Periodontitis is the most widespread oral disease and is closely related to the oral microbiota. The oral microbiota is adversely affected by some pharmacologic treatments. Systemic antibiotics are widely used for infectious diseases but can lead to gut dysbiosis, causing negative effects on the human body. Whether systemic antibiotic-induced gut dysbiosis can affect the oral microbiota or even periodontitis has not yet been addressed. In this research, mice were exposed to drinking water containing a cocktail of four antibiotics to explore how systemic antibiotics affect microbiota pathogenicity and oral bone loss. The results demonstrated, for the first time, that gut dysbiosis caused by long-term use of antibiotics can disturb the oral microbiota and aggravate periodontitis. Moreover, the expression of cytokines related to Th17 was increased while transcription factors and cytokines related to Treg were decreased in the periodontal tissue. Fecal microbiota transplantation with normal mice feces restored the gut microbiota and barrier, decreased the pathogenicity of the oral microbiota, reversed the Th17/Treg imbalance in periodontal tissue, and alleviated alveolar bone loss. This study highlights the potential adverse effects of long-term systemic antibiotics-induced gut dysbiosis on the oral microbiota and periodontitis. A Th17/Treg imbalance might be related to this relationship. Importantly, these results reveal that the periodontal condition of patients should be assessed regularly when using systemic antibiotics in clinical practice.
Humans ; Mice ; Animals ; Dysbiosis ; Anti-Bacterial Agents/pharmacology* ; Virulence ; Microbiota ; Periodontitis/chemically induced* ; Cytokines

OBJECTIVETo establish the three-dimensional images of rat's alveolar bone and to evaluate the effects of nicotine on alveolar bone loss during the process of ligature-induced periodontitis with micro-computed tomography (micro-CT).

METHODSThirty-six adult male SD rats received silk ligatures around the cervix of the right second maxillary molars. Then the animals were randomly assigned to three groups and received daily intraperitoneal injections as follows: group A (control), saline solution; group B, nicotine, 0.83 mg x kg(-1) x d(-1); and group C, nicotine, 1.67 mg x kg(-1) x d(-1). Six animals in each group were randomly selected and sacrificed at day 14 and 28. Micro-CT examinations were used to evaluate the periodontal breakdown.

RESULTSWith the nicotine dose increased, bone mineral density (BMD), bone volume fraction (BVF), and trabecular thickness (TT) gradually reduced, while the trabecular spacing (TS) and alveolar bone loss (ABL) increased. At day 28, the ABL of group C (left, right) was (0.61 +/- 0.14) mm and (1.39 +/- 0.09) mm, and significantly higher than that of group B [(0.39 +/- 0.10) mm and (1.31 +/- 0.06) mm] and group A[(0.30 +/- 0.06) mm and (0.94 +/- 0.07) mm]. The BMD of group C, group B and group A at day 28 was [(617.86 +/- 34.27), (572.46 +/- 31.62) mg/cm3], [(660.04 +/- 36.73), (604.97 +/- 32.59) mg/cm3] and [(709.15 +/- 34.95), (657.04 +/- 30.06) mg/cm3] respectively.

CONCLUSIONSDaily administration of nicotine results in significant bone loss and microstructure deteriorations in the trabeculae of alveolar bone.

Alveolar Bone Loss ; chemically induced ; diagnostic imaging ; Animals ; Male ; Nicotine ; toxicity ; Periodontitis ; diagnostic imaging ; Rats ; Rats, Sprague-Dawley ; Tooth Socket ; diagnostic imaging ; X-Ray Microtomography

OBJECTIVETo characterize the expression of lipopolysaccharide (LPS) receptors-CD14 and TLR4 in rat peri-radicular tissue and to investigate the signal transduction pathway of LPS and its receptors in periapical periodontitis.

METHODSAfter establishment of a model of rat molar LPS-induced apical periodontitis, CD14 and TLR4 expression in healthy and inflammatory periapical tissue were determined by immunohistochemistry.

RESULTSCD14 and TLR4 were not detected in healthy periapical tissue but strongly positive in inflammatory periapical tissue. Positive cells were mostly monocytes/macrophages.

CONCLUSIONSCD14 and TLR4 may play an important role in the pathogenesis of periapical periodontitis, probably via immune cells such as monocytes/macrophages and neutrophils.

Animals ; Disease Models, Animal ; Lipopolysaccharide Receptors ; metabolism ; Lipopolysaccharides ; toxicity ; Periapical Periodontitis ; chemically induced ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Toll-Like Receptor 4 ; metabolism

This study is to prepare the in situ forming sustained-release injection which can perform sustained release behavior at the periodontal site for 7 days and to evaluate its in vitro and in vivo properties. After preparation of in situ forming sustained-release injection the in situ time was studied. And the surface of the solid injection was characterized by SEM. The rheological curve at 0 degrees C, 25 degrees C, 37 degrees C was determined and the impact of the temperature on the viscosity was examined. The in vitro release behavior was investigated. At last, rabbit periodontitis model was established to study its pharmacokinetics. The injection was stable, hard to stratify and decompose. The in situ forming time was about 6 seconds. It can easily adhere into periodontal pockets. There were lots of holes on the surface of the solid injection for the drug to diffuse. The drug releasing curves could be fit by Korsmeyer-Peppas equation. The drug smoothly released for 7 days at pH 7.4 PBS buffer with a very slight burst release and maintained a certain concentration. In vivo pharmacokinetics results indicated that after administration with the in situ forming injection, achievement of tinidazole (TNZ) concentration in gingival crevicular fluid (GCF) was more comparable and long-lasting than usual solution of TNZ management and relatively constant TNZ levels were attained until 168 h. All these results supported the prospect of tinidazole in situ forming sustained-release injection in clinical applications.
Animals ; Antitrichomonal Agents ; administration & dosage ; pharmacokinetics ; Delayed-Action Preparations ; Drug Carriers ; Drug Compounding ; methods ; Endotoxins ; Gingival Crevicular Fluid ; metabolism ; Injections ; Periodontal Pocket ; metabolism ; Periodontitis ; chemically induced ; metabolism ; Polyesters ; chemical synthesis ; pharmacokinetics ; Polyethylene Glycols ; chemical synthesis ; pharmacokinetics ; Rabbits ; Random Allocation ; Rheology ; Tinidazole ; administration & dosage ; pharmacokinetics