Evaluation of periodontal status of 380 pregnant women and analysis of the related factors / 实用口腔医学杂志

Objective: To evaluate periodontal status of 380 pregnant women and its related factors. Methods: 380 healthy pregnant women aged 20 to 43 at 10-35 weeks of gestation were enrolled and received a questionnaire and a periodontal examination, in order to compare and analyse the effects of different ages, gestational weeks and educational levels on periodontal condition. Results: The prevalence of periodontal disease of the subjects was 87. 1％. In first (10-15 weeks), second (16-27 weeks) and third (28-35 weeks) trimester PD (mm) was 2. 48 ± 0. 54, 2. 60 ± 0. 54 and 2. 71 ± 0. 48 respectively (P ＜ 0. 05) ; the percentage of PD≥4 mm in 2 or more sites were 76. 5％, 84. 1％ and 93. 5％ respectively (P ＜ 0. 05) ; GI and BI did not show significant differences among of the 3 groups trimester stages (P＞ 0. 05) ; PD in maternal age (year) 20-27, 28-35 and 36-43 years was2. 39 ± 0. 51, 2. 61 ± 0. 53 and 2. 61 ± 0. 56 respectively (P ＜ 0. 05) . A significantly positive linear trend was observed between age and GI (P ＜ 0. 05) or PD (P ＜ 0. 05), but without significant correlation between age and BI. Significant correlation was found between pregnant weeks and PD (P ＜ 0. 05), but without correlation between pregnant weeks and GI (P＞ 0. 05) or BI (P＞ 0. 05) .Conclusion: The prevalence of periodontal disease during pregnancy is high. Meanwhile, the periodontal inflammation is increasing worse with the increase of gestational weeks and maternal age.

Salivary interleukin 6 and sialic acid in periodontitis

Aim: Periodontitis is the major multi ­factorial chronic infectious oral diseases in dentate people. Sialic acid regulates innate immunity response that release cytokines. The study aimed to evaluate interleukin-6 levels in periodontittsis and its relation to clinical features, total sialic acid and its fraction and total proteins to clarify its role. Material and Methods: The study was observational case-control study, carried out in periodontology clinic, College of Dentistry / Erbil /Iraq. A total of 60 participants were recruited in this study, They were divided into three groups: control group represent systemically and periodontally healthy subjects, clinically, diagnosed dentate periodontitis group and partial edentulous group.The data was collected through interview questionnaire, clinical periodontal examination, and biochemical tests for salivary; IL-6.total sialic acid and its fraction, and salivary total proteins Statistical analysis was done by statistical Package for Social Sciences. Results: Statistical analysis showed a significant (P≤ 0.01) highest value of total sialic acid in periodontitis. While the highest value of IL-6 was in partial edentulous group. Old ages increased salivary IL-6 significantly. In periodontitis there was significantly association of IL-6 with probe pocket depth, mobility scores of teeth, protein bonund sialic acid and significant negative association with lipid bound sialic acid in precipitate. While in partial edentulous IL-6 associated significantly with gingival index and free sialic acid in precipitate and negatively with probe pocket depth. Conclusions: Salivary sialic acid and IL-6 are periodontitis biomarkers in dentate. Pleiotropic role of IL-6 can be diagnosed by sialic acid levels. It depends on age, (which affects number of teeth and salivary flow rate), and treatment conditions

Diabetes y su impacto en los tejidos periodontales / Diabetes and its impact on periodontal tissues

Periodontal disease is an infectious disease of inflammatory character whose pathognomonic sign is the formation of periodontal pocket. Your etiological factor is bacteria; necessary but not sufficient for its development as a susceptible host is necessary, because it is a multifactorial disease that responds to risk factors such as snuff and diabetes. The hyperglycemia promotes the formation of advanced glycation end products (AGEs), they alter the stability of collagen and vascular integrity; reducing chemotaxis, phagocytosis and intracellular killing of PMNN; favoringbacterial persistence in the periodontal pocket and periodontal destruction. Monocytes, macrophages and endothelial cells are associated with these AGEs. They secrete more IL-1 and TNF-a; increasing its concentration in the crevicular fluid. Metalloproteinases (MMP), such as collagenase, diabetics are increased by altering the homeostasis of collagen. Alterations in endotelial cells produce changes in coagulation leading to a focal thrombosis and vasoconstriction. Systemic inflammation has an important role in insulin sensitivity function and glucose dynamics, since swelling induces insulin resistance, and this usually accompanies systemic infections. Similarly, periodontal infection may enhance the systemic inflammatory state and aggravate insulin resistance. These events affect the emergence, evolution and periodontal regeneration; having a bidirectional relationship control Periodontitis and diabetes, as both share the same way of perpetuating the disease, inflammation.

PPARgamma Inhibits Inflammation through the Suppression of ERK1/2 Kinase Activity in Human Gingival Fibroblasts

Periodontal disease is a major oral disorder and comprises a group of infections that lead to inflammation of the gingiva and the destruction of periodontal tissues. PPARgamma plays an important role in the regulation of several metabolic pathways and has recently been implicated in inflammatory response pathways. However, its effects on periodontal inflammation have yet to be clarified. In our current study, we evaluated the anti-inflammatory effects of PPARgamma on periodontal disease. Human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) showed high levels of intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-2 (MMP-2), and -9 (MMP-9). Moreover, these cells also showed upregulated activities for extracellular signal regulated kinase (ERK1/2), inducible nitric oxide synthase (iNOS) and cyclooxygnase-2. However, cells treated with Ad/PPARgamma and rosiglitazone in same culture system showed reduced ICAM-1, VCAM-1, MMP-2, -9 and COX-2. Finally, the anti-inflammatory effects of PPARgamma appear to be mediated via the suppression of the ERK1/2 pathway and consequent inhibition of NF-kB translocation. Our present findings thus suggest that PPARgamma indeed has a pivotal role in gingival inflammation and may be a putative molecular target for future therapeutic strategies to control chronic periodontal disease.