Cigarette smoking is a well-established risk factor for periodontal disease and it is the strongest factor among the modifiable ones 1. Research evidence suggests that smokers have a higher tendency to problems such as teeth and bone loss and gingival recession compared to non-smokers, and to the formation of periodontal pockets, which increase the probability to suffer from more severe periodontal disease 2 - 5.
Tobacco can affect the function and proliferation of periodontal cells such as gingival fibroblasts, periodontal membrane cells, periodontal ligament cells and other cells, thus inducing cell apoptosis. It can also affect the invasion of periodontal disease, inhibit the autoimmune defense, and aggravate the inflammation reaction to damage and destroy the alveolar bone.
Oral cancer is a common health hazard, which is also closely related to tobacco. This article reviews the relationship among tobacco, periodontal disease and oral cancer. Searches were limited to studies in English and published from to Inclusion criteria were: articles focused on tobacco and nicotine and focused on any of the six key themes periodontal disease, oral cancer, inflammation, alveolar bone, periodontal cells, and oral bacterial species according to the objective of this review.
Firstly, titles and abstracts were assessed, and then articles were included or excluded based on their relevance. In this review, clinical, microbiological and immunological data regarding tobacco, periodontal disease and oral cancer were collected, compared, analyzed and studied, and the relationship among them was summarized.
Periodontal disease is a common chronic inflammatory disease that causes tooth loss in adults, and it is characterized by the destruction of the supporting structures of teeth including the gingiva, cementum, periodontal ligament, and alveolar bone 6 , 7. It is now recognized that periodontal disease is a multifactorial disease in which plaque is the triggering factor of periodontal disease. Common risk factors for periodontal disease include gender, poor lifestyle such as smoking habit and alcohol consumption, certain systemic diseases such as diabetes, prediabetes, obesity and metabolic syndrome, and genetic factors 8.
The first observation on the relationship between smoking and periodontal tissues occurred in thes, when Pindborg 9 , 10 demonstrated that necrotizing ulcerative gingivitis was associated with tobacco consumption. In general, evidence indicates that smokers have more severe periodontal diseases, with increased bone attachment and tooth loss, gingival recession, and pocket formation compared to non-smokers and there is a dose-response relationship between the number of cigarettes smoked per day and odds of periodontal disease 14 , The dangers of passive smoking have also been emphasized as some evidence linked passive smoking to diseases and death in non-smokers Oral cancer is a common health hazard, with approximately new patients and 2.
Oral cancer is considered as a multi-factor disease, in which tobacco, alcohol and betel quid are the major risk factors Smoking has a significant epidemiological correlation with oral cancer and plays an important role in its occurrence and development.
Smokers are 7 to 10 times more likely to develop oral cancer and 3 times more likely to develop a second primary cancer than non-smokers 20 , In addition, some studies reported a positive correlation between periodontal disease and oral cancer, suggesting that periodontal disease is an independent risk factor for oral cancer, and smoking promotes this correlation 22 - Periodontal ligament cells hPDLCs are the main cell components in the periodontal membrane, and they have chemotactic adhesion, proliferation, biosynthesis and differentiation into cementite and osteoblasts.
Various tissues, such as cementum and alveolar bone, are formed, playing an important role in the maintenance, regeneration and repair of tooth support tissues. Table 1 summarizes the effect of tobacco on periodontal cells. Many of the underlying effects of tobacco products on periodontal tissues may be due to a direct inhibition of normal fibroblast function.
Both gingival fibroblasts hGFs and periodontal ligament fibroblasts PDLFs display reduced cell viability with increasing concentrations of cigarette smoke extract CSE and nicotine 27 , Du et al.
In addition to the direct damage to cells, a study shows that the combination of CSE increases the collagen-degrading ability of hGFs Nicotine, as the main active ingredient in tobacco, increases human gingival fibroblast-mediated collagen degradation, in part through the activation of membrane-associated matrix metalloproteinases MMPs. Indeed, MMP and MMP-2 produced by the nicotine-treated human gingival fibroblasts undergo more readily zymogen activation. Nicotine has an additive effect on human gingival fibroblast-mediated collagen degradation when combined with the presence of P.
Deveci et al. They observed that nicotine increases periodontitis by disrupting the periodontal membrane and prevents the anchorage of teeth in the dental alveoli by disrupting the epithelial structure.
Studies show that nicotine may alter periodontal cells directly via nAChRs, leading to pathophysiological effects and the development of tobacco-related diseases in these cells 34 - Cigarette smoking contributes to the development of destructive periodontal diseases and delays the healing process. Moga et al. They found that nicotine exerts dose- and time-dependent cytotoxic effects.
