title: Peptidoglycan of Actinomyces naeslundii induces inflammatory cytokine production and stimulates osteoclastogenesis in alveolar bone resorption.
abstract: OBJECTIVE
  Actinomyces naeslundii, plays an important role in forming dental biofilms and causes gingival inflammation. Although peptidoglycan, the major cell wall component of Gram-positive bacteria, has been demonstrated to induce inflammatory cytokines, little is known about the association of peptidoglycan with alveolar bone resorption. This study investigated the involvement of peptidoglycan from A. naeslundii in osteoclast formation and bone resorption.
  
  
  METHODS
  Osteoclast formation and function induced by peptidoglycan of A. naeslundii T14V were examined using the co-culture system of MCTC3/PA6 cells and BALB/c mouse bone marrow cells. Osteoclast formation was evaluated to count TRAP-positive multi-nuclei cells as osteoclasts. The function of osteoclasts was assessed by measuring the areas of pits absorbed. Inflammatory cytokine genes expressions, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, were examined by RT-PCR analysis using murine peritoneal macrophages. Experimental periodontitis was performed in Sprague-Dawley rats orally infected with A. naeslundii.
  
  
  RESULTS
  TRAP-positive multi-nuclei cells and the areas of pits induced by peptidoglycan were significantly greater than controls (p<0.01). Gene expression levels of IL-1β, IL-6, and TNF-α induced by A. naeslundii PGN were stronger than controls. In experimental periodontitis, bone loss of A. naeslundii-infected rats was comparable to that of rats induced by Porphyromonas gingivalis, which has been reported to be a periodontal pathogenic agent, being significantly greater than that of the sham group (p<0.01).
  
  
  CONCLUSIONS
  These results suggest that peptidoglycan of A. naeslundii is an important virulence factor in the development of periodontitis.
authors.affiliation: Department of Oral Medicine, Division of Endodontics, Kanagawa Dental College, Yokosuka 238-8580, Japan.
authors.forename: Takenori
authors.initials: T
authors.lastname: Sato
authors.forename: Kiyoko
authors.initials: K
authors.lastname: Watanabe
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Kumada
authors.forename: Toshizo
authors.initials: T
authors.lastname: Toyama
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Tani-Ishii
authors.forename: Nobushiro
authors.initials: N
authors.lastname: Hamada
mesh_terms: D000190:Actinomyces / Q000378:metabolism* / Q000472:pathogenicity; D000196:Actinomycosis / Q000150:complications*; D016301:Alveolar Bone Loss / Q000209:etiology*; D000704:Analysis of Variance; D000818:Animals; D016207:Cytokines / Q000009:adverse effects* / Q000096:biosynthesis / Q000378:metabolism; D015870:Gene Expression; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010010:Osteoclasts / Q000378:metabolism*; D010457:Peptidoglycan / Q000009:adverse effects*; D010518:Periodontitis / Q000382:microbiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D037521:Virulence Factors / Q000009:adverse effects
chemical_list: D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D010457:Peptidoglycan; D014409:Tumor Necrosis Factor-alpha; D037521:Virulence Factors