title: Lipopolysaccharide-mediated enhancement of bone metabolism in estrogen-deficient mice.
abstract: BACKGROUND
  Osteoporosis may be a risk factor in periodontal disease. However, biologic mechanisms explaining the apparent interaction between these two diseases have not been defined. It is well known that lipopolysaccharide (LPS) increases the resorption of alveolar bone. We hypothesized that LPS and estrogen deficiency have synergistic effects on bone metabolism and may lead to enhanced bone resorption.
  
  
  METHODS
  Eighty 8-week-old female ddY mice were divided into two groups and underwent a sham operation or bilateral ovariectomy. They were maintained for 4 weeks to assess estrogen-deficient bone loss. Osteoblasts and bone marrow cells (BMCs) were collected from ovariectomized (OVX) and sham-operated mice. Osteoclast differentiation in a coculture of osteoblasts and BMCs was investigated by tartrate-resistant acid phosphatase staining. Receptor activator of nuclear factor-kappa B ligand (RANKL) mRNA expression in LPS-treated osteoblasts was investigated using real-time polymerase chain reaction. Interferon-gamma (IFN-gamma) and interleukin (IL)-6 and -10 levels in the culture supernatants were evaluated by enzyme-linked immunosorbent assay. Group means were compared by analysis of variance followed by Tukey's honestly significant difference.
  
  
  RESULTS
  There was a significant increase in the number of osteoclasts in LPS-treated cocultures from OVX mice compared to sham controls (P <0.05). RANKL mRNA expression in LPS-treated osteoblasts from OVX mice was greater than in sham mice (P <0.05). In contrast, the production of IFN-gamma in LPS-treated coculture from OVX mice was significantly lower than in sham mice (P <0.05).
  
  
  CONCLUSIONS
  LPS-bearing Gram-negative organisms are abundant in periodontal disease, and the results supported the hypothesis that bone resorption is increased in estrogen-deficient patients.
authors.affiliation: Department of Periodontology, Aichi-Gakuin University, Nagoya, Japan.
authors.forename: Sachiko
authors.initials: S
authors.lastname: Fujita
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kikuchi
authors.forename: Takanori
authors.initials: T
authors.lastname: Sobue
authors.forename: Mariyo
authors.initials: M
authors.lastname: Suzuki
authors.forename: Masanori
authors.initials: M
authors.lastname: Koide
authors.forename: Toshihide
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism*; D000818:Animals; D016723:Bone Remodeling / Q000276:immunology / Q000502:physiology*; D001862:Bone Resorption / Q000276:immunology / Q000378:metabolism*; D001842:Bone and Bones / Q000166:cytology / Q000378:metabolism*; D004967:Estrogens / Q000172:deficiency* / Q000502:physiology; D005260:Female; D007375:Interleukin-1 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D010010:Osteoclasts / Q000276:immunology / Q000502:physiology; D017698:Postmenopause / Q000378:metabolism; D053245:RANK Ligand / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004967:Estrogens; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D053245:RANK Ligand; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D000469:Alkaline Phosphatase