title: Expression and regulation of a disintegrin and metalloproteinase-8 and -17 in development of rat periradicular lesion.
abstract: BACKGROUND
  A disintegrin and metalloproteinases (ADAMs) are a family of transmembrane proteins that share a common domain structure. However, little is known about the possible involvement of ADAM-8 and ADAM-17 in the development of periradicular lesions. Here we demonstrated the expression of ADAM-8 and ADAM-17 in rat periradicular lesions.
  
  
  METHODS
  We induced experimentally periradicular lesions in rats. The animals were killed at 0, 2, 4, 6, and 8 weeks after pulp exposure. The left molars underwent immunofluorescence analysis for both ADAMs and for neutrophil elastase, and right molars were used for reverse transcription-polymerase chain reaction analysis of ADAM-8 and ADAM-17. The areas of these lesions were measured histometrically, and the numbers of all antigen-positive cells in the periapical portion were counted per unit area.
  
  
  RESULTS
  The area of the periradicular lesions gradually expanded from 0 to 4 weeks, showing a large increase from week 2 to week 4. Both ADAM-8-positive and ADAM-17-positive cells gradually increased in number from 0 to 4 weeks and then decreased from 4 to 8 weeks. There were more ADAM-17-expressing cells than ADAM-8-expressing ones at all experimental periods except at 4 weeks. The highest expression of ADAM-8 mRNA was observed at 4 weeks, and there were significant differences between 0 and 2 weeks and between 4 and 6 weeks. The expression of ADAM-17 mRNA increased from 0 to 4 weeks and subsequently decreased from 4 to 8 weeks, with a significant difference between 4 and 6 weeks.
  
  
  CONCLUSIONS
  Our results suggest that ADAM-8 and ADAM-17 may be related to the development of rat periradicular lesions.
authors.affiliation: Department of Endodontics, School of Dentistry, Aichi Gakuin University, Nagoya, Japan. tsuyoshi5585@gmail.com
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Tanaka
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Ozeki
authors.forename: Rie
authors.initials: R
authors.lastname: Kawai
authors.forename: Ichiro
authors.initials: I
authors.lastname: Imaizumi
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakata
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakamura
mesh_terms: D051722:ADAM Proteins / Q000032:analysis / Q000502:physiology*; D000072198:ADAM17 Protein; D016301:Alveolar Bone Loss / Q000209:etiology / Q000473:pathology; D000818:Animals; D002452:Cell Count; D003789:Dental Pulp Exposure / Q000150:complications; D003790:Dental Pulp Necrosis / Q000209:etiology / Q000473:pathology; D019272:Leukocyte Elastase / Q000032:analysis; D008297:Male; D008565:Membrane Proteins / Q000032:analysis / Q000502:physiology*; D008963:Molar / Q000473:pathology; D010482:Periapical Abscess / Q000209:etiology / Q000473:pathology; D010483:Periapical Diseases / Q000209:etiology* / Q000473:pathology; D010486:Periapical Tissue / Q000473:pathology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D019227:Tooth Apex / Q000473:pathology
chemical_list: D008565:Membrane Proteins; D019272:Leukocyte Elastase; D051722:ADAM Proteins; D000072198:ADAM17 Protein; C000606464:Adam17 protein, rat