Ng et al. Generally, smokers have more calculus deposit than non-smokers, and the calculus from smokers is stiffer and more tightly attached to teeth than that from non-smokers. Acquired pellicle attaching to a tooth surface is the initial step for dental biofilm formation, followed by bacterial cell attachment to the acquired pellicle In vitro experiments showed that lower concentrations of nicotine can stimulate oral biofilm formation and influence cell metabolism of biofilm microorganisms Unfortunately, there are still questions regarding the ability of nicotine in increasing the metabolic activity of microorganisms in the oral cavity.
Some studies reported no differences in the prevalence of subgingival species between smokers and non-smokers with periodontitis 41 , Cogo et al. Moreover, the species considered in their study appear not to metabolize these compounds. However, some authors showed that smoking increases the prevalence and amount of some oral bacterial strains Table 2 is a summary of some of the results attesting the factors that increase the bacterial invasiveness due to the presence of tobacco.
Streptococcus gordonii S. Huang et al. Furthermore, Shan et al. These effects may promote later pathogen attachment to tooth surfaces, the accumulation of tooth calculus, and the development of periodontal disease in cigarette smokers.
Moreover, it is found in significantly higher numbers in smokers than in non-smokers, and infection is more persistent in smokers compared to non-smokers With this in mind, the consequences of the presence of P. High doses of CSE and nicotine inhibit bacterial growth, while low doses can increase the biofilm formation of the gingival porphyrins and associated actinobacteria, as confirmed by previous reports 40 , Their results revealed the changes in the proteome of P.
However, Baek et al. It cannot be excluded that a significant change in the protein profile actually occurred, but it was not detectable by visual inspection of gel electrophoresis. Considering the limitations of the current study, it can only be concluded that nicotine has the potential to elicit a stress reaction, and therefore may serve as an environmental modulating factor for bacterial metabolism and survival.
The multiple defence barriers of the periodontal tissue are represented by the epithelial barrier, immune cells, saliva and gingival fluid. This mechanism plays an important role in the persistence of dental plaque in the gingival furrow and the protection of periodontal tissue from bacterial invasion and destruction. Table 3 summarizes the mechanisms by which tobacco can reduce the immune defense of periodontal tissues.
Epithelial cells are recognized as the first line of defence against bacterial infection and environmental harmful stimuli such as cigarette smoke CS. Although previous studies explored the effects of nicotine on host cells, mechanisms used by CS to affect cellular functions remain uncertain.
CSE exposure reduces the pro-inflammatory cytokine burden, which may promote P. Moreover, cell migration and proliferation are key aspects of many biological processes, including wound healing and tissue regeneration During the wound healing process, epithelial cells at the wound edges start to migrate and proliferate to cover the denuded area. This cell migration is necessary for re-epithelialization.
The Imamura et al. It has been reported that neutrophils pretreated with CSE exhibited reduced speed, velocity and directionality compared to untreated neutrophils In addition, tobacco affects the secretion of cytokines and inflammatory mediators from immune cells such as neutrophils and mononuclear cells.
Tobacco may impair the chemotaxis and phagocytosis of neutrophils, modifying the production of cytokines or inflammatory mediators The functional roles of T cells in periodontal disease lesions remain to be elucidated.
On the other hand, P. However, DCs cultured in the presence of nicotine significantly impair T-cell proliferation and reduce host immunity DCs are key mediators between innate and adaptive immunity, and they stimulate naive T cells to differentiate to effector T-cell subsets that may be actively involved in the immunopathogenesis of periodontal diseases.
Other effects of smoking are the decrease in blood flow and impairment of revascularization in the periodontal tissues, thereby causing delayed wound healing. Nicotine causes the contraction of vascular endothelial cells 61 , reducing blood flow, making gingivitis less clinically evident and easy to be missed, reduces the immune cells and gingival crevicular fluid GCF , and may reduce the host immunity during early periodontitis.
Leptin emerges as a pleiotropic molecule involved in several physiological and pathological conditions, and higher leptin levels in healthy sites in periodontitis patients may play a protective role against periodontal disease.
However, Bozkurt et al. Monocyte chemoattractant protein-1 MCP-1 is involved in the activation and recruitment of inflammatory and immune cells to infected sites, thereby mediating a variety of pathophysiological conditions. The Sukumaran et al.
This last aspect is described in detail in the next section. Table 4 shows a summary of the mechanisms by which tobacco aggravates periodontal inflammation. The mechanism of immune inflammation that can accurately explain the aggravation and progression of periodontal disease with nicotine has not been fully elucidated.
Nevertheless, oxidative stress and changes in the immune inflammatory system seem to play an important role. Tobacco exacerbates periodontal tissue inflammatory response. Proteases from host and microorganism play an important role in periodontitis tissue destruction. Proteases break down proteins by hydrolyzing peptides. MMPs are a family of proteolytic enzymes associated with periodontal tissue destruction, which mainly degrade extracellular matrix molecules such as collagen, gel, and elastin Nicotine, which is the major ingredient of cigarette smoke, up-regulates MMP-1, MMP-2 and MMP-3 gene expression in arterial smooth muscle cells, vascular endothelial cells, periodontal ligament fibroblasts and osteoclasts.
