A.actinomycetemcomitans-induced periodontal disease promotes systemic and local responses in rat periodontium.
OBJECTIVE
To characterize the histologic and cellular response to A. actinomycetemcomitans (Aa) infection.


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).


CONCLUSIONS
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.
Department of Prosthodontics and Periodontics, Piracicaba Dental School, University of Campinas, Piracicaba, São Paulo, Brazil.
Beatriz de Brito
Bde B
Bezerra
Oelisoa
O
Andriankaja
Jun
J
Kang
Sandra
S
Pacios
Hyung Jin
HJ
Bae
Yu
Y
Li
Vincent
V
Tsiagbe
Helen
H
Schreiner
Daniel H
DH
Fine
Dana T
DT
Graves
D000189:Actinobacillus Infections / Q000188:drug therapy; D016976:Aggregatibacter actinomycetemcomitans / Q000276:immunology*; D010520:Aggressive Periodontitis / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology*; D016301:Alveolar Bone Loss / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology*; D000667:Ampicillin / Q000627:therapeutic use; D000818:Animals; D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000907:Antibodies, Bacterial / Q000096:biosynthesis / Q000097:blood; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002634:Chemotaxis, Leukocyte; D004195:Disease Models, Animal; D004846:Epithelial Attachment / Q000276:immunology; D007612:Kanamycin / Q000627:therapeutic use; D009000:Monocytes / Q000276:immunology; D018375:Neutrophil Activation; D010010:Osteoclasts / Q000382:microbiology; D017622:Periodontal Attachment Loss / Q000188:drug therapy / Q000276:immunology* / Q000382:microbiology*; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D000900:Anti-Bacterial Agents; D000907:Antibodies, Bacterial; D014409:Tumor Necrosis Factor-alpha; D007612:Kanamycin; D000667:Ampicillin