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However, further studies are needed to demystify this phenomenon. GCF as an inflammatory exudate, responds to the current events within the periodontium and the state of the periodontal tissues that produce it. Leptin has only recently been identified in the GCF, but various other GCF components have already faithfully served as potential diagnostic or prognostic markers for the progression of periodontitis. Since the host response is a critical parameter in evaluating the pathogenesis and progression of periodontal disease, the risk of developing the disease is evaluated using various inflammatory mediators. Results from a pilot longitudinal study pointed to the idea that inflammatory mediator levels within GCF increase over time in periodontitis patients, both in sites with more bone loss as well as relatively stable sites without bone loss [15]. Collection of GCF using micropipettes appears to be the gold standard as it provides an undiluted sample of apparently ��native�� GCF whose volume can be assessed accurately (Griffiths et al.,) [16]. The present biochemical study was aimed to evaluate and S6 Kinase compare the GCF concentrations of leptin in periodontally healthy and diseased subjects with respect to Body Mass Index (BMI) among the study groups as well as to obtain an insight into leptin��s possible role in the initiation and progression of periodontal disease. 60 subjects; 31 males (51.7%) and 29 females (48.3%) between the ages of 30-50 y (Mean age of 39.0 �� 6) who reported to the Department of Periodontology at Meenakshi Ammal Dental College, Chennai, were recruited into the study. The subjects were divided into 3 groups; each group comprising of 20 subjects as Group I (Healthy periodontium), Group II (Gingivitis) and Group III (Chronic periodontitis). Havel PJ et al.,[17] had stated that the concentrations of leptin are significantly higher in women than in men of the same BMI but that the exact cause of higher leptinemia in women remained unclear. Some studies had shown that the leptin levels varied significantly throughout the menstrual cycle [18]. In the present study, we accounted for this variation by evaluating the mean leptin levels (pg/mL) in the males and females [Table/Fig-11] separately although it was not found to be statistically significant in this study. Pregnant women had been excluded from the study because it has been demonstrated that serum leptin levels are higher in pregnant women than in puerperal women, possibly due to an excessive increase of leptin production from maternal adipose tissue that is stimulated by high concentrations of serum estradiol and leptin production from the placenta [19]. The clinical parameters recorded in this study were Modified Gingival Index (MGI), Clinical attachment level (CAL), and radiographic evidence of bone loss.