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Background and Objective Occlusal trauma is an important factor that influences the progression of periodontitis, but it is unclear whether occlusal trauma influences periodontal destruction at the onset of periodontitis. We established an experimental periodontitis model with both site-specific loss of attachment and alveolar bone resorption. The purpose of the present study was to investigate the effects of occlusal trauma on periodontal destruction, particularly loss of attachment, at the onset of experimental periodontitis. Material and Methods Sixty rats were used in the present study. Forty-eight rats immunized with lipopolysaccharide ( LPS) intraperitoneally were divided into four groups. In the trauma ( T) group, occlusal trauma was induced by placing an excessively high metal wire in the occlusal surface of the mandibular right first molar. In the inflammation ( I) group, periodontal inflammation was induced by topical application of LPS into the palatal gingival sulcus of maxillary right first molars. In the trauma + inflammation ( T+ I) group, both trauma and periodontal inflammation were simultaneously induced. The PBS group was administered phosphate-buffered saline only. Another 12 nonimmunized rats (the n−( T+ I) group) were treated as described for the T+ I group. All rats were killed after 5 or 10 d, and their maxillary first molars with surrounding tissues were observed histopathologically. Loss of attachment and osteoclasts on the alveolar bone crest were investigated histopathologically. To detect immune complexes, immunohistological staining for C1q B was performed. Collagen fibers were also observed using the picrosirius red-polarization method. Results There were significant increases in loss of attachment and in the number of osteoclasts in the T+ I group compared with the other groups. Moreover, widespread distribution of immune complexes was observed in the T + I group, and collagen fibers oriented from the root surface to the alveolar bone crest had partially disappeared in the T, T+ I and n−( T+ I) groups. Conclusion When inflammation was combined with occlusal trauma, immune complexes were confirmed in more expanding areas than in the area of the I group without occlusal trauma, and loss of attachment at the onset of experimental periodontitis was increased. Damage of collagen fibers by occlusal trauma may elevate the permeability of the antigen through the tissue and result in expansion of the area of immune-complex formation and accelerating inflammatory reaction. The periodontal tissue destruction was thus greater in the T+ I group than in the I group. [ABSTRACT FROM AUTHOR]

Background and objective Periodontitis is generally accepted to relate to gram-negative bacteria, and the host defense system influences its onset and progression. However, little is known about the relation between gram-positive bacteria and periodontitis. In this study, we topically applied gram-positive and gram-negative bacterial suspensions to the gingival sulcus in rats after immunization, and then histopathologically examined their influence on periodontal destruction. Materials and Methods Rats previously immunized with heat-treated and sonicated Staphylococcus aureus or Aggregatibacter actinomycetemcomitans were used as immunized groups. The non-immunized group received only sterile phosphate-buffered saline. In each animal, S. aureus or A. actinomycetemcomitans suspension was applied topically to the palatal gingival sulcus of first molars every 24 h for 10 d. Blood samples were collected and the serum level of anti- S. aureus or anti- A. actinomycetemcomitans immunoglobulin G (IgG) antibodies was determined by enzyme-linked immunosorbent assay. The first molar regions were resected and observed histopathologically. Osteoclasts were stained with tartrate-resistant acid phosphatase ( TRAP). The formation of immune complexes was confirmed by immunohistological staining of C1qB. Results Serum levels of anti- S. aureus and anti- A. actinomycetemcomitans IgG antibodies in the immunized groups were significantly higher than those in the non-immunized groups were. The loss of attachment, increase in apical migration of the junctional epithelium, and decreases in alveolar bone level and number of TRAP-positive multinuclear cells in each immunized group were significantly greater than in each non-immunized group. The presence of C1qB was observed in the junctional epithelium and adjacent connective tissue in the immunized groups. Conclusions Heat-treated and sonicated S. aureus and A. actinomycetemcomitans induced attachment loss in rats immunized with their suspensions. Our results suggest that not only gram-negative but also gram-positive bacteria are able to induce periodontal destruction. [ABSTRACT FROM AUTHOR]

Yoshinaga Y, Ukai T, Kaneko T, Nakatsu S, Shiraishi C, Kuramoto A, Oshino K, Ichimura I, Hara Y. Topical application of lipopolysaccharide into gingival sulcus promotes periodontal destruction in rats immunized with lipopolysaccharide. J Periodont Res 2012; 47: 674-680. © 2012 John Wiley & Sons A/S Background and Objective: The causes of periodontitis are bacteria and the host immune system, but the role of the immune system in the onset and progression of periodontal disease is still unclear. Our previous report showed that the formation of an immune complex in the gingival sulcus induces periodontal destruction. This study was carried out to investigate how the immune system, particularly immunization, is involved in periodontal destruction. Material and Methods: Animals immunized intraperitoneally with lipopolysaccharide (LPS) were used as the immunized group. The nonimmunized group received only phosphate-buffered saline. LPS was applied daily onto the palatal gingival sulcus in both groups 1 d after the booster injection. Serum levels of anti-LPS IgG were determined. Loss of attachment and the level of alveolar bone were histopathologically and histometrically investigated. RANKL-bearing cells and the expression of C1qB were immunohistologically evaluated. Results: The serum levels of anti-LPS IgG were elevated in the early experimental period in the immunized group. There were significant increases in loss of attachment, level of alveolar bone and the number of RANKL-bearing cells in the immunized group. C1qB was observed in the junctional epithelium and adjacent connective tissue. The nonimmunized group showed similar findings at and after the time when the serum level of anti-LPS IgG was elevated. Conclusion: Topical application of LPS as an antigen induced periodontal destruction when the serum level of anti-LPS IgG was elevated in rats immunized with LPS. The presence of C1qB suggests that the formation of immune complexes is involved in this destruction. [ABSTRACT FROM AUTHOR]