The impact of smoking on periodontal health: A comprehensive review

Introduction

Periodontal disease, also known as gum disease, is a chronic inflammatory condition affecting the tissues surrounding and supporting the teeth.1 Comprising the periodontium are four primary tissues: the gingiva, periodontal ligament (PDL), cementum, and alveolar bone.

Smoking has long been recognized as a significant risk factor for periodontal (gum) disease, a chronic inflammatory condition that affects the supporting structures of the teeth. The detrimental effects of smoking on periodontal health are well-documented and profound. Smoking compromises the immune response, impairs wound healing, and reduces the effectiveness of periodontal treatments.

Periodontal disease begins with gingivitis, characterized by inflammation and bleeding of the gums. Continued smoking exacerbates this condition, leading to periodontitis, where the gums recede, bone structure supporting the teeth is damaged, and teeth may loosen or even be lost. Nicotine and other compounds in tobacco smoke change the oral environment, fostering the proliferation of harmful bacteria and impairing blood flow to the gums.

Figure 1

Progression of periodontal disease

Periodontal disease primarily caused by bacterial plaque, a sticky, colorless film that constantly forms on teeth. If not removed daily through brushing and flossing, plaque can harden into tartar, which is more challenging to remove and requires professional cleaning. The disease follows a chronic course characterized by periods of activity and remission.1 Eventually, it leads to the affected tooth either falling out or being extracted or necessitates the therapeutic removal of dental plaque.

The disease is influenced by tooth modifiable and non modifiable factors. Modifiable factors include those that can be changed or controlled such as oral hygiene, diet, stress, and various systemic diseases.1 While non-modifiable factors include genetic predispositions and age.

Indeed, the manifestation and progression of periodontal disease can vary significantly based on individual factors such as bacterial flora composition and specific local and systemic influences. Factors like genetics, oral hygiene practices, smoking habits, systemic conditions like diabetes and medications can all influence the development and severity of periodontal disease.2

Smoking is widely recognized as a significant risk factor for periodontitis.

Pathophysiology of Periodontal Disease / Periodontal Microbiology of Smokers

Periodontal disease is triggered by an imbalance in the oral micro biome where harmful bacteria outnumber beneficial bacteria.3

Secondary bacteria such as Fusobacterium nucleatum, take the advantage of that entire oral environment. The oral microbiome, which consists of a complex community of microorganisms, plays a significant role in maintaining oral health. However, an imbalance in this micro biome, referred to as dysbiosis, can be associated with poor host health (i.e. poor oral hygiene tobacco use.4 It can cause harmful bacteria to gather below the gum line. These bacteria release molecules known as pathogen-associated molecular patterns (PAMPs), which then spark inflammation in the intermediate area.

This leads to a rise in Gingival Crevicular Fluid (GCF) from the bloodstream providing a favorable environment for bacteria to thrive. The bacterial community that forms in the periodontal pocket further drives the immune response.

Neutrophils and natural killer (NK) cells are mobilized as part of the innate immune response to fight infection and inflammation. The resulting environment abundant in pro inflammatory cytokines further strengthens the influx of immune cells and the breakdown of nearby tissue.5 This triggers an adaptive immune response where dendritic cells pick up specific antigens and present them to naive T cells. Consequently, T helper cells type 1,2 and 17 are generated, producing a receptor activator of nuclear factor - K B ligand (RANK-L), which accelerates bone loss.1

Normally, harmful organisms would be eliminated, and the recruited immune cells would undergo programmed cell death, allowing for reversible tissue damage, characteristics of gingivitis.1 However, in circumstances not entirely clear, these harmful bacteria persist, evading control by the initial immune response, leading to chronic and unresolved inflammation. This chronic inflammation progresses to fibrous and irreversible damage to gum, tissues, and local bone, defining periodontal disease.6

Smoking affects oral bacteria by altering the oral environment. While smoking is associated with increased plaque accumulation, there isn't substantial evidence to suggest that smoking directly accelerates the rate at which plaque develops. Cigarette smoke contain harmful chemicals that can reduce the mouth's natural defense mechanisms and disrupt the balance of oral organisms. Smoking can lower the oxidation-reduction potential (Eh) in the oral cavity. This change in Eh may create conditions that are more favorable for the growth of anaerobic bacteria, which thrive in low oxygen environments. 4

Effect of Smoking on Periodontal Health

Smoking and Alveolar Bone Loss

Periodontal damage was noted around canines and premolars, which aren't associated with the Molar- Incisor pattern typically observed in localized juvenile periodontitis. Some studies have shown that smoking decreases the mineral content in bone, yet the connection between smoking, osteoporosis, and periodontitis remains ambiguous.15 Furcation defects with severe periodontal damage are typically rare, even among young adults. However, when they do, their treatment tends to be intricate & the prognosis often becomes poorer.

