Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As introduced by different studies, dental plaque is known as a reservoir of Helicobacter Pylori (HP) and a potential source for gastric re-infection. Also, it has been demonstrated that individuals with gastric HP infection manifest a greater plaque index and a higher incidence rate for gingivitis. The goal of the present research was survey of severity and prevalence of periodontal diseases associated with gastric HP infection among patients having referred to the endoscopy wards of Imam Khomeini and Milad hospitals. In this research, 122 patients with gastric HP infection were investigated for determining 4 indices: plaque index (PI), gingival index (GI), clinical attachment loss (CAL) and pocket depth (PD), for all existing teeth, using RUT (rapid urease test). The results indicated that about 86.9% of patients had developed gingivitis of various degrees and 100% of them were afflicted with periodontitis of different degrees, and about 64.8% of patients showed a weak PI, and 61.5% had a low level of education. This low-level education seen in majority of the studied subjects, addresses a high degree of importance and influence of the oral hygiene in gastric HP infections. Hence, gastroentrologists are required to refer patients to dentists in line of preserving oral and dental health.
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PMID:Correlation between oral hygiene and Helicobacter pylori infection. 2113 68

Periodontitis can cause damage to dental support tissue and affect the function of periodontal ligament cells. Rutin, a common flavonoid, plays a key role in anti-inflammatory responses, tissue repair and bone development. The purpose of this study was to investigate the effects of rutin on the oxidative stress, proliferation, and osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) in an inflammatory environment and the underlying mechanism. Lipopolysaccharide (LPS) was used to stimulate PDLSCs to mimic an inflammatory environment model. Reactive oxygen species (ROS) levels were detected by the dichlorodihydrofluorescein diacetate (DCFH-DA) probe and the oxidative stress factors were tested by an oxidative stress factor detection kit. Moreover, the proliferation of PDLSCs was evaluated by cell counting kit-8 (CCK-8) assay. In addition, the osteogenic differentiation of PDLSCs was determined by alkaline phosphatase (ALP) staining, ALP activity test, alizarin red staining, and alizarin red semi-quantitative analysis. Furthermore, the protein levels of AKT and p-AKT were detected by Western blot. The results showed that rutin inhibited the release of ROS and increased the secretion of oxidative stress factors [superoxide dismutase (SOD) and glutathione (GSH)] and promoted the proliferation of PDLSCs in an inflammatory environment. Moreover, rutin upregulated ALP activity and enhanced the number of mineralized nodules. Conversely, the use of LY294002 (an inhibitor of PI3K) blocked the activation of the PI3K/AKT signaling pathway and prevented the beneficial effects of rutin. In conclusion, rutin promoted the antioxidative stress ability, proliferation and osteogenic differentiation of PDLSCs through PI3K/AKT signaling pathway in LPS-induced inflammatory environment.
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PMID:Effects of rutin on the oxidative stress, proliferation and osteogenic differentiation of periodontal ligament stem cells in LPS-induced inflammatory environment and the underlying mechanism. 3222 58