title: Remodeling of the rat gingiva induced by CO2 laser coagulation mode.
abstract: OBJECTIVE
  This study was conducted to clarify the morphologic characteristics and subsequent repair process of coagulation necrosis produced by pulsed CO(2) laser irradiation with relatively low fluence, and thereby to evaluate the clinical efficacy of this irradiation mode.
  
  
  METHODS
  Wounding of rat gingiva to produce coagulation necrosis was done with a CO(2) laser with a fluence of 326 J/cm(2). The structural characteristics of the wound and subsequent repair process were examined by means of histology, immunohistochemistry, and electron microscopy.
  
  
  RESULTS
  At 6 hours after irradiation, the cells in the laser wound appeared histologically intact but had lost the immunoreactivity to antibodies against Hsp47 and exhibited various ultrastructural signs of cell death. This wound area was lined by Hsp70-positive cells. At 1-day post-irradiation, the uptake of BrdU rapidly increased in the adjacent epithelium and connective tissue. The re-epithelization commenced at 1 day and was completed by 7 days. The necrotic tissue gradually became integrated within the newly formed connective tissue and the original contour of the gingiva was retained during the repair process. The repair process of the laser-induced wound progressed more rapidly than that of a scalpel-made wound.
  
  
  CONCLUSIONS
  The present study suggests that the coagulation necrosis produced by the low fluence pulsed CO(2) laser does not disturb the repair process but promotes its steady progress and subsequent tissue remodeling. This laser mode will pave the way for more conservative and minimally invasive surgery for treating a wide variety of oral soft tissue disorders.
authors.affiliation: Department of Oral Medical Sciences, Division of Oral Pathology, Ohu University School of Dentistry, Koriyama, Fukushima 963-8611, Japan. a-yamasaki@den.ohu-u.ac.jp
authors.forename: Akira
authors.initials: A
authors.lastname: Yamasaki
authors.forename: Kiyoharu
authors.initials: K
authors.lastname: Tamamura
authors.forename: Yuuko
authors.initials: Y
authors.lastname: Sakurai
authors.forename: Noriko
authors.initials: N
authors.lastname: Okuyama
authors.forename: Junko
authors.initials: J
authors.lastname: Yusa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ito
mesh_terms: D000818:Animals; D001973:Bromodeoxyuridine / Q000493:pharmacokinetics; D016923:Cell Death; D049109:Cell Proliferation; D003238:Connective Tissue / Q000378:metabolism / Q000502:physiology / Q000648:ultrastructure; D004848:Epithelium / Q000473:pathology / Q000502:physiology; D005347:Fibroblasts / Q000378:metabolism; D005881:Gingiva / Q000293:injuries / Q000473:pathology* / Q000528:radiation effects*; D050958:HSP47 Heat-Shock Proteins / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D007150:Immunohistochemistry; D017075:Laser Coagulation; D054020:Lasers, Gas; D008297:Male; D008854:Microscopy, Electron; D009336:Necrosis; D011838:Radiation-Sensitizing Agents / Q000493:pharmacokinetics; D051381:Rats; D017208:Rats, Wistar; D012038:Regeneration; D014945:Wound Healing
chemical_list: D050958:HSP47 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D011838:Radiation-Sensitizing Agents; C494662:Serpinh1 protein, rat; D001973:Bromodeoxyuridine