In a radiographic investigation conducted within an older adult population referred to a specialist periodontal clinic. The study revealed that among cigarette smokers, the prevalence of molar furcation was twice as high as compared to non-smokers.16 The present findings conclude that tobacco smoking significantly impacts alveolar bone loss.19 The analysis reveals the influence of tobacco extends beyond soft tissue alone, impacting alveolar bone as well. Tobacco consumption may serve as a complicating factor in the etiology of periodontal disease.

Smoking and Host Immune Response

Smoking impact on the inflammatory response and its impairment of protective mechanisms play a significant role in accelerating periodontal destruction.20 Immune response in the subgingival (below the gumline) environment plays a crucial role in shaping the microbial community present in the oral cavity.

Polymorphonuclear leukocyte PMNs (Neutrophils) are indeed the primary type for defending the body against bacterial invasion through a process called phagocytosis.20 Corberand in 1980 highlights the complex effects of tobacco smoke on PMNs.According to the study, PMN motility was severely depressed by a solution of tobacco smoke concentrate, indicating impairment in the ability of these immune cells to migrate to sites of infection / inflammation.20 Smokers generally have elevated blood levels of PMNs (polymorphonuclear leukocytes) compared to non-smokers. However, the suppression of chemotaxis in smokers relative to now smokers is concerning.16

Cigarette smoking has been shown to activate the release of elastase, an enzyme (released by neutrophils) that plays a role in breakdown of elastin, a key component of connective tissue.2 Elastase has the capacity to cause tissue damage. Destructive effects of elastase, particularly in the context of cigarette smoke exposure, are prominently displayed in lung diseases such as emphysema. When exposed to cigarette smoke, elastase- defined animal models do not develop emphysema. This demonstrates the crucial role of clastase in mediating the tissue damage associated with cigarette smoke exposure and the pathogenesis by emphysema. Moreover, the heightened production of oxygen species induced by cigarette smoking can diminish the tissue levels of α- 1 protease inhibitors. Consequently, this enables elastase & other enzymes, which have the potential to inflict tissue damage, to persist unchecked at active sites within the tissue. Smokers cohibit lower levels of functional elastase & its inhibitor-complex in gingival crevicular fluid compared to non-smoking controls.

Nicotine metabolites have been found to accumulate within the periodontium. This contribute to vasoconstriction, a narrowing of blood vessels, which in turn reduces blood flow to the gums and surrounding tissues. This affects the activity of crucial immune cells including Polymorphonuclear leukocytes and macrophages.

Tobacco use has been associated with elevated levels of neutrophils in peripheral blood. Furthermore, it facilitates their migration through capillary walls.20

Smoking ang Serum IgG

P. gingivalis has the capability to modulate innate host defense functions, including immune subversion of IL-8 secretion, complement activity TLRA activation, through various virulence factors. This modulation ultimately leads to impaired host defense against periodontal pathogens.

In vitro studies have highlighted that nicotine exposure can hinder antimicrobial activities, such as the production of superoxide anion and hydrogen peroxide.13

Separate investigations have also revealed a reduced number of helper lymphocytes among cigarette smokers. This decline could potentially affect both B cell function & antibody production.

Toothbrushing Behavior in Smokers and Non-Smokers

While the exact reasons why smokers tend to have more plaque buildup than non-smokers aren't fully understood.20 One significant factor is the impact of smoking and oral hygiene behaviors. Smokers may be likely to engage in proper oral hygiene practices such as regular brushing, flossing and dental checkups.

Toothbrushing behavior indeed plays a significant role in oral cleanliness. People who brush their teeth regularly tend to have less plaque buildup compared to those who brush less frequently or inconsistently.22

Smokers often exhibit lower toothbrushing efficiency compared to non-smokers. This could be due to various factors such as the adverse effects of smoking on gum health, reduced saliva production and possibly the presence of tobacco stains that may make it harder to visually assess plaque removal.

