Smoking as a risk factor for periodontitis

1) Introduction:

Periodontal diseases are a group of conditions affecting the supporting structures of the dentition. These are multifactorial diseases where many risk factors affect the progression of the disease. Among those risk factors identified for periodontitis are bacterial colonisation, age, gender, socioeconomic status, genetic predisposition, certain systemic conditions and smoking. Tobacco smoking has been found to be a major environmental risk factor associated with generalized forms of severe periodontitis in several studies 1-4. Cigarette smoke contains at least 500 potentially toxic substances, including hydrogen cyanide, carbon monoxide (resulting in carboxyhaemoglobin), free radicals, nicotine, nitrosamines (potent carcinogens) and a variety of oxidant gases (causing platelet activation and endothelial dysfunction).

2) Who is a current smoker, a non smoker and a former smoker ?

According to Centre for Disease Control (CDC) and Prevention, the smokers are classified as:

Current smokers: Those that had smoked ≥ 100 cigarettes over their lifetime and smoked at the time of interview.

Non smokers: Those that had not smoked ≥ 100 cigarettes in their lifetime.

Former smokers: Those that had smoked ≥100 cigarettes over their lifetime but were not currently smoking.

According to number of cigarettes smoked/day, smokers can be classified as:

                Heavy smokers: smoked ≥ 20 cigarettes/day.

                Light smokers: smoked ≤ 19 cigarettes/day.

3) Pharmacology of tobacco smoke products:

Tobacco smokes has two distinct phases: Vapour and particulate phase.

  • Vapour phase: Contains CO2 and upto 5% of CO.
  • Particulate phase:  It is in the form of aerosols and has liquid droplets and solid sub microscopically particles (diameter 0.8 – 1.6μm). It contains tar droplets of the free substance suspended on these tar particles.

Measurement of exposure:

Patient’s exposure to tobacco can be measured by simple question, sophisticated questionnaire and biochemical analysis. The biochemical analysis includes exhaled CO in breath and cotinine (a metabolite of nicotine) in saliva, plasma / serum or urine. Cotinine measurements are more reliable in determining a subject exposure to tobacco smoke because its half life is 14 – 20 hours as compared to nicotine (2-3 hours). Mean plasma and salivary cotinine concentration of regular smokers are approx 300 ngm/ml for non smoker is 2 ngm/ml.

Pharmacokinetics of nicotine:

Nicotine is the main alkaloid found in tobacco, and is responsible for its addictive potential.  Its half life is approximately 2-3 hours and it is most active compound in smoke. During smoking the inhaled nicotine is absorbed through the pulmonary venous rather than the systemic venous system, and thus reaches the brain in 10-20 seconds. It is highly lipid soluble and rapidly enters cell membrane. It is not well absorbed through oral mucosa because of its ionized form. It has action on all parts if body but has predilection for brain and other nervous tissue. Nicotine acts on the nicotinic acetylcholine receptors, specifically the ganglion type nicotinic receptor and one CNS nicotinic receptor. By binding to nicotinic acetylcholine receptors, nicotine increases the levels of several neurotransmitters including dopamine. It is thought that increased levels of dopamine in the reward circuits of the brain are responsible for the euphoria and relaxation and eventual addiction caused by nicotine consumption.

Reward circuit of the brain :The reward circuit of the brain includes the ventral tegmental area (VTA), which is connected to the nucleus accumbens and the prefrontal cortex in the pathway where they communicate through neurons. This is called as reward circuit because it functions to reward and initiates associated pleasurable feelings in response to life sustaining functions, such as eating, to encourage repetition of that function. The main neurotransmitter involved in this circuit is dopamine. When this circuit is activated there is release of dopamine that induces a pleasurable feeling, from the neurons in the VTA. Nicotine and other drugs of abuse increase dopamine levels to sometimes much higher than natural response which causes addiction to these drugs.


 Mechanism of nicotine addiction

Nicotine addiction

4) Evidence for relationship of smoking with periodontitis:

A study done on healthy male Spanish military recruits to find out the degree of periodontal disease and its relationship to smoking revealed higher plaque and bleeding indices in non-smokers although probing depths and attachment loss were greater in smokers 4. Another clinical study done in northern Ireland demonstrated periodontal probing depth in excess of 4mm was more than double in young smokers (15%) compared with 6% in nonsmokers 5. Several studies have shown smoking as a major environmental factor associated with generalized forms of aggressive periodontitis 6-7. Overall many studies in which smokers and non-smokers had similar plaque accumulation or where it was adjusted, have demonstrated that smokers had deeper probing depths 8-11, greater attachment loss 12, 9, 5, 13-14, greater alveolar bone loss 15-17 and greater tooth loss 9, 13.

