Affiliations: Department of Implantology, the 2nd Affiliated
Hospital, Harbin Medical University, Harbin, Heilongjiang, China | Department of Orthodontics, the 1st Affiliated
Hospital, Harbin Medical University, Harbin, Heilongjiang, China | Department of Oral and Maxillofacial Surgery, the 2nd
Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang, China
Note: [] Corresponding authors: Bin Zhang and Cheng-Chao Guan, Department
of Implantology, the 2nd Affiliated Hospital, Harbin Medical University, Harbin
150086, Heilongjiang, China. E-mail: [email protected],
[email protected]
Abstract: OBJECTIVE: In this study, we sought to investigate the dynamic
changes in the levels of TNF-α, IL-1β and LPS in the gingival
crevicular fluid (GCF) in a rat model of diabetes mellitus (DM) and
periodontitis (PD). Additionally, we evaluated alveolar bone loss and the
histopathological response associated with experimental diabetes mellitus and
experimental periodontitis. METHODS: DM and PD were induced together in 15 rats (group 1) by
streptozotocin injection and ligature induction. Periodontitis alone was
produced by ligature induction in 15 rats (group 2), diabetes alone was
produced by streptozotocin injection in 15 rats (group 3), and fifteen
systemically and periodontally healthy rats were used as controls (group 4).
The gingival TNF-α, IL-1β and LPS levels were measured by using
ELISA method. Periodontal destruction was assessed by measuring the alveolar
bone loss. Periodontal inflammation was quantified by histopathological grading
in H&E stained samples. RESULTS: Higher levels of TNF-α, IL1-β and LPS, increased
alveolar bone loss and more serve histopathology were found in group 1 compared
with group 2, group 3 and group 4 (p< 0.05). The quantities of TNF-α,
IL1-β and LPS, the amount of alveolar bone loss and the severity of the
histopathological finding were greater in group 2 than group 3 and group 4
(p< 0.05). Group 3 demonstrated higher levels of TNF-α, IL1-β and
LPS, increased alveolar bone loss and more serve histopathology than group 4
(p< 0.05). Statistically significant differences were noted between all of
the groups. CONCLUSIONS: These data indicate that DM may lead to enhanced
TNF-α, IL1-β and LPS production in the periodontal tissues. The
resorption values of alveolar bone and the histological inflammation were more
severe in rats with periodontitis and diabetes mellitus than in those with
periodontitis alone, diabetes mellitus alone and control rats. Our findings are
consistent with the hypothesis that hyperglycemia contributes to the heightened
inflammatory response associated with periodontitis.
