Periodontal Status and Hyperlipidemia: Statin Users Versus Non-Users
Dept of Periodontics & Oral Implantology, Government Dental College, Rohtak, Haryana (INDIA).Journal of Periodontology (Impact Factor: 2.71). 04/2012; 84(1). DOI: 10.1902/jop.2012.110756
Background: The association between serum lipids and periodontal disease has been studied predominantly in chronic periodontitis patients with limited data available regarding periodontal status of hyperlipidemic subjects. Meanwhile, the impact of statins on the periodontal health of the population also remains largely under-explored. This study aims to assess the periodontal status among hyperlipidemic subjects and statin users. Methods: In this cross-sectional study, 94 hyperlipidemic subjects (50 on statins and 44 on non-pharmacologic therapy), and 46 normolipidemic controls underwent periodontal examination [plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment level (CAL)]. Biochemical parameters measured included serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) levels. Results: PD and GI were significantly higher in non-statin hyperlipidemics compared to normolipidemic [(P <0.001(PD) and P <0.05 (GI)] and statin group [(P=0.001 (PD) and P <0.05 (GI)]. Periodontal parameters between statin and normolipidemic group did not differ significantly. After adjusting for confounders, positive and significant correlations were observed between PD and TG, TC and LDL while CAL shared correlation with TC and LDL. GI was correlated with TG and TC. Regression analyses revealed that while TC was significantly associated with PD (P <0.001), LDL showed significant association with CAL (P=0.013). TG showed significant association with GI (P=0.020). Conclusions: Our findings suggest that relative to the general population, hyperlipidemic subjects are more prone to periodontal disease. Also, within the limits of this study, it may be stated that statins have a positive impact on periodontal health.
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- "Another reason for the anti-inflammatory effect of statins could be due to the beneficial effects of statins which is mediated through the lowered LDL cholesterol levels, which has been suggested to have anti-inflammatory properties as given by Matsuura et al. Sangwan et al., in his study found that hyperlipidemic patients are more prone to periodontal disease and statins have positive impact on periodontal health. "
ABSTRACT: Statins are the group of lipid-lowering drugs commonly used to control cardiovascular and cerebrovascular diseases. Statins have potential anti-inflammatory effect by blocking the intermediate metabolites of the mevalonate pathway. The objective of this study was to evaluate the anti-inflammatory effect of statin medication in chronic periodontitis patients. Thirty patients of age group between 40 and 60 years were selected from the outpatient pool of Department of Periodontics, Thaimoogambigai Dental College and Hospital, Chennai. Thirty patients selected were grouped into two groups, Group-I consists of patients with generalized chronic periodontitis and on statin medication and Group-II consists of patients with generalized chronic periodontitis. Clinical parameters were recorded and gingival crevicular fluid (GCF) samples were analyzed for interleukin (IL)-1β using commercially available enzyme-linked immunosorbent assay. The mean GCF IL-1β levels in generalized chronic periodontitis patients who are on statin medication (Group-I) were lower than the generalized chronic periodontitis patients without statin medication (Group-II). Reduction of GCF IL-1β levels in statin users indicate that statins have anti-inflammatory effect on periodontal disease.Indian Journal of Pharmacology 07/2013; 45(4):391-4. DOI:10.4103/0253-7613.115017 · 0.69 Impact Factor
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ABSTRACT: Background: Simvastatin is a cholesterol-lowering drug whose pleiotropic effects may have a therapeutic impact on bone. This study evaluates the effect of simvastatin on rats subjected to experimental periodontal disease. Methods: Periodontitis was induced by ligature placement around the maxillary left second molar of rats for 11 days. Groups of six animals received oral saline or simvastatin (3, 10, and 30 mg/kg/day) until sacrifice on day 11. Alveolar bone loss was determined by macroscopic and histologic examination. The serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total alkaline phosphatase (TAP) were evaluated. Gingival myeloperoxidase activity and gingival levels of interleukin-1β (IL-1β), tumor necrosis factor-α, IL-10, reduced glutathione, malonaldehyde, and nitrate/nitrite were analyzed to investigate oxidative stress and inflammation. Expression of inducible nitric oxide synthase (iNOS), matrix metalloproteinases 1 and 8 (MMP-1 and -8), bone morphogenetic protein-2 (BMP-2), receptor activator of nuclear factor κB (RANK), RANK ligand (RANKL), and osteoprotegerin (OPG) were also investigated by immunohistochemistry to assess bone turnover and metabolism. Immunofluorescence microscopy was used to confirm the expression of RANKL in rats' maxillae. Results: Treatment with simvastatin improved alveolar bone loss within all of the parameters studied, thus demonstrating anti-inflammatory and antioxidant activity. Simvastatin reduced expression of iNOS, MMP-1 and -8, RANK, and RANKL and increased BMP-2 and OPG levels in the periodontal tissue. Simvastatin (30 mg/kg) increased TAP activity on day 11 compared with the saline group. No differences were found in the levels of AST and ALT in any of the groups studied. Conclusion: The present data suggest that simvastatin prevents inflammatory bone resorption in experimental periodontitis, which may be mediated by its anti-inflammatory and antioxidant properties.Journal of Periodontology 11/2012; 84(8). DOI:10.1902/jop.2012.120114 · 2.71 Impact Factor
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ABSTRACT: Parodontitis und Atherosklerose zeigen eine hohe Prävalenz, gemeinsame Risikofaktoren und pathogenetische Mechanismen. Der Entzündungsprozess stellt, wie schon von Virchow angenommen, das kausale Verbindungsglied dar. Einige der involvierten Pathomechanismen werden diskutiert. Trotz einer verfrühten Schlussfolgerung der American Heart Association, die auf einer inkompletten Literatursuche basiert, deuten biochemische und klinische Daten auf mehr als nur eine Assoziation hin. Eine Verbesserung der Mundhygiene und Behandlung der Parodontitis wie auch der gemeinsamen Risikofaktoren sollte nicht nur das Fortschreiten der Atherosklerose bremsen, sondern auch zu einer Reduktion bzw. einem späteren Auftreten von Gefäßereignissen führen. Abstract Periodontitis and atherosclerosis have a high prevalence and have many risk factors and pathogenetic mechanisms in common. The inflammatory process, as already claimed by Virchow, seems to be the common link. Some of the pathomechanisms involved are discussed. Despite a premature conclusion based on an incomplete literature search by the American Heart Association, biochemical and clinical data indicate that there is more than only an association. Improving oral health and treatment of periodontal disease and the common modifiable cardiovascular risk factors may impede the progression of atherosclerosis and decrease or delay the later occurrence of vascular events.Stomatologie 03/2013; 110(1-2):27-31. DOI:10.1007/s00715-012-0198-5
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