Effects of improvement in periodontal inflammation by toothbrushing on serum lipopolysaccharide concentration and liver injury in rats.
OBJECTIVE
Periodontitis increases the serum lipopolysaccharide level, contributing to liver injury. Toothbrushing improves periodontitis and may also affect serum lipopolysaccharide concentration and periodontitis-induced liver injury. The purpose of the present study was to examine whether the improvement in periodontal inflammation by toothbrushing clinically affects the serum lipopolysaccharide level and hepatic pathological changes in rat periodontitis.


METHODS
Thirty male Wistar rats were divided into 5 groups, 2 groups receiving topical application of pyrogen-free water to the gingival sulcus for 4 or 8 weeks. The next 2 groups received topical application of lipopolysaccharide and proteases for 4 or 8 weeks. The last group received topical application of lipopolysaccharide and proteases for 8 weeks, and the palatal gingiva was brushed with a powered toothbrush once a day for 4 weeks prior to the end of the experimental period.


RESULTS
Topical application of lipopolysaccharide and proteases induced not only periodontal inflammation but also an elevation in the serum lipopolysaccharide concentration, with increasing hepatic inflammation, steatosis and 8-hydroxydeoxyguanosine levels in a time-dependent manner. The rats that received gingival stimulation showed decreased polymorphonuclear leukocyte infiltration and collagen loss levels in the periodontal lesions. Furthermore, this group also showed a decrease in serum lipopolysaccharide concentration and hepatic inflammation, steatosis and 8-hydroxydeoxyguanosine levels, compared with the group receiving no treatment.


CONCLUSIONS
Toothbrushing promoted healing of periodontal lesions, decreased serum lipopolysaccharide concentration and suppressed liver injury in a rat periodontitis model.
Tomofuji
Takaaki
T
Department of Preventive Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Ekuni
Daisuke
D
Sanbe
Toshihiro
T
Azuma
Tetsuji
T
Tamaki
Naofumi
N
Irie
Koichiro
K
Maruyama
Takayuki
T
Yamamoto
Tatsuo
T
Watanabe
Tatsuo
T
Miyauchi
Mutsumi
M
Takata
Takashi
T
D000080242:8-Hydroxy-2'-Deoxyguanosine; D016301:Alveolar Bone Loss / Q000517:prevention & control; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000517:prevention & control; D003094:Collagen / Q000187:drug effects; D003238:Connective Tissue / Q000187:drug effects / Q000473:pathology; D004272:DNA, Mitochondrial / Q000032:analysis; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000097:blood; D004846:Epithelial Attachment / Q000187:drug effects / Q000473:pathology; D004926:Escherichia coli; D005234:Fatty Liver / Q000517:prevention & control; D005881:Gingiva / Q000187:drug effects / Q000473:pathology; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000009:adverse effects / Q000097:blood*; D008107:Liver Diseases / Q000097:blood / Q000517:prevention & control*; D008297:Male; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects; D010447:Peptide Hydrolases / Q000009:adverse effects; D017622:Periodontal Attachment Loss / Q000517:prevention & control; D010518:Periodontitis / Q000097:blood / Q000517:prevention & control*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000097:blood; D013305:Streptomyces griseus / Q000201:enzymology; D014099:Toothbrushing; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
D004272:DNA, Mitochondrial; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D003094:Collagen; D010447:Peptide Hydrolases; D003849:Deoxyguanosine