title: Periapical lesion progression and cytokine expression in an LPS hyporesponsive model.
abstract: OBJECTIVE
  The purpose of this study was to compare periapical lesion progression and the expression of the bone modulating cytokines IL-1alpha, TNF-alpha, IL-4, IL-6 and IL-11 in periapical lesions of normal and C3H/HeJ (LPS hyporesponsive) mice.
  
  
  METHODS
  Pulps of both mandibular first molars from C3H/HeJ and BALB/c (normal) mice were exposed and inoculated with normal mouse oral microorganisms for 2, 4, 6, and 8 weeks. After euthanasia, specimens were prepared for histological examination. A quantitative evaluation of the lesional area and immunohistochemical stain counts was performed.
  
  
  RESULTS
  There were no statistically significant differences in progression of periapical lesions for both mouse strains with time (two-factor ANOVA, P > 0.05). The immunohistochemical staining revealed no overall differences between the two strains in levels of expression of the cytokines (P > 0.05). IL-11 expression did not change from control levels in BALB/c mice, but correlated with the expression of IL-6 and IL-4 in C3H/HeJ mice.
  
  
  CONCLUSIONS
  Responsiveness to LPS may not be significant in the pathogenesis of periapical lesions and in cytokine expression within the lesions, when the lesions are induced by non-specific oral flora.
authors.affiliation: Department of Endodontology, University of Connecticut Health Center, Farmington 06030-1715, USA. fouad@nso.uchc.edu
authors.forename: A F
authors.initials: AF
authors.lastname: Fouad
authors.forename: A W
authors.initials: AW
authors.lastname: Acosta
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004396:Coloring Agents; D016207:Cytokines / Q000276:immunology* / Q000502:physiology; D003782:Dental Pulp / Q000382:microbiology; D003789:Dental Pulp Exposure / Q000382:microbiology; D003790:Dental Pulp Necrosis / Q000382:microbiology; D004195:Disease Models, Animal; D018450:Disease Progression; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000276:immunology; D017370:Interleukin-11 / Q000276:immunology; D015847:Interleukin-4 / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008815:Mice, Inbred Strains; D010483:Periapical Diseases / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D004396:Coloring Agents; D016207:Cytokines; D007375:Interleukin-1; D017370:Interleukin-11; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4