Influence of Smoking on Interleukin-34 Levels in Gingival Crevicular Fluid and Plasma in Periodontal Health and Disease: A Clinico-biochemical Study

Objective: Interleukins (IL) -1β, -34, receptor activator of nuclear factor-kB ligand (RANKL) and osteoprotegerin (OPG) play a crucial role in osteoclastogenesis and bone resorption through modulating inflammatory processes and osteoclastogenesis. Smoking is the major risk factor in the initiation and progression of periodontitis, and adversely affects the outcomes of non-surgical periodontal therapy. To date, there is no study investigating both gingival crevicular fluid (GCF) IL-1β, IL-34, RANKL and OPG levels before and after non-surgical periodontal therapy in smoking and non-smoking patients with periodontitis stage 3, grade B and C. The aim of current research was to examine the GCF levels of some osteoclastogenesis-related cytokines in periodontitis in relation to smoking before and after periodontal therapy. Methods: At baseline, full-mouth periodontal status together with GCF samples were collected from 116 individuals, including 60 periodontitis patients (30 smokers and 30 nonsmokers) and 56 periodontally healthy controls (28 smokers and 28 nonsmokers). Non-surgical periodontal therapy, consisting of instruction for daily plaque control and scaling and root planing (SRP), was performed. GCF sampling and full-mouth periodontal measurements were repeated 6 weeks after completion of SRP. The GCF levels of biomarkers were measured by enzyme-linked immunosorbent assay. Results: The periodontitis groups exhibited significant improvement in clinical parameters. At baseline, the GCF IL-1β levels in periodontitis groups were significantly higher than periodontally healthy controls (p

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“…GCF IL-34 levels decreased in all periodontitis groups at 6-week. This is consistent with the results of other studies with IL-34 (5,(32)(33).…”

Section: Discussionsupporting

confidence: 93%

GCF Levels of Osteoclastogenesis-Related Cytokines in Periodontitis in Relation to Smoking During Non-Surgical Periodontal Therapy

ERENLER¹,

Görgün

2023

Middle Black Sea Journal of Health Science

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“…Salivary and serum IL-34 levels were decreased significantly in smoker and non-smoker periodontitis patients after NSPT. These findings were in accordance with previous reports of altered levels of these markers in GCF (21,24,47) and serum (24,47) in periodontitis and decreased after NSPT (21,47). However, some studies reported that healthy controls showed higher IL-34 levels in saliva (48,49) and elevated after NSPT (49).…”

Section: Discussionsupporting

confidence: 93%

“…In RANKLinduced osteoclastogenesis, IL-34 can replace macrophage colony-stimulating factor (M-CSF) and promote osteoclast differentiation as M-CSF does. A recent study showed that serum and GCF IL-34 levels in smokers were higher than in non-smoker patients, which suggested that smoking may be an essential factor in releasing IL-34 (24). To our knowledge, no study that reported the relationship between smoking and the salivary IL-34 before and after NSPT.…”

Section: Introductionmentioning

confidence: 86%

Clinical and Biochemical Effects of Smoking on Non-Surgical Periodontal Treatment in Grade III Stage C Periodontitis Patients

Arıkan

Görgülü

Dogan

2023

Clinical and Experimental Health Sciences

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Objective: The purpose of this study was to evaluate the effect of smoking on clinical parameters and the serum and saliva levels of RANKL, OPG, and IL-34 in periodontitis stage III grade C (III-C) patients after non-surgical periodontal treatment (NSPT). Methods: A total of 60 subjects, 40 periodontitis-III-C patients (20 smokers and 20 non-smokers) and 20 non-smoker periodontally healthy individuals, were included. All clinical periodontal parameters were recorded, and unstimulated saliva and serum samples were collected from all patients at baseline, but at 1 and 3 months only from periodontitis patients (N=40). Saliva and serum levels of RANKL, OPG, and IL-34 were analyzed by ELISA. Results: At baseline only whole mouth probing depth (PD) and percent of sites with PD>5mm were higher in smokers than non-smoker periodontitis patients (p

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Nicotine suppresses proliferation and mineralized tissue‐associated gene expressions of cementoblasts

Bozkurt

Hakkı

2019

Journal of Periodontology

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BackgroundPrevious studies reported that nicotine, which is the prominent constituent of tobacco, has negative effects on periodontium cells. However, the precise role of nicotine in cementoblast functions remains unclear. In the present study, we investigated the effects of nicotine on the functions of cementoblasts (OCCM‐30) in terms of proliferation, migration, and mineralized tissue‐associated gene expression.MethodsImmortalized murine cementoblasts were exposed to various concentrations (0, 10−6, 10−5, 10−4, 10−3, 10−2, 10−1, 1, 2.5, 5, and 10 mM) of nicotine, and cementoblast proliferation was then evaluated using a real‐time cell analyzer for 142 hours. Using an in vitro wound healing assay, cell migration was evaluated 2, 4, 6, and 24 hours after exposure to different concentrations of nicotine (1, 2.5, 5, and 10 mM). The mRNA expressions of bone sialoprotein (BSP), collagen type I (COL‐I), osteocalcin (OCN), runt‐related transcription factor 2 (Runx2), and alkaline phosphatase (ALP) were assessed in the nicotine‐treated (0, 10−3, 10−2, 10−1, 1, 2.5, 5, and 10 mM) OCCM‐30 cells by reverse transcription quantitative polymerase chain reaction at 8 and 24 hours exposure.ResultsAt concentrations of 1 to 10 mM, nicotine significantly reduced cementoblast proliferation (P <0.01). Exposure to nicotine at other concentrations (1, 2.5, and 5 mM) significantly reduced wound healing rates, whereas nicotine at a concentration of 10 mM immediately decreased the viability of OCCM‐30 cells. Similar results were observed in inverted microscopy images at the highest nicotine concentrations. All concentrations of nicotine decreased the transcripts of BSP and COL‐I in a dose‐ and time‐dependent manner (P <0.001). Nicotine concentrations higher than 1 mM reduced the expression of OCN, RunX2, and ALP in a time‐dependent manner (P <0.001).ConclusionsThis study indicated that nicotine inhibited the proliferation, migration, and mineralized tissue‐associated gene expression of OCCM‐30 cells. These findings suggest that nicotine negatively affects cementoblast function and the formation of new cementum, which is critical for new attachment.

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Influence of Smoking on Interleukin-34 Levels in Gingival Crevicular Fluid and Plasma in Periodontal Health and Disease: A Clinico-biochemical Study

Cited by 9 publications

References 41 publications

GCF Levels of Osteoclastogenesis-Related Cytokines in Periodontitis in Relation to Smoking During Non-Surgical Periodontal Therapy

GCF Levels of Osteoclastogenesis-Related Cytokines in Periodontitis in Relation to Smoking During Non-Surgical Periodontal Therapy

Clinical and Biochemical Effects of Smoking on Non-Surgical Periodontal Treatment in Grade III Stage C Periodontitis Patients

Nicotine suppresses proliferation and mineralized tissue‐associated gene expressions of cementoblasts

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