It has been demonstrated that diabetes mellitus (DM) may have an inductive effect on the vascular endothelial growth factor (VEGF) levels of periodontium during periodontal disease. The aim of this study is to confirm this phenomenon, investigating whether it is also valid for diabetic periodontitis patients under good metabolic control. Sixteen type II DM patients, all with a glycosylated hemoglobin (HbA1c) value less than 7 (test), and 15 systemically healthy (control) chronic periodontitis patients were included in the study. The VEGF concentrations in the gingival supernatants and gingival crevicular fluid (GCF) samples of the study groups were measured by enzyme-linked immunosorbent assay. The data were analyzed by Student's t test in statistical means. The VEGF levels were significantly higher in the gingival supernatants of the test group (55.89 +/- 8.11 pg/ml) than that of the control group (24.81 +/- 2.04 pg/ml; p < 0.01). However, there was no statistically significant difference in the VEGF levels of GCF between the study groups (38.96 +/- 4.89 pg/ml in the test and 32.20 +/- 4.02 pg/ml in the control group; p > 0.05). Our study confirms that DM affects the VEGF levels of periodontal soft tissues in periodontal disease, and our results also suggest that this effect may not be influenced by the metabolic control of DM.

The results of this study suggest that increased VEGF expression may be associated with the pathogenesis of CsA-induced gingival overgrowth.

Preeclampsia is a human pregnancy-specific disorder characterized by a placental pro-inflammatory response in combination with an imbalance of angiogenic factors and clinical symptoms, including hypertension and proteinuria. Insufficient uteroplacental oxygenation in preeclampsia due to impaired trophoblast invasion during placentation is believed to be responsible for many of the molecular events leading to the clinical manifestations of this disease. We investigated the use of hypoxic treatment of the dual placental perfusion system as a model for preeclampsia. A modified perfusion technique allowed us to achieve a mean soluble oxygen tension within the intervillous space (IVS) of 5-7% for normoxia and o3% for hypoxia (as a model for preeclampsia). We assayed for the levels of different inflammatory cytokines, oxidative stress markers, as well as other factors, such as endothelin (ET)-1 that are known to be implicated as part of the inflammatory response in preeclampsia. Our results show a significant increase under hypoxia in the levels of different inflammatory cytokines, including IL-6 (P ¼ 0.002), IL-8 (Po0.0001), TNF-a (P ¼ 0.032) and IFN-g (P ¼ 0.009) at 360 min in maternal venous samples (n ¼ 6). There was also a significant increase in ET-1 levels under hypoxia both on the maternal side at 30 min (P ¼ 0.003) and fetal side at 360 min (P ¼ 0.036) (n ¼ 6). Other markers of oxidative stress, including malondialdehyde and 8-iso-protaglandin F2a (P ¼ 0.009) also show increased levels. Overall, these findings indicate that exposure of ex vivo dually perfused placental tissue to hypoxia provides a useful model for mimicking the inflammatory response characteristic of preeclampsia. This would therefore provide a powerful tool for studying and further delineating the molecular mechanisms involved in the underlying pathophysiology of preeclampsia.

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