Gingival crevicular fluid leptin levels in periodontitis patients with long-term and heavy smoking
ABSTRACT The aim of the present study was to evaluate gingival crevicular fluid (GCF) leptin levels and the influence of long-term and heavy smoking on GCF leptin levels in patients with chronic periodontitis.
In this study, 143 individuals were divided into three groups: non-smokers (NS), smokers (S), and control (C). Three subgroups of NS and S were grouped as follows: a) probing depth (PD) <or=3 mm; b) PD = 4 to 5 mm; and c) PD >5 mm. For each patient, PD, gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), and clinical attachment level (CAL) values were recorded. The GCF leptin levels obtained from sampling sites were determined by using enzyme-linked immunosorbent assay kits.
The GCF leptin levels were found significantly lower in the a and b subgroups in the S group than those in the NS group (P <0.05). The inflammatory markers GI and GBTI showed significant correlations with leptin in NS (P <0.05).
Our results suggest that higher leptin GCF levels in healthy sites in periodontitis patients may play a protective role in periodontal disease. Further studies are needed to determine the cellular origin of the leptin in the gingiva and the effect of plasma leptin levels on GCF leptin concentrations.
- SourceAvailable from: Víctor Sánchez-Margalet
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- "It has been suggested that leptin orchestrates the immune host response by enhancing cytokine production and phagocytosis by macrophages (Fantuzzi & Faggioni 2000, Sánchez-Margalet et al. 2003a,b, Fernández-Riejos et al. 2010). The presence of leptin has been reported both in healthy and inflamed gingival tissues (Johnson & Serio 2001), in gingival crevicular fluid (Bozkurt et al. 2006, Karthikeyan & Pradeep 2007a,b, Dilsiza et al. 2010) and in human chronic periapical lesions (Haghighi et al. 2010). Elevated serum leptin concentration has been associated with increased chronic periodontitis (Gundala et al. 2012). "
ABSTRACT: AIM: To investigate the expression of leptin in healthy and inflamed human dental pulp. METHODOLOGY: Twenty-one pulp samples were obtained from freshly caries- and restoration-free extracted human third molars. In seven-third molars (inflamed pulp group), inflammation was induced prior to extraction. Pulp samples were processed, and leptin expression was determined by quantitative real-time PCR (qRT-PCR) and the amount of leptin by immunoblot. RESULTS: All healthy and inflamed dental pulp samples expressed leptin. Western blot analysis revealed the presence of a protein with an apparent molecular weight of ~16 kDa in human dental pulp, which corresponds to the estimated molecular weight of leptin. The expression of leptin mRNA in dental pulp was confirmed by qRT-PCR analysis, and the size of the amplified fragments (296 bp for leptin and 194 bp for cyclophilin) was confirmed by agarose gel electrophoresis. The expression of leptin in the inflamed pulp group was significantly greater (P < 0.05) than in healthy teeth. The relative amount of leptin in inflamed pulps was almost twice than in healthy pulps. CONCLUSIONS: For the first time, the presence of leptin in human dental pulp tissues has been demonstrated. The upregulation of leptin expression in inflamed pulp samples suggests that leptin can play a role in pulpal inflammatory and immune responses.International Endodontic Journal 09/2012; DOI:10.1111/iej.12009 · 2.27 Impact Factor
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- "One possible explanation is speculated that the secreted leptin may be used up as a substrate during inflammation. Furthermore, the levels of leptin in GCF were demonstrated to be significantly lower in smokers than in non-smokers . "
ABSTRACT: Obesity is associated with an increased risk for developing characteristic features of metabolic syndrome, including hypertension, type 2 diabetes, and dyslipidemia. Interestingly, chronic exposure to periodontal pathogens' endotoxin and increased cytokine production have been proposed to enhance the risk for causing type 2 diabetes and cardiovascular complications. Obesity has also recently been reported to be associated with periodontitis. Obesity induces macrophage accumulation in adipose tissue, promotes chronic low-grade inflammation, and increases adipokines derived from adipocytes. In this review, we summarize recent advances in understanding the roles of adipokines in chronic inflammatory states such as periodontitis and focus primarily on adiponectin, leptin, and resistin. Understanding the role of adipokines may help elucidate relationships among periodontitis, obesity, type 2 diabetes, and cardiovascular diseasesJapanese Dental Science Review 08/2010; 46(2). DOI:10.1016/j.jdsr.2010.01.001
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- "A decreasing leptin level in GCF and gingival tissue is associated with a more deteriorated periodontal status (Johnson and Serio, 2001), and smokers also show reduced GCF leptin levels (Bozkurt et al., 2006), suggesting a protective role of leptin for the periodontium. The relationship between GCF and serum levels of leptin has been recently reported (Karthikeyan and Pradeep, 2007a,b). "
ABSTRACT: A review of pathological mechanisms that can explain the relationship between periodontitis and cardiovascular disease (CVD) is necessary to improve the management of both conditions. Metabolic syndrome is a combination of obesity, hypertension, impaired glucose tolerance or diabetes, hyperinsulinemia, and dyslipidemia. All these have been examined in recent years in terms of their relationship to periodontitis. Reviewed data indicate an association between some of them (body mass index, high-density lipoprotein-cholesterol [HDL-C], triglycerides, high blood pressure, among others) and periodontitis. Oxidative stress may act as a potential common link to explain relationships between each component of metabolic syndrome and periodontitis. Both conditions show increased serum levels of products derived from oxidative damage, with a pro-inflammatory state likely influencing each other bidirectionally. Adipocytokines might modulate the oxidant/anti-oxidant balance in this relationship.Journal of dental research 07/2009; 88(6):503-18. DOI:10.1177/0022034509337479 · 4.14 Impact Factor