Gingival Crevicular Fluid Leptin Levels in Periodontitis Patients With Long-Term and Heavy Smoking

Department of Periodontology, Faculty of Dentistry, Süleyman Demirel University, Isparta, Turkey.
Journal of Periodontology (Impact Factor: 2.71). 05/2006; 77(4):634-40. DOI: 10.1902/jop.2006.050277
Source: PubMed


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.

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    • "Research has shown that leptin is mainly produced by the adipose tissue and, at lower levels, by tissues such as the stomach, skeletal muscle and placenta (La Cava and Matarese 2004). Although leptin has been identified in gingival crevicular fluid (GCF; Bozkurt et al. 2006; Karthikeyan and Pradeep 2007a, 2007b; Zimmermann et al. 2012), gingival tissues (Johnson and Serio 2001), dental pulp (Martin-Gonzalez et al. 2012) and even chronic periapical lesions (Kangarlou Haghighi et al. 2010), no systematic study has been conducted to unveil the expression of leptin and its distribution in dental and periodontal tissues. Moreover, insufficient evidence has been obtained in order to determine whether leptin is a result of local production or is transported by circulation, let alone to pinpoint its cellular sources. "
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    ABSTRACT: Imbalance or disruption in the expression of inflammatory mediators contributes greatly to the destruction of the periodontal supporting tissues. Leptin, through binding to its receptor - OBR, has potent effects on immunity and inflammation. However, to date, researches only indicated a role of leptin in periodontitis. No direct or valid evidence exists about how they are regulated by local inflammation, what effects they have and the underlying mechanisms. Experimental periodontitis was induced by ligation of mandibular second molars in beagle dogs. The expressions of leptin, OBR and interleukin (IL)-1β were examined by immunohistochemistry. Meanwhile recombinant human IL-1β was employed to stimulate human periodontal ligament cells (hPDLCs) in vitro, messenger ribonucleic acid (mRNA) and protein levels of leptin were measured using real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Then mRNA and protein levels of IL-6 and IL-8 were measured using real-time PCR and ELISA, after stimulation with various concentrations of leptin, knocking down of all or just the long form of OBR-OBRb by small interfering RNA (siRNA) and incubation with multiple intracellular signaling pathway inhibitors, respectively. Leptin and OBR increased greatly in inflammatory periodontal tissues, which correlated well with the extent of inflammatory infiltration and was a result from the up-regulation in resident cells themselves. High-dose of leptin could induce the expression of mRNA and protein of IL-6 and IL-8 in hPDLCs through binding with OBRb and activating different intracellular signaling pathways. Up-regulated leptin and OBR in periodontitis in turn stimulated pro-inflammatory cytokines expression in periodontal ligament cells to further promote local inflammation.
    Journal of Periodontology 04/2015; 86(7):1-18. DOI:10.1902/jop.2015.150030 · 2.71 Impact Factor
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    • "By contrast, leptin levels are decreased in GCF and gingival tissues in periodontitis patients, as compared to periodontally healthy individuals [53, 62, 66, 67]. In addition, smoking and biomechanical forces also lead to reduced leptin levels in GCF [68, 69]. These studies suggest that periodontitis, smoking, and biomechanical forces impact the local leptin synthesis in periodontium. "
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    ABSTRACT: Obesity is increasing throughout the globe and characterized by excess adipose tissue, which represents a complex endocrine organ. Adipose tissue secrets bioactive molecules called adipokines, which act at endocrine, paracrine, and autocrine levels. Obesity has recently been shown to be associated with periodontitis, a disease characterized by the irreversible destruction of the tooth-supporting tissues, that is, periodontium, and also with compromised periodontal healing. Although the underlying mechanisms for these associations are not clear yet, increased levels of proinflammatory adipokines, such as leptin, as found in obese individuals, might be a critical pathomechanistic link. The objective of this study was to examine the impact of leptin on the regenerative capacity of human periodontal ligament (PDL) cells and also to study the local leptin production by these cells. Leptin caused a significant downregulation of growth (TGF β 1, and VEGFA) and transcription (RUNX2) factors as well as matrix molecules (collagen, and periostin) and inhibited SMAD signaling under regenerative conditions. Moreover, the local expression of leptin and its full-length receptor was significantly downregulated by inflammatory, microbial, and biomechanical signals. This study demonstrates that the hormone leptin negatively interferes with the regenerative capacity of PDL cells, suggesting leptin as a pathomechanistic link between obesity and compromised periodontal healing.
    International Journal of Endocrinology 07/2014; 2014(6):180304. DOI:10.1155/2014/180304 · 1.95 Impact Factor
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    • "They also suggested that a high gingival leptin concentration might be protective in nature for gingiva. Later, Bozkurt et al. [24] evaluated the effects of long-term heavy smoking on GCF leptin levels in periodontitis patients and found that the GCF leptin level was significantly different when nonsmokers and smokers were compared with healthy individuals. The authors suggested the possible role of the leptin receptor expression in the gingiva during inflammation to explain the decrease in GCF leptin levels with increasing clinical inflammatory parameters. "
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    ABSTRACT: Purpose: The present split mouth study evaluates the effect of nonsurgical periodontal treatment on the gingival crevicular fluid (GCF) leptin level in chronic periodontitis. Methods: Ninety sites from 30 nonobese chronic periodontitis patients were selected and divided as follows: group I, 30 healthy sites receiving no treatment; group II, 30 periodontitis sites receiving scaling and root planing (SRP); and group III, 30 periodontitis sites receiving SRP with tetracycline local drug delivery. At baseline, after GCF sampling and clinical parameter recording, the assigned treatment was performed for the study groups. During recall visits, GCF sampling followed by clinical parameter recording was done for groups II and III. Results: Reductions in the probing depth and the clinical attachment level (CAL) were highly significant at different time intervals (except between day 0 and 45) in both groups II and III. Upon comparison, group III showed significant gain in CAL between day 0 and 15 and between day 0 and 45. After treatment, the reduction in the GCF leptin level was more significant in group III than in group II at day 15 but re-elevated almost to the pretreatment levels at day 45. Conclusions: Nonsurgical periodontal therapies were not effective in maintaining stable reduction in the GCF leptin level during the study period.
    Journal of periodontal & implant science 06/2014; 44(3):118-25. DOI:10.5051/jpis.2014.44.3.118 · 1.15 Impact Factor
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