Nicotine administration also causes a change in fibroblast activity due to the change of collagen fiber synthesis and decreased MMP2 expression Cytokines are proteins secreted by cells that act as information molecules to transmit signals to other cells. Cytokines have many roles, including initiation and maintenance of immune and inflammatory responses, regulating cell growth and differentiation.
The two cytokines, interleukin IL and tumor necrosis factor TNF , play an important role in periodontal tissue destruction. Reduced growth factor expression by nicotine might contribute, at least in part, to the overall detrimental effects of tobacco use in wound healing and skin diseases. Smoking produces an adverse effect on clinical periodontal variables and alveolar bone height and density, acting as a potential risk factor for alveolar bone loss 73 , These observations highlight the destruction of periodontal tissue by smoking and the unfavorable clinical course of periodontal disease in patients with a cigarette smoking habit.
Table 5 summarizes the effect of tobacco on the alveolar bone. Smoking alters alveolar bone metabolism and therefore can synergistically act on alveolar bone loss Hapidin et al. Eratilla et al. Furthermore, cigarette smoking has a detrimental effect on early bone tissue response around sandblasted acid-etched implant surface topographies and narghile smoking increases peri-implant soft-tissue inflammation and crestal bone loss 80 - Overall, tobacco accelerates the loss of alveolar bone and has a negative effect on the remodeling of alveolar bone during implantation and orthodontic treatment proportional to the dose of CSE and nicotine.
Osteoclast and osteoblast play a key role in bone resorption caused by periodontal disease. Tooth loss is mainly a result of alveolar bone resorption, which reflects an increased osteoclast formation and activation.
Kubota et al. Thus, nicotine at levels found in the plasma of the smokers, has the ability to act directly on osteoclast precursors, inducing its osteoclastogenic differentiation, while in the presence of growth factors such as inflammatory cytokines, the osteoclastogenesis enhancers M-CSF and RANKL induce a significant resorbing increase Nicotine, which is the major ingredient of cigarette smoke, can also inhibit osteoblast differentiation 86 , Katono et al. MMP-2 levels were higher in the exposed rats compared with the non-exposed rats, suggesting that MMP may be one of the molecules responsible for the increased tissue degradation observed in the periodontal tissues of smokers.
MMP is considered as an important factor in periodontal tissue damage because of strong matrix degradation ability. How Is Gum Disease Treated? Prescription mouth rinse or medicine. Surgery to remove tartar deep under the gums. Surgery to help heal bone or gums lost to periodontitis. Your dentist may use small bits of bone to fill places where bone has been lost. Or your dentist may move tissue from one place in your mouth to cover exposed tooth roots.
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Cell Infect. Song, L. Smoking and gum periodontal disease Smoking can cause gum disease. The two stages of gum disease are gingivitis and periodontitis. Preventing tooth loss is important It is important to prevent tooth loss. Teeth also play an important part in holding the shape of the lower part of the face. Smoking increases gum disease risk The risk of gum disease is higher: For a person who smokes less than 10 cigarettes a day, compared to someone who smokes none.
This increases 4 to 5 times more likely for people who smoke heavily. Gum disease may be harder to detect. Bleeding gums — usually an indication of gum disease — may not be present as tobacco causes poor blood supply to the gums. Not respond as well to gum treatment professional dental cleaning as non-smokers.
Severe periodontal disease — the risk increases with alcohol use. At a higher risk of developing acute necrotizing ulcerative gingivitis. This is very painful condition that causes a terrible smell and taste.
Will my gums get better if I stop smoking? Smoking and symptoms of gum disease If you smoke, it is important to see your dentist for regular check-ups. Symptoms of gum disease to watch for include: Red, swollen, tender, bleeding gums.
Discharge pus coming from your gums. Gums that are loose and pull away from your teeth. A bad taste or bad breath. Loose teeth. This can change the feel of your bite when your teeth are placed together or make dentures fit differently.
Spaces opening between your teeth. Smoking and slow healing after dental treatment Tobacco use makes it harder for the immune system to fight infections. Smoking may lead to: Dry socket — a slow healing tooth socket after a tooth removal which is very painful.
Increased pain after oral and gum surgery. Less success if you have dental implants. Contact your dentist if you have any problems after dental treatment. Mouth cancer and smoking risk Mouth cancer or oral cancer is cancer of the mouth including the tongue, cheek, roof or floor of the mouth, and lips. Symptoms of mouth cancer Please see your dentist or doctor immediately if you notice any: Persistent ulcer in your mouth or on your lip that does not disappear after 7 to 10 days, particularly if the ulcer is not painful.
White or red patch in your mouth. Swelling in your mouth. Dentures suddenly not fitting properly. Health risks of vaping Smoking e-cigarettes or water pipes known as vaping — may seem less harmful than smoking regular cigarettes. These include: Nicotine. Heavy metals.
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