasts and alpha-SMA-positive cells in VKC papillae. Morphometric analysis showed that the number of cell nuclei in VKC papillae was 7.3 times higher versus in normal controls (P < 0.05). Furthermore, the immunoreactive area for fibronectin was 4.5 times larger versus in normal controls (P < 0.05), although collagens were not significantly different between the 2 groups.
  
  
  CONCLUSIONS
  Giant papillary formation in VKC is thought to occur in relation to tissue remodeling. However, the most relevant factor for the exacerbation of VKC seems to be inflammation rather than fibrosis.
authors.affiliation: Department of Ophthalmology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. naokato@bc.iij4u.or.jp
authors.forename: Naoko
authors.initials: N
authors.lastname: Kato
authors.forename: Kazumi
authors.initials: K
authors.lastname: Fukagawa
authors.forename: Murat
authors.initials: M
authors.lastname: Dogru
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Fujishima
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tsubota
mesh_terms: D000199:Actins / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D003228:Conjunctiva / Q000378:metabolism / Q000473:pathology*; D003233:Conjunctivitis, Allergic / Q000378:metabolism / Q000473:pathology*; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology*; D005353:Fibronectins / Q000378:metabolism; D005355:Fibrosis; D019084:Fluorescent Antibody Technique, Indirect; D006801:Humans; D007124:Immunoenzyme Techniques; D007797:Laminin / Q000378:metabolism
chemical_list: D000199:Actins; D005353:Fibronectins; D007797:Laminin; D003094:Collagen