Periodontal and systemic responses in various mice models of experimental periodontitis: respective roles of inflammation duration and Porphyromonas gingivalis infection.
BACKGROUND
The great variability of periodontal and systemic responses to experimental periodontitis reflects the inherent pathogenic complexity of mice models and could limit the resulting interpretations and their extension to human diseases. This study compared the effect of Porphyromonas gingivalis (Pg) infection and experimental periodontitis duration at local and systemic levels in various models.


METHODS
Periodontitis was induced in C57BL/6J mice by ligatures previously incubated with Pg (LIGPG group) or not (LIG group) or by oral gavage (GAV) with Pg ATCC 33277. Blood samples were taken, and mice were euthanized at different times. Periodontal tissue destruction, osteoclast number, and inflammation were assessed by histomorphometry, tartrate-resistant acid phosphatase histoenzymology, and cathepsin B (CATB) and matrix metalloproteinase 9 (MMP9) immunochemistry. Serum levels of interleukin-6 (IL-6) and IL-1β were measured using enzyme-linked immunosorbent assay bioplex methods.


RESULTS
Periodontal tissue destruction and osteoclast numbers were significantly elevated in LIGPG models compared to LIG and GAV models. They increased with time with the exception of osteoclast numbers in the LIG model. CATB and MMP9 expression was related to bone destruction processes and Pg infection. The highest serum levels of IL-6 and IL-1β were observed in the LIGPG group. A decrease of IL-6 and an increase of IL-1β serum level were observed with time in LIGPG group contrary to LIG group.


CONCLUSIONS
These data indicate that Pg infection worsened periodontal tissue destruction through specific pathogenic pathways and modified systemic response to periodontal inflammation. Furthermore, the blood cytokine response to ligature models showed their relevance for evaluating the systemic impact of periodontal disease.
Department of Periodontology, Dental Faculty, University of Strasbourg, Strasbourg, France.
Kenza
K
Saadi-Thiers
Olivier
O
Huck
Pierre
P
Simonis
Peggy
P
Tilly
Jean-Etienne
JE
Fabre
Henri
H
Tenenbaum
Jean-Luc
JL
Davideau
D016301:Alveolar Bone Loss / Q000378:metabolism / Q000473:pathology; D000818:Animals; D002401:Cathepsin B / Q000378:metabolism; D004195:Disease Models, Animal; D005751:Gastric Lavage; D007249:Inflammation / Q000503:physiopathology*; D053583:Interleukin-1beta / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008026:Ligation; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D010010:Osteoclasts / Q000473:pathology; D010518:Periodontitis / Q000201:enzymology* / Q000382:microbiology* / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000502:physiology*; D013997:Time Factors; D014774:Virulence
D053583:Interleukin-1beta; D015850:Interleukin-6; D002401:Cathepsin B; D020780:Matrix Metalloproteinase 9