title: Actinobacillus actinomycetemcomitans lipopolysaccharide-mediated experimental bone loss model for aggressive periodontitis.
abstract: BACKGROUND
  Bacterial constituents, such as Gram-negative derived lipopolysaccharide (LPS), can initiate inflammatory bone loss through induction of host-derived inflammatory cytokines. The aim of this study was to establish a model of aggressive inflammatory alveolar bone loss in rats using LPS derived from the periodontal pathogen Actinobacillus actinomycetemcomitans.
  
  
  METHODS
  Eighteen female Sprague-Dawley rats were divided into LPS test (N = 12) and saline control (N = 6) groups. All animals received injections to the palatal molar gingiva three times per week for 8 weeks. At 8 weeks, linear and volumetric alveolar bone loss was measured by micro-computed tomography (microCT). The prevalence of inflammatory infiltrate, proinflammatory cytokines, and osteoclasts was assessed from hematoxylin and eosin, immunohistochemical, or tartrate-resistant acid phosphatase (TRAP)-stained sections. Statistical analysis was performed.
  
  
  RESULTS
  A. actinomycetemcomitans LPS induced severe bone loss over 8 weeks, whereas control groups were unchanged. Linear and volumetric analysis of maxillae by microCT indicated significant loss of bone with LPS administration. Histologic examination revealed increased inflammatory infiltrate, significantly increased immunostaining for interleukin IL-6 and -1beta and tumor necrosis factor-alpha, and more TRAP-positive osteoclasts in the LPS group compared to controls.
  
  
  CONCLUSIONS
  Oral injections of LPS derived from the periodontal pathogen A. actinomycetemcomitans can induce severe alveolar bone loss and proinflammatory cytokine production in rats by 8 weeks.
authors.affiliation: Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI 48109-1078, USA.
authors.forename: Jill E
authors.initials: JE
authors.lastname: Rogers
authors.forename: Fei
authors.initials: F
authors.lastname: Li
authors.forename: Derek D
authors.initials: DD
authors.lastname: Coatney
authors.forename: Carlos
authors.initials: C
authors.lastname: Rossa
authors.forename: Paul
authors.initials: P
authors.lastname: Bronson
authors.forename: Jaclynn M
authors.initials: JM
authors.lastname: Krieder
authors.forename: William V
authors.initials: WV
authors.lastname: Giannobile
authors.forename: Keith L
authors.initials: KL
authors.lastname: Kirkwood
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans / Q000472:pathogenicity*; D016301:Alveolar Bone Loss / Q000000981:diagnostic imaging / Q000382:microbiology* / Q000473:pathology; D000704:Analysis of Variance; D000818:Animals; D016207:Cytokines / Q000096:biosynthesis*; D004195:Disease Models, Animal; D005260:Female; D007124:Immunoenzyme Techniques; D053583:Interleukin-1beta / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000008:administration & dosage; D010010:Osteoclasts; D010518:Periodontitis / Q000000981:diagnostic imaging / Q000382:microbiology* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014057:Tomography, X-Ray Computed / Q000379:methods; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha