Effect of nicotine on human gingival, periodontal ligament and oral epithelial cells. A systematic review of the literature.

  title={Effect of nicotine on human gingival, periodontal ligament and oral epithelial cells. A systematic review of the literature.},
  author={Richard Holliday and James Campbell and Philip M. Preshaw},
  journal={Journal of dentistry},

Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

First evidence was provided in vitro that nicotine probably exerts a suppressive effect on the production of inflammatory mediators and antimicrobial peptides in human oral epithelial cells.

Long-term exposure to cigarette smoke influences characteristics in human gingival fibroblasts.

The data suggest that long-term smoking habits may reduce wound healing ability, modulate ECM protein homeostasis, stimulate the inflammatory response, and accelerate cellular senescence in HGFs, and consequently accelerate the progression of periodontal diseases.

Evaluation of Salivary Biomarkers of Periodontal Disease Based on Smoking Status: A Systematic Review

The results were interpreted with caution because of limitations in the number of included studies and the study design, and mixed results were observed some studies in detecting glutathione peroxidase, M MP-8, and MMP-14.

Ineffectiveness of ozone therapy in nonsurgical periodontal treatment: a systematic review and metaanalysis of randomized clinical trials

The current evidence indicates that ozone has antimicrobial activity and good biocompatibility with periodontal cells and gingival fibroblasts, but no evidence was found for a positive effect of OT as an adjunct to scaling and root planing.

Heat‐not‐burn tobacco (IQOS), oral fibroblasts and keratinocytes: cytotoxicity, morphological analysis, apoptosis and cellular cycle. An in vitro study

In conclusion IQOS smoke seemed to induce proliferation as highlighted by a viability assay, and migration and cell cycle analysis, and the increased cell proliferation induced by IQOS devices must be carefully investigated for its possible clinical effects on oral cell populations.

Effect of switching from cigarette smoking to the use of the tobacco heating system on periodontitis treatment outcome: Periodontal parameter results from a multicenter Japanese study

The results indicate that SRP improves the course of periodontitis similarly in cigarette smokers and THS users, with a trend toward more favorable outcomes in BoP, PCR, and PD improvement at sites with higher initial PD.

Assessment of oral changes resulting from the use of electronic cigarettes: Literature review

The PubMed database was used and books were used, with the following terms and operators: “electronic cigarette” OR "e-cigarette" OR "electronic cigarettes" AND “oral health” from January 2015 to January 2020.

The effect of smoking on periodontal tissues

This article is a review of the work of domestic and foreign authors on the effect of smoking on periodontal tissues, the mechanism of action of nicotine on the microvasculature, hygiene and soft

The Impact of Smoking on Subgingival Plaque and the Development of Periodontitis: A Literature Review

The mechanism of smoking on subgingival plaque microorganisms represented by the red complex and its effect on the periodontal microecology still need to be further explored.



The effect of nicotine and cotinine on human gingival fibroblasts attachment to root surfaces

Low concentrations of nicotine and cotinine caused a reduction in the initial cell adhesion in comparison with the control group, however, no significant adverse effects on the proliferation of attached cells were seen in the longer period.

Mechanisms of cytotoxicity of nicotine in human periodontal ligament fibroblast cultures in vitro.

Results indicate that thiol depletion could be the mechanism for nicotine cytotoxicity and suggest that factors that induce glutathione synthesis of human PDLF may be used for further chemoprevention of cigarette smoking-related periodontal diseases.

Nicotine-induced alterations in human primary periodontal ligament and gingiva fibroblast cultures

The results confirm clinical oberservations regarding the important role of nicotine as a risk factor in the etiology and progression of periodontal disease.

Effects of tobacco products on the attachment and growth of periodontal ligament fibroblasts.

Tobacco products inhibit attachment and growth of human PDL fibroblasts, which may partly explain the role of these substances in the progression of periodontitis.

Matrix remodeling response of human periodontal tissue cells toward fibrosis upon nicotine exposure

  • Hiroko Takeuchi-IgarashiSatoshi Kubota Yukihiro Numabe
  • Biology, Medicine
  • 2014
Results indicate that nicotine not only impairs fibroblast motility, and induces cellular degenerative changes, but also alters ECM-remodeling systems of periodontal cells.

Effects of nicotine on proliferation and extracellular matrix production of human gingival fibroblasts in vitro.

Results show that, in vitro, nicotine inhibits the growth of gingival fibroblasts and their production of FN and collagen, while also promoting collagen breakdown, which suggests that nicotine itself may augment the destruction of theGingival ECM occurring during periodontal inflammation associated with smokeless tobacco use.

Effects of nicotine on periodontal ligament fibroblasts in vitro.

The results show that nicotine can have direct adverse effects on various functions of the periodontal cells through proliferation, attachment, alkaline phosphatase production and chemotaxis.

Effects of nicotine on the strength of attachment of gingival fibroblasts to glass and non-diseased human root surfaces.

It is shown that the nature of cell attachment to either glass or root surfaces is altered by nicotine, and marked detachment was noted when nicotine exposure was coupled with vigorous agitation at different rpm.

Nicotine increases the collagen-degrading ability of human gingival fibroblasts.

Nicotine increased human gingival fibroblast-mediated collagen degradation, in part through the activation of membrane-associated MMPs.

The effects of nicotine and age on replication and viability of human gingival fibroblasts in vitro.

It appears that the smoking history and the patient age could be relevant for final evaluation of the results, since HGF from smokers are less sensitive to nicotine than H GF from non-smokers, and cells from older donors are more resistant to Nicotine than cells from younger donors.