To investigate the changes of vaspin and TNF-α levels in gingival crevicular fluid (GCF) of type 2 diabetic (T2DM) patients with chronic periodontitis (CP) after non-surgical periodontal treatment.

60 subjects were divided into 4 groups: DM-CP group (patients with both T2DM and CP, n＝15); CP group (CP patients without T2DM, n＝15); DM group (T2DM patients without CP, n＝15), and CTRL group (systemically and periodontally healthy individuals, n＝15). The clinical parameters of periodontal tissue and GCF were measured before and 8 weeks after non-surgical periodontal treatment. The levels of vaspin and TNF-α were measured by ELISA.

The levels of vaspin and TNF-α in CP group were significantly higher than those in CTRL group (P < 0.05), while the levels of vaspin and TNF-α in CP group were significantly decreased after treatment (P < 0.05). There was a statistically significant positive correlation between the total amount of vaspin and the total amount of TNF-α, the level of HbA1c, gingival index (GI) and probing depth (PD) (P < 0.05).

The results shows that vaspin and TNF- α are greatly decreased in periodontitis after non-surgical periodontal treatment. It suggests that vaspin and TNF- α in GCF may serve as inflammatory markers for the diagnosis and prognosis of diabetes and periodontitis.

To evaluate the expression of the receptor for advanced glycation end products (RAGE) in gingival tissue endothelial cells from type 2 diabetic rats with chronic periodontitis and to explore the role of RAGE in the pathogenesis of diabetes in cases with chronic periodontitis.

Sixty 7-week-old female Wistar diabetic obese rats were randomly divided into two groups. Periodontitis was induced in 30 rats by silk ligation, and the other 30 rats were used as the control group in which the periodontal tissues were not treated. One week after periodontal ligation and inoculation, the periodontitis and control group rats were randomly divided into two subgroups; the first subgroup was fed a high-fat diet, and the second group was fed a low-fat diet. Thus, 15 rats per group were included in the high-fat diet periodontitis (HF/P), low-fat diet periodontitis (LF/P), high-fat diet periodontal health (HF/C), and low-fat diet periodontal health (LF/C) groups. Glucose tolerance tests were performed weekly to measure the fasting insulin and blood glucose levels and the insulin resistance index to verify successful construction of the rat diabetes model. After successful modeling of chronic periodontitis, the rats were sacrificed at the 13th week after measurement of the serum necrosis factor-α (TNF-α), interleukin-6 (IL-6) and leptin levels. The tooth periodontal tissues were prepared and sectioned to observe histological changes. Immunofluorescence double staining was used to detect the density of RAGE-positive endothelial cells in the gingival tissues of the four groups.

The serum fasting blood glucose and insulin levels and insulin resistance index were significantly higher in the HF/P and HF/C groups than in the LF/P and LF/C groups (P < 0.01). The serum TNF-α and IL-6 levels were significantly higher in the HF/P and LF/P groups than in the HF/C and LF/C groups (P < 0.01). The serum leptin levels were significantly higher in the HF/P group than in the other three groups. The density of RAGE-positive endothelial cells was significantly higher in the HF/P and HF/C groups than in the LF/P (P＝0.001) and LF/C groups (P＝0.040). The density of RAGE-positive endothelial cells in the HF/P group was higher than that in the HF/C group (P＝0.027).

Endothelial cells in type 2 diabetic rats with periodontitis have increased gingival tissue RAGE and serum leptin levels.

To observe the expression of interleukin-33 (IL-33) in macrophages of chronic periapical periodontitis and apical cyst tissue, and to provide a basis for the study of the pathogenesis of IL-33 in periapical diseases.

The apical tissues of 20 normal control group, 15 chronic periapical periodontitis group and 15 apical cyst group were collected for HE staining and optical microscopy respectively. CD14 was used as the marker of macrophages and double immunofluorescence staining was used to observe the changes of periapical tissues under fluorescence microscopy. The expression of IL-33 in CD14-positive macrophages was observed.

The macrophage density (cell/mm²) of IL-33 and CD14 positive expression in normal control group, chronic periapical periodontitis group and root cyst group were (23.81 ± 5.16, 62.97 ± 8.54, 119.83 ± 14.61) respectively, and there were significant differences among the three groups (F＝87.17, P < 0.01). The density of IL-33 and CD14 positive macrophages in root cyst group was significantly higher than that in chronic periapical periodontitis group and control group (P < 0.01).

IL-33 and CD14 positive macrophages increased in normal apical tissue, chronic periapical periodontitis tissue and apical cyst tissue in turn.