The strongest evidence in support of this relationship comes from the National Health and Nutrition examination survey (NHANES III), where 12,329 U.S. adults (18 yrs or older) were evaluated for periodontal status in smokers and non-smokers. Results of the study demonstrated that approximately 75% of periodontitis cases were due to smoking.  Out of total periodontitis cases approximately half were either current (41.9%) or past smokers (10.9%) 18.

5) Biological effects of smoking in periodontal disease:

i) Reduced clinical signs of inflammation:

One of the most important biological effects of smoking on periodontal tissues is reduced clinical signs of inflammation. Nicotine in smoke may cause vasoconstriction in the peripheral blood vessels, thus may reduce the clinical signs of gingivitis 19. Many studies have shown decreased clinical signs of inflammation in presence of same amount of local factors in smoking patients as compared to non-smoking patients 20-22. This has been reported that the reduction in clinical signs of gingivitis in smokers is independent of plaque levels 19.

ii) Effect on gingival epithelium:

Heavy smokers often present with a thickened, fibrotic appearance of their gingival tissues. It has been shown that heavy smokers have grayish discoloration and hyperkeratosis of the gingiva. Changes in the epithelium were described as keratotic, hyperkeratotic and hyperplastic 23. Prolonger irritation from tobacco smoke causes changes in oral mucosa causing benign smoker’s keratosis, leukoplakia etc.

iii) Effect on gingival bleeding:

As already explained the initial signs of inflammation of gingiva are suppressed in smokers. Bleeding on probing is the initial sign of inflammation of gingiva. The nicotine present in cigarette smoke stimulates sympathetic ganglia which release neurotransmitters including catecholamines 24. Catecholamines are potent vasoconstrictors causing reduction in blood flow in gingiva. This results in decreased gingival bleeding on probing. The decreased gingival bleeding in smokers can also be attributed to the heavier keratinization of the gingivae in smokers 3. Recent studies done on measurement of gingival blood flow using Doppler Flowmetry have shown either no change or increased blood  flow 25-27. The reason for this may be due to increased blood pressure which overcomes the vasoconstrictive effects of smoking 27.

iv) Effects on gingival crevicular fluid:

Studies have shown a decreased secretion of gingival crevicular fluid in smokers as compared to non smokers 28-29. The reason for this decrease in GCF flow has been suggested to be the vasoconstriction which causes decreased blood flow and hence decreased GCF production.

v) Effects on host immune response:

Various aspects of host immune response are affected by smoking. These include adverse effect on fibroblast function 30, defective chemotaxis and phagocytosis by neutrophils 31-32 and disturbance in immunoglobulin production 33-34. Studies have shown elevated levels of TNF-α in the gingival crevicular fluid of  smokers 35 as well as elevated levels of PGE 2, neutrophil elastase and matrix metalloproteinase-8 (MMP-8) 36. 

Effects of smoking on host response
Changes in vasculature.
Reduced clinical signs of inflammation.
Altered fibroblast attachment and functions.
Altered neutrophil functions.
Increased TNF-α and PGE2 in GCF.
Increased neutrophil collagenases and elastases in GCF.
Increased production of PGE2 by monocytes.
Decreased immunoglobulin production.
Decreased lymphocyte proliferation.
Increase in subgingival pathogenic micro-flora.
Altered cytokine production.

vi) Effects on humoral immune system:

Humoral immune system is also affected by smoking. Macrophages are components of both cellular and humoral immunity. It has been demonstrated that alveolar macrophages from smokers exhibit reduced expression of class II MHC 37-38. Further investigations have shown decreased concentration of serum IgG in smokers 39-43. Along with this serum IgG titers against P. intermedia and F. Nucleatum has been shown to be reduced in smokers 44.

In a study effect of smoking on Immunoglobulin G subclass in young adults with aggressive forms of periodontitis was investigated. Results showed that smoker group with aggressive form of periodontal diseases had depressed IgG immunoglobulin subclasses as compared to non smoker group. Also smoking was not found to depress serum levels of IgG2 in Black subjects except for those with generalized periodontal destruction 45.

vii) Effects on cytokine production:

Recent studies have suggested that smoking influences host cytokine levels. It has been shown that exposure to bacterial lipopolysaccharides in smokers results in significantly more tumor necrosis factor alpha (TNF-α) and Interleukin-6 (IL-6) and also the acute phase protein α2-macroglobulin 46. Other investigations have shown increased levels of tumor necrosis factor alpha (TNF-α) in GCF of smokers as compared to non-smokers 47.

