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Updated: Apr 11, 2026
Inducing Apical Periodontitis in Mice
Published on: August 6, 2019
Expression of Interleukin-1β and Matrix Metalloproteinase-8 in Cytolytic and Noncytolytic Enterococcus
Bingling Lu1, Jinxiu Zhang1, Xiaojing Huang1
1School and Hospital of Stomatology, Fujian Medical University, Fuzhou, Fujian, China; Key Laboratory of Stomatology (FMU), Fujian Province University, Fuzhou, Fujian, China.
Introduction:
Cytolytic Enterococcus faecalis possesses a highly toxic and proinflammatory capacity. Cytokines and proteases play important roles in the host inflammatory response. The aim of this study was to compare the local expression of interleukin (IL)-1β and matrix metalloproteinase-8 (MMP-8) between persistent apical periodontitis (AP) infected by cytolytic and noncytolytic E. faecalis.
Methods:
Eighty-four left upper first rat molars were divided into 4 groups: chronic AP group (n = 6), disinfection group (n = 6), cytolytic E. faecalis-infected persistent AP group (n = 36), and noncytolytic E. faecalis-infected persistent AP group (n = 36). Periradicular lesions were established after pulp exposure. After 3 weeks, root canals were prepared, and disinfected. E. faecalis strains ATCC 29212 or ATCC 700802 suspensions were inoculated into root canals 2 weeks later. Six samples were collected at different time points (1, 2, 3, 4, 5, and 6 weeks). The expression levels of IL-1β and MMP-8 were detected by immunohistochemical staining.
Results:
IL-1β and MMP-8 expression trends in the cytolytic groups were similar to those of the noncytolytic group although at different time points the expression levels in the cytolytic group were significantly higher than those in the noncytolytic group (P < .01). IL-1β expression enhancement occurred during the early phase of infection, whereas increased MMP-8 expression lasted for a prolonged period.
Conclusions:
Both E. faecalis strains could induce local IL-1β and MMP-8 expression in persistent AP. Compared with noncytolytic E. faecalis, cytolytic E. faecalis may cause more severe local inflammation and tissue destruction in persistent AP.