Furthermore, there is higher calcium concentration in the dental plaque of smokers compared to non-smokers.23 The Male smokers tend to spend less time brushing their teeth compared to age-matched male non-smokers.24

Danielsen's findings between 13 smokers and 16 non-smokers.They indicate that within the confines of an experimental gingivitis model and among healthy adults who already maintain good oral hygiene,there were no significant differences observed in the rate of plaque accumulation between smokers and non-smokers.20

The correlation you've highlighted between smoking behavior and grooming habits, particularly in adolescence, is fascinating. It suggests that while smokers may exhibit less well developed health related behaviors compared to now smokers, they may place a higher emphasis on grooming behaviors.

Individuals with extroverted trails may engage in more impulsive behaviors, such as smoking. Behavioral differences between smokers and non-smokers likely play a significant role in the observed disparities in oral cleanliness.

Smoking and Genetic Variability

Variations among individuals within the species can arise from typical genetic diversity or variations known as polymorphisms. Differences in how individuals respond to conditions or treatments can also be attributed to unique genetic variations among individuals. Having a positive IL-1 genotype boosts the risk of tooth loss by 2.7 times, whereas smoking raises it by 2.9 times. The combined effect results in an estimated 7.7 times higher risk of tooth loss. There was significant attachment loss in genotype positive patients who were smokers.25

In a study involving 323 maintenance patients, researchers observed a correlation between bleeding upon probing and a positive IL-1 genotype among non-smokers.However, the association between bleeding on probing and a positive IL-1 genotype did not achieve statistical significance among smokers. The authors propose that smoking might have a more pronounced effect on the likelihood of bleeding, which could overshadow any detectable influence of the IL-1 genotype within this subgroup.25

In a study involving 154 patients, the authors examined the potential pharmacogenetic interaction between arylamines found in tobacco smoke and the N-acetyltransferase 2 (NAT2) profile in individuals diagnosed with periodontal disease. The process of acetylation plays a role in detoxifying arylamines present in tobacco smoke. NAT2 polymorphisms in the population determine whether individuals are rapid or slow acetylators, influencing this detoxification process. The study results showed that patients with the most severe periodontal disease tended to be slow acetylators, (risk ratio of more than 2). The authors suggest that the impaired metabolism of arylamines could potentially impact the immune response, possibly acting as immunosuppressants.26

In another study, patients with a positive NAT2 genotype were significantly linked to greater severity of bone loss, particularly notable among smokers aged 40-55 years.26 In summary, polymorphisms appear to account for some of the variability observed in disease among patients. However, further studies are needed to fully understand the specific roles these genetic variations play.

Smoking and Cessation

A recent epidemiological study from the United States highlighted a significant drop in teenage smoking after a peak in the mid-1990s, attributed to successful campaigns aimed at deterring smoking among adolescents.27 Many young smokers are addicted to nicotine, and like adults, they face similar challenges with relapse when attempting to quit. Effective prevention programs have shown promise in reducing adolescent smoking rates, emphasizing that preventing smoking initiation during youth can greatly reduce future tobacco use. However, it's important to note that damage done to periodontal tissues from previous smoking cannot be reversed.

In a literature review focusing on health promotion and behavioral strategies to prevent periodontal diseases, Kallio28 outlines the various approaches available to dental professionals at the chair side and within society. Key chair side interventions include taking a brief smoking history and offering advice on quitting smoking, assessing how family and peer influences impact patient behavior, and providing written educational materials.

Collaboration between dental professionals, along with other healthcare providers and administrators, in shaping school policies to implement smoking bans has been highlighted as a successful model of community engagement. A youth intervention study29 demonstrated significant impact, revealing a 22% reduction in lifetime cigarette consumption among participants in the test group compared to controls over a span of 15 years.

Periodontal Treatment in Smokers

Following non-surgical therapy, which includes scaling, root planing and professional teeth cleaning, smokers experienced less favorable healing outcomes in terms of gingival bleeding reduction and pocket depth reduction compared to non-smokers.30

Non- surgical treatments for periodontal disease have shown promising results in both smokers and non-smokers. However, smokers tend to have deeper periodontal pockets. A 5-year study examining non surgical periodontal treatments in 40 patients has revealed significant findings regarding smokers & their oral health outcomes.

Those who smoked were more prone to requiring new surgical interventions compared to non smokers. Smokers in contrast to non-smokers demonstrated poorer outcomes following flap debridement surgery regarding reduction in pocket depth and improvement in attachment levels, particularly in areas with initially deep periodontal pockets.

