TY - JOUR
T1 - A.actinomycetemcomitans-induced periodontal disease promotes systemic and local responses in rat periodontium
AU - De Brito Bezerra, Beatriz
AU - Andriankaja, Oelisoa
AU - Kang, Jun
AU - Pacios, Sandra
AU - Bae, Hyung Jin
AU - Li, Yu
AU - Tsiagbe, Vincent
AU - Schreiner, Helen
AU - Fine, Daniel H.
AU - Graves, Dana T.
PY - 2012/4
Y1 - 2012/4
N2 - Aim To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. Material & Methods Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF-α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. Results An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p < 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p < 0.05). TNF-α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF-α expression in the connective tissue (p < 0.05). PMN recruitment significantly increased after Aa infection (p < 0.05). Aa also increased the number of CD8 + T cells (p < 0.05), but not CD4 + T cells or regulatory T cells (Tregs) (p > 0.05). Conclusion Aa infection stimulated a local response that increased numbers of PMNs and TNF-α expression in the junctional epithelium and loss of attachment. Both TNF-α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF-α in the connective tissue, osteoclast numbers and CD8 + T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction.
AB - Aim To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection. Material & Methods Wistar rats infected with Aa were evaluated for antibody response, oral Aa colonization, loss of attachment, PMN recruitment, TNF-α in the junctional epithelium and connective tissue, osteoclasts and adaptive immune response in local lymph nodes at baseline and 4, 5 or 6 weeks after infection. Some groups were given antibacterial treatment at 4 weeks. Results An antibody response against Aa occurred within 4 weeks of infection, and 78% of inoculated rats had detectable Aa in the oral cavity (p < 0.05). Aa infection significantly increased loss of attachment that was reversed by antibacterial treatment (p < 0.05). TNF-α expression in the junctional epithelium followed the same pattern. Aa stimulated high osteoclast formation and TNF-α expression in the connective tissue (p < 0.05). PMN recruitment significantly increased after Aa infection (p < 0.05). Aa also increased the number of CD8 + T cells (p < 0.05), but not CD4 + T cells or regulatory T cells (Tregs) (p > 0.05). Conclusion Aa infection stimulated a local response that increased numbers of PMNs and TNF-α expression in the junctional epithelium and loss of attachment. Both TNF-α expression in JE and loss of attachment was reversed by antibiotic treatment. Aa infection also increased TNF-α in the connective tissue, osteoclast numbers and CD8 + T cells in lymph nodes. The results link Aa infection with important characteristics of periodontal destruction.
KW - A.actinomycetemcomitans
KW - animals
KW - bone resorption
KW - disease models
KW - host-pathogen interactions
KW - periodontal disease
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U2 - 10.1111/j.1600-051X.2011.01847.x
DO - 10.1111/j.1600-051X.2011.01847.x
M3 - Article
C2 - 22313458
AN - SCOPUS:84862822799
SN - 0303-6979
VL - 39
SP - 333
EP - 341
JO - Journal of Clinical Periodontology
JF - Journal of Clinical Periodontology
IS - 4
ER -