Flow chart showing relationship of tobacco smoking and periodontal disease progression

Effects of smoking

viii) Acute necrotizing ulcerative gingivitis and smoking:

Acute necrotizing ulcerative gingivitis occurs more frequently in smokers. Possible mechanisms for this increased susceptibility include vasoconstriction of gingival blood vessels, reduced activity of leukocytes and proliferation of anaerobic, fuso-spirochaetal micro-organisms. Along with this other factors like poor oral hygiene and mental stress are jointly implicated in the etiology of acute necrotizing ulcerative gingivitis.

ix) Effects of smoking on subgingival micro-flora:

Smoking does not appear to increase the amount of plaque formation when controlling for other factors 48. Smoking causes change in subgingival environment conditions by lowering of the oxidation-reduction potential (Eh), and this could cause an increase in anaerobic plaque bacteria 29. One investigation showed a statistically significant increase in the proportion of Gram-positive to Gram-negative bacteria in 3-day-old plaque from smokers, when compared with the non-smokers 49. Studies have demonstrated an increase in subgingival pathogenic bacteria in smokers. These include Tenerella forsythensis, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans and Treponema denticola 49-51. The changes in oral ecosystem which among other effects also predispose smokers to increased risk of candidiasis. As far as calculus formation is concerned, smokers show more calculus formation as compared to non smokers 52. This may be due to the increased salivary flow rates. There is an increased calcium concentration in fresh saliva in smokers following smoking 53.

x) Effects of smoking on periodontal treatment and post-operative healing:

Smoking has adverse effects on periodontal treatment outcome and post-operative healing. One investigation showed that past smokers and non-smokers responded similarly to treatment and heavy smokers (over 20/day) had higher plaque levels during maintenance and the poorest response to treatment, but did not significantly differ from light smokers 54. Another micro-biological study showed that current smokers had less healing and reduction in subgingival B. forsythus and P. gingivalis after treatment compared with former and non-smokers 55.

Smokers have been shown to have deeper pockets after periodontal therapy than non-smokers, and these pockets continue to harbour quantitatively and qualitatively more pathogenic bacteria than shallower pockets 29. Another factor responsible for reduced healing is reduced fibroblast, PMN and epithelial cell function as well as reduced host defense response. Fibroblasts have been shown to bind and internalize nicotine which is detrimental to their function because of which there is slow production of collagen fibers by these cells and thus periodontal healing is delayed 56.

xi) Effects of smoking on regenerative therapy:

Research has shown that recession sites treated using connective tissue with a partial thickness pedicle graft 55 and a coronally positioned flap alone or with a bioabsorbable membrane 58 found no difference in root coverage between smokers and non-smokers. On the other hand, when guided tissue regeneration procedures were used smokers had significantly less root coverage (57%) compared to non-smokers (78%) 57. Many studies conclude that smoking significantly influenced bone gain or bone fill in periodontal defects after surgery and reduces success of regenerative therapy 60-63.

xii) Effects of smoking on implant therapy:

Studies have shown detrimental effects of smoking on success of implant therapy. One of the initial studies done on smoking and its effects on implant therapy found overall failure rate of 5.92% and specifically implant failure in smokers was 11.28% as compared to 4.76% in non-smokers 64. In fact, success rate of dental implant has been found to be twice in non-smokers as compared to smokers and that too maxillary implants are more affected 65. The smokers showed a higher score in bleeding index with greater peri-implant pocket depth and radiographically discernible bone resorption around the implant, particularly in the maxilla 66. Also studies have shown the benefit of smoking cessation on success rate as well as osseointegration 67. So, patients who are in habit of smoking should be advised to follow a smoking cessation protocol.

6) Smoking cessation:

Studies have shown beneficial effects of smoking cessation on periodontal health. Dentists play an important role in smoking cessation reason being patients visit their dentist more often than their physician, so dentists have more opportunity for patient counselling. Secondly, oral effects of smoking e.g. staining of teeth are visible to patient which can help the dentist to explain effects of smoking on oral and systemic health.

Transtheoretical model of smoking cessation:

This is the most widely used model used for smoking cessation (Prochaska & DiClemente 1983) 68. There are five stages in this model which help the health care providers to understand at what stage the patient is in and what type of support is indicated for smoking cessation by the patient.

Precontemplation stage:

In this stage patient is not aware that the habit is the cause of his/her problem and has no intention of quitting. Here the aim of health provider is to increase the awareness of the problem and to guide them into the contemplation stage.