Investigators studying the longevity of osseointegrated implants in patients with a positive IL-1 genotype observed a notable impact of patients smoking habits on implant survival. They found that smoking influenced the success rate of implants. Smokers explained a 2.5 times higher rate of implant failure, whereas the genetic status (IL-1 genotype) did not emerge as a significant factor affecting implant survival.25

In a follow up study of 3-5 years, focusing on patients with severely resorbed maxilla rehabilitated with implants, researchers noted that the failure rate stabilized after initial 2 years, smokers exhibited a higher incidence of implant failures compared to non-smokers during this period.25

Complications following implant placement were found to be more frequent in smokers, especially in implants where the cover screw was placed. Additionally, the severity of complications was linked to the duration of smoking habits. Smokers (65.3%) exhibited a lower success rate compared to non-smokers (82.7%) implants severely placed in grafted maxillary sinuses.25 Previous studies examining healing outcomes associated with connective tissue grafting have consistently reported a negative influence and poorer root coverage among smokers. Nevertheless, outcomes from guided tissue regeneration procedures in Miller Class 1 or 2 Buccal recessions remained stable over a 4-year period, regardless of whether the patients were smokers and non-smokers.31 The success rate of implant loading in augmented ridges using deproteinized bone mineral after 4-6 years was reported as 43% for smokers and 100% for non-smokers.

In summary, the majority of evidence indicates that surgical and non-surgical treatments are less successful in smokers compared to non-smokers. Clinical studies consistently demonstrated a significant reduction in pocket depth and the number of diseased sites in both smokers and non-smokers.32, 33, 34 Tobacco smoking hinders the healing process following non-surgical periodontal therapy.

Discussion

Smoking is a well-established risk factor for numerous health problems, and oral health is no exception. It significantly increases the risk and severity of periodontal disease, the leading cause of tooth loss in adults. This discussion will delve into the detrimental effects of smoking on each aspect of periodontal health and explore the supporting evidence from various studies.

The foundation of a healthy oral cavity lies in a balanced oral microbiome, where beneficial bacteria coexist with a minimal presence of harmful ones. Smoking disrupts this delicate balance. Study published in the (2020) by Y Jiang et al.21 found that smoking alters the composition of the oral microbiome, promoting the growth of pathogenic bacteria associated with gum disease. This shift weakens the body's natural defense against infection, making individuals more susceptible to developing gingivitis, the initial stage of gum disease.

Smoking triggers a chronic inflammatory response throughout the body, including the gums. This inflammation, as evidenced by study (2018) by FRM Leite et al.35 damages the delicate tissues supporting the teeth. This damage weakens the defense ability to fight off infection and can lead to the progression of gingivitis to periodontitis, a more severe form of gum disease characterized by bone loss and receding gums.

Even when individuals with periodontitis attempt to quit smoking, the damage may already be done. Study (2022) by PM Duarte et al36 demonstrate that smoking hinders the body's ability to heal from periodontal treatment. This can make it more challenging to control periodontal disease and prevent tooth loss Smoking can mask the early signs of gum disease. Healthy gums typically exhibit a pink color and firm texture. However, smoking can constrict blood vessels in the gums, making them appear pale, even when inflammation is present. Consequently, this can delay the identification and management of the condition, allowing the disease to develop further.

The severity of the impact of smoking on periodontal health is directly related to the intensity and duration of the habit. According to the study by Tomar et al. (2000),33 the likelihood of developing periodontitis grows with the number of cigarettes smoked per day and the length of time a person has been smoking. The consequences of neglecting oral health due to smoking extend beyond periodontal diseases.

Conclusion

Although the exact ways in which smoking affects gum tissues aren't fully understood, it remains the most significant avoidable risk factor for periodontal disease. The impact varies based on how long and how much a person smokes. Additionally, the smoking habits of family members may influence behavior and could potentially lead to passive smoking effects, an area that requires more investigation. In addition to its broader systemic effects that can change how the body responds, smoking seems to have substantial local effects that could contribute to the early onset of periodontal disease in young adults who are susceptible.

To effectively pursue our goals of prevention, early disease detection, and timely intervention, the dental profession must prioritize educating young patients about how smoking impacts their gum health. By doing so, dentistry can play a vital role in promoting the overall health and well-being of our youth and future generations. This proactive approach not only addresses periodontal health but also contributes meaningfully to broader public health initiatives.

Source of Funding

None.

Conflict of Interest

None.