Smoking and periodontal disease

Rivera‐Hidalgo, Francisco

doi:10.1046/j.0906-6713.2003.03205.x

Cited by 110 publications

(96 citation statements)

References 80 publications

(80 reference statements)

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“…Smoking has been shown as a major risk factor for the onset and development of periodontal diseases [Rivera-Hidalgo, 2003], and a delayed healing response subsequent to periodontal therapies has been demonstrated in smokers [Grossi et al, 1996]. However, it is not clear if nicotine inhibits the wound healing process by delaying wound contraction.…”

Section: Discussionmentioning

confidence: 99%

Nicotine inhibits myofibroblast differentiation in human gingival fibroblasts

Fang

Svoboda

2005

J of Cellular Biochemistry

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Cigarette smoking has been suggested as a risk factor for several periodontal diseases. It has also been found that smokers respond less favorably than non-smokers to periodontal therapy. Previous work in our lab has shown that nicotine inhibits human gingival cell migration. Since myofibroblasts play an important role in wound closure, we asked if nicotine affects gingival wound healing process by regulating myofibroblast differentiation. Human gingival fibroblasts (HGFs) from two patients were cultured in 10% fetal bovine serum cell culture medium. Cells were pretreated with different doses of nicotine (0, 0.01, 0.1, and 1 mM) for 2 h, and then incubated with transforming growth factor beta (TGF-β1) (0, 0.25, 0.5, and 1 ng/ml) with or without nicotine for 30 h. The expression level of α-smooth muscle actin (α-SMA), a specific marker for myofibroblasts, was analyzed by Western blots, immunocytochemistry, and real-time polymerase chain reaction (real-time PCR). Phosphorylated p38 mitogen-activated protein kinase (Phospho-p38 MAPK) activity was analyzed by Western blots. TGF-β1 induced an increase of α-SMA protein and mRNA expression, while nicotine (1 mM) inhibited the TGF-β1-induced expression of α-SMA but not β-actin. Nicotine treatment down-regulated TGF-β1-induced p38 MAPK phosphorylation. Our results demonstrated for the first time that nicotine inhibits myofibroblast differentiation in human gingival fibroblasts in vitro; supporting the hypothesis that delayed wound healing in smokers may be due to decreased wound contraction by myofibroblasts. Keywordshuman gingival fibroblasts; myofibroblasts; α smooth muscle actin; TGFβ; p38 MAP kinase Myofibroblasts are contractile cells that share characteristics of fibroblasts and smooth muscle cells [Tomasek et al., 2002]. One of the major features of myofibroblast differentiation is the expression of smooth muscle cell markers. These markers include α-SMA, γ-SMA, smooth muscle 22 (SM22), calponin, smoothelin, meta-vinculin, h-caldesmon [Halayko and Solway, 2001]. Among these, α-SMA has been suggested as the most reliable marker of myofibroblast differentiation [Gabbiani, 2003]. Also, Dr. Masur's lab demonstrated that myofibroblast differentiation was cell density dependent in corneal fibroblasts. They found that the lower the cell density when cells were seeded in culture, the more cells differentiated into myofibroblasts. However, the myofibroblast phenotype was not terminal. The cells lost the myofibroblast

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Section: Discussionmentioning

confidence: 99%

Nicotine inhibits myofibroblast differentiation in human gingival fibroblasts

Fang

Svoboda

2005

J of Cellular Biochemistry

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“…27 Periodontal parameters, GCF volume and flow rate might be different between smokers and non-smokers. 28 Since the confounding effects of smoking have been neglected in most studies pertaining to gingival enlargement, smokers were excluded from the present study.…”

Section: Discussionmentioning

confidence: 99%

Clinical and pharmacological variables as a risk factor for nifedipine‐induced gingival overgrowth

Güncü¹,

Çağlayan²,

Dinçel³

et al. 2007

Australian Dental Journal

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Background: Gingival enlargement is usually noted within one to two months after the initiation of nifedipine therapy. The aetiology of nifedipineinduced gingival overgrowth is uncertain. The aim of this study was to determine the relationship between plasma and gingival crevice fluid (GCF) nifedipine concentrations and the degree of gingival overgrowth in patients treated with nifedipine, and also to assess the correlations between clinical and pharmacological variables. Methods: Eighteen patients taking nifedipine in regular doses for at least six months participated in the study. Gingival enlargement was evaluated with two indices to score vertical and horizontal overgrowth. Gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), probing depth (PD) and clinical attachment level (CAL) were also evaluated.GCF and plasma nifedipine concentrations were determined by using high performance liquid chromatography. Results: There was no significant difference between responders and non-responders for PI, GI and GBTI. The mean concentration of nifedipine in GCF was significantly greater than concentration in plasma. No significant difference was observed for GCF and plasma nifedipine concentration between responders and non-responders. Conclusions: The present study showed that neither GCF nor plasma nifedipine levels appeared to be a risk factor for nifedipine-induced gingival overgrowth. Improving the oral hygiene in patients using nifedipine may help control the degree of druginduced gingival enlargement.

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“…The survival of osseointegrated implants were signifi cantly infl uenced by the smoking status of the patients. Implant failure was 2.5 times greater in smokers than in non -smokers [83] . In conclusion, smoking is evidently associated with more severe periodontal tissue pathology and poorer response to treatment, as well as a reduction in the regenerative capacity of the oral tissues.…”

Section: Dental Caries 265mentioning

confidence: 94%