Smoking Modulates Gene Expression of Type I Collagen, Bone Sialoprotein, and Osteocalcin in Human Alveolar Bone

Campos, Juliana Medeiros de; Prati, Alexandre Javaroni; Cirano, Fabiano Ribeiro; Pimentel, Suzana Peres; Pastore, Gabriel Pires; Pecorari, Vanessa Gallego Arias; Ribeiro, Fernanda Vieira; Casati, Márcio Zaffalon; Casarin, Renato Corrêa Viana

doi:10.1016/j.joms.2015.06.168

Cited by 26 publications

(22 citation statements)

References 53 publications

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“…Experimental animal studies have shown that the regulation of specific molecular ties between collagen fibrils and other matrix components is essential for bone strength and biomechanical properties . Interestingly, molecular analysis of bone biopsies from sites planned to receive dental implants in smokers and nonsmokers, revealed lower expression of OC and BSP, but higher expression of collagen 1 in the biopsies from smokers compared to nonsmokers . Seemingly inconsistent with this finding, the present molecular analysis of the crevicular fluid during the first month after surgical trauma, demonstrated a generally higher expression of OC in smokers compared to nonsmokers.…”

Section: Discussioncontrasting

confidence: 75%

Gene expression in peri‐implant crevicular fluid of smokers and nonsmokers. 1. The early phase of osseointegration

Sayardoust

Omar

Thomsen

2017

Clin Implant Dent Rel Res

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During the early phase of osseointegration, postoperative pain is linked to the inflammatory cell response and, may tentatively serve as an indicator of biological complication and implant loss. The present study suggests that smokers have an altered bone composition and (ultra)structure based on the observations that ISQ values are higher and correlate to recipient bone quality and quantity in smokers.

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Section: Discussioncontrasting

confidence: 75%

Gene expression in peri‐implant crevicular fluid of smokers and nonsmokers. 1. The early phase of osseointegration

Sayardoust

Omar

Thomsen

2017

Clin Implant Dent Rel Res

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“…Clinical studies have indicated that an increased smoking exposure suppresses osteoprotegerin production [32] and increases soluble receptor activator of nuclear factor kappa-B ligand concentration via kappa-B pathway activation [29]. Inflammation and oxidative stress induced by cigarette smoking damage collagen metabolism [33], which is a vital biochemical marker of bone metabolism [34]. In addition, smoking can directly exert toxicity on bone cells [33,35] and increase calcitonin resistance [36], which impedes bone angiogenesis [31].…”

Section: Discussionmentioning

confidence: 99%

Associations of Smoking and Alcohol and Coffee Intake with Fracture and Bone Mineral Density: A Mendelian Randomization Study

et al. 2019

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The causal associations of smoking and alcohol and coffee intake with fracture and bone mineral density are unknown. We investigated the associations using Mendelian randomization (MR). Summary-level data from UK Biobank for bone fractures (main outcome) (53,184 cases; 373,611 non-cases) and estimated bone mineral density (eBMD) (n = 426,824 individuals) were used. Single-nucleotide polymorphisms associated with smoking initiation (n = 378) and alcohol (n = 99) and coffee (n = 15) intake at the genome-wide significance threshold (P = 5 × 10 −8) were identified from published genome-wide association studies. Univariable and multivariable inverse-variance weighted, weighted median, MR-Egger, and MR-PRESSO methods were used for statistical analyses. Genetic predisposition to smoking initiation was associated with fracture but not eBMD. The odds ratio of fracture per one-unit increase in log odds of smoking was 1.09 (95% confidence interval 1.04, 1.15; P = 8.58 × 10 −4) after adjustment for alcohol intake in the multivariable MR analysis. The association remained in complementary analyses. Genetically predicted alcohol and coffee intake was not associated with fracture or eBMD. Nevertheless, genetic liability to alcohol dependence, based on variants in the ALD1B gene, was associated with fracture and lower eBMD. The odds ratio was 1.06 (95% confidence interval 1.01, 1.12; P = 0.018) per genetically predicted one-unit higher log odds of liability to alcohol dependence. This MR study strengthens the causal inference on an association between smoking and higher fracture risk but found no linear association of modestly higher alcohol and coffee intake with fracture or BMD. However, alcohol dependence may increase fracture risk. Keywords Alcohol • Bone mineral density • Coffee • Fracture • Mendelian randomization • Smoking Abbreviations BMD Bone mineral density BMI Body mass index CI Confidence interval DXA Dual-energy X-ray absorptiometry eBMD Estimated bone mineral density MR Mendelian randomization OR Odds ratio SNPs Single-nucleotide polymorphisms Electronic supplementary material The online version of this article (

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“…Smoking and its derivatives deeply affect gingival/peri‐implant tissues, altering capillary density and blood flow, reducing pO 2 , inducing the presence of toxic agents in gingival fluid and altering bone‐related gene expression in bones and the cytokine profile in peri‐implant tissues, which could explain these dissimilarities in microbiota. Additionally, smoking has been demonstrated to have the capacity to alter bacterial functionality or medium characteristics.…”

Section: Discussionmentioning

confidence: 99%

Smoking habit modulates peri‐implant microbiome: A case‐control study

Pimentel

Fontes

Ribeiro

et al. 2018

J of Periodontal Research

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Background and Objective Smoking is a recognized risk factor for peri‐implant disease and leads to microbiological changes in mucositis and peri‐implantitis. However, there is no knowledge about the impact of smoking in healthy peri‐implant tissue. The aim of the study was to evaluate the microbiome in a peri‐implant environment in smokers with healthy peri‐implant conditions. Methods Peri‐implant biofilm was collected around single clinically healthy, screwed‐retained, teeth‐surrounded implants in 12 non‐smoker (NSMK) and 12 smoker (SMK) non‐periodontitis subjects (no bleeding and probing depth <4 mm). Bacterial DNA was isolated and 16S ribosomal RNA gene libraries were sequenced using pyrosequencing, targeting the V3‐V4 region. Datasets were processed using the Quantitative Insights into Microbial Ecology, Greengenes and the Human Oral Microbiome Database databases. Results An evident difference in the SMK peri‐implant microbiome was observed compared to the NSMK microbiome, with a large abundance of species, even with a healthy peri‐implant. The SMK core‐microbiome showed an abundance of Fusobacterium, Tannerella and Mogibacterium, while the NSMK core revealed an abundance of Actinomyces, Capnocytophaga and Streptococcus, genera that are usually related to periodontal health. The microbiome inter‐relationship was shown to be more inter‐generic in SMK then in NSMK, indicating different microbiome cohesion. Conclusion Smoking negatively affected the peri‐implant microbiome, leading to a disease‐associated state, even in clinically healthy individuals.

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Smoking Modulates Gene Expression of Type I Collagen, Bone Sialoprotein, and Osteocalcin in Human Alveolar Bone

Cited by 26 publications

References 53 publications

Gene expression in peri‐implant crevicular fluid of smokers and nonsmokers. 1. The early phase of osseointegration

Gene expression in peri‐implant crevicular fluid of smokers and nonsmokers. 1. The early phase of osseointegration

Associations of Smoking and Alcohol and Coffee Intake with Fracture and Bone Mineral Density: A Mendelian Randomization Study

Smoking habit modulates peri‐implant microbiome: A case‐control study

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