title: Antigenicity of primary endodontic infection against macrophages by the levels of PGE(2) production.
abstract: BACKGROUND
  Root canal contents are potent stimuli for proinflammatory cytokines involved in apical periodontitis. This study investigated target gram-negative bacterial species and endotoxins in primary endodontic infection with apical periodontitis, determined their antigenicity against macrophages through the levels of PGE(2), and evaluated their relationship with clinical findings.
  
  
  METHODS
  Samples were taken from 21 root canals with primary infection and apical periodontitis by using paper points. Polymerase chain reaction (16S rDNA) was used for bacterial detection and limulus amebocyte lysate assay for endotoxin measurement. Levels of prostaglandin E2 (PGE(2)) were measured by enzyme-linked immunosorbent assay (Duoset Kit; R&D, Minneapolis, MN).
  
  
  RESULTS
  Prevotella nigrescens (13/21), Fusobacterium nucleatum (6/21), and Porphyromonas endodontalis (6/21) were the most frequently observed species. A positive association was found between F. nucleatum and P. endodontalis (P < .05). A correlation was found between the number of gram-negative bacterial species and the levels of endotoxins, such as PGE(2) (P < .05). Higher levels of endotoxin were detected in teeth with exudation, whereas elevated levels of PGE(2) were found in teeth with tenderness to percussion and pain on palpation.
  
  
  CONCLUSIONS
  Our findings imply an additive effect between the number of gram-negative bacterial species involved in endodontic infection regarding the induction of proinflammatory cytokine by macrophage cells. Moreover, teeth with clinical symptomatology were related to higher levels of endotoxins and PGE(2) secretion.
authors.affiliation: Department of Restorative Dentistry, State University of Campinas, Piracicaba, São Paulo, Brazil.
authors.forename: Frederico C
authors.initials: FC
authors.lastname: Martinho
authors.forename: Wanderson Miguel Maia
authors.initials: WM
authors.lastname: Chiesa
authors.forename: Fabio R M
authors.initials: FR
authors.lastname: Leite
authors.forename: Joni A
authors.initials: JA
authors.lastname: Cirelli
authors.forename: Brenda P F A
authors.initials: BP
authors.lastname: Gomes
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000276:immunology*; D018929:Cell Culture Techniques; D002470:Cell Survival / Q000502:physiology; D016207:Cytokines / Q000032:analysis / Q000276:immunology; D003790:Dental Pulp Necrosis / Q000276:immunology / Q000382:microbiology*; D015232:Dinoprostone / Q000032:analysis / Q000276:immunology*; D004731:Endotoxins / Q000032:analysis / Q000276:immunology; D005122:Exudates and Transudates / Q000737:chemistry; D005674:Fusobacterium Infections / Q000276:immunology; D016967:Fusobacterium nucleatum / Q000276:immunology; D016905:Gram-Negative Bacterial Infections / Q000276:immunology*; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology; D008264:Macrophages / Q000276:immunology*; D008875:Middle Aged; D010485:Periapical Periodontitis / Q000276:immunology / Q000382:microbiology; D045202:Porphyromonas endodontalis / Q000276:immunology; D016966:Porphyromonas gingivalis / Q000276:immunology; D018713:Prevotella intermedia / Q000276:immunology; D045242:Prevotella nigrescens / Q000276:immunology; D012329:RNA, Bacterial / Q000032:analysis; D055815:Young Adult
chemical_list: D000942:Antigens, Bacterial; D016207:Cytokines; D004731:Endotoxins; D018836:Inflammation Mediators; D012329:RNA, Bacterial; D015232:Dinoprostone