Contemplation stage:

Now the patient is aware of the fact that smoking is the reason for his/her problems and expresses an intention to stop within 6 months. The aim of health worker is to reinforce and encourage the patient to follow through with their intentions.

Preparation stage:

The patient intends to stop the habit within less than 1 month. Most of the patients at this stage have previously attempted to quit, but without success. Patients are most responsive. Adjunctive therapies should be offered to help the patient in smoking cessation.

Action stage:

In this stage the patient stops the habit and maintains early abstinence. Significant effort should he made to control withdrawal symptoms at this stage, otherwise there are chances of relapse.

Maintenance stage:

The patient has stopped the habit for six continuous months. Continued efforts should he made to prevent relapse.

Cessation advice for health care providers:

The guidelines for health care providers when giving smoking cessation advice include the ‘Five A’s’ which are,

Ask at each appointment about current and past smoking status.

Advise all smokers to quit.

Assess the smoker’s current stage in the transtheoretical model.

Assist the patient in the preparation stage including nicotine replacement therapy (NRT).

Arrange for proper follow-up, and refer the patient to a smoking cessation clinic, if necessary.

Nicotine withdrawal:

There are two types of nicotine withdrawal agents: nicotine containing and non-nicotine containing. These agents are used to replace nicotine and gradually lower patients dependency on smoking.

Nicotine containing nicotine replacement agents:

These contain nicotine and deliver measured amount of nicotine so that gradually the nicotine intake can be reduced. These are available in following forms,

  • Patch: Habitrol, nicoderm. 
  • Gum: Nicoritte
  • Nasal spray: Nicotrol NS
  • Inhaler: Inhaler nicotrol

Nicotine patch:

Patch often preferred route for clinical use because of little compliance problem. Patch is applying to a different skin area to minimize irritation. Three bands of patch are available in different strength according to the patch size and are used for 16 – 24 hours each. Largest patch is used for initial 4 weeks and next smaller size for 2 weeks during stepped withdrawal period. Mid size patch is used initially by patients that are light smokers (i.e. < 10 cigarettes per day) or patients of small stature. One patch used for 16 hours only. Patches are used for 6 weeks after which use is discontinued entirely.

Nicotine Gum:

4 mg nicotine gum is usually preferred when:

  • Skin disease or adhesive allergy result in contraindication to patch.
  • When the patient is not been successful with using the patch
  • As a supplement to patch
  • When gum is preferred by the patient for any reason.

One piece should be used every 1 – 2 hours for 6 weeks, then 2 -4 hours for the next 3 weeks, 4-8 hours for next 3 weeks. The “chew and park” routine is followed for about 30 minutes per piece. Patient must be instructed to chew the gum until the peppery taste is noticeable and then to park the gum as nicotine absorption occurs.

Nicotine nasal spray:

 It’s an option that simulates the rapid delivery affect of cigarette smoking. Recommended dose is 1 spray into each nostril 8 – 16 times daily.

Nicotine oral inhaler:

It resembles smoking. Dosage is 16 cartridges per day.

Use of any of the products is recommended for 8 – 10 week period continued use of nicotine replacement agents beyond 10 – 12 weeks is not recommended.


These are similar for all nicotine supplements.

  • Patient in an immediate post myocardial infarction period.
  • Patient having severe arrhythmias.
  • Patient having severe or worsening angina pectoris.

Specific contraindications:

Skin patches: skin disorder

Nasal spray and inhalation system: asthma/ chronic nasal disorder.

Nicotine gum: TMJ disorder/ denture

Non nicotine agents:

Bupropion hydrochloride:

It is nicotine replacement alternative. It is used as a centrally acting non nicotine agent. Patient strongly depend on nicotine may use bupropion in combinations with a nicotine replacement. Patient medical history, current medical status and behaviour must be carefully evaluated before recommending bupropion. It interacts with may drugs including alcohol antipsychotic agents, hepatic enzyme induces and inhibitor, levodopa and MAO inhibitors. These are concerns because many of these agents potentiate risk of seizures. Use of bupropion differs from nicotine replacement in that bupropion treatment should begin 7-10 days before the patient selected quit date, where as pharmaceutical nicotine substitution should begin on the quit date.

7) Conclusion:

From the above discussion it is clear that tobacco smoking has got adverse effects on various aspects of periodontal health. The toxic substances present in tobacco smoke are one of the risk factors for periodontal disease progression. Studies have shown adverse effects of smoking on healing after non-surgical or surgical periodontal therapy. Also, cessation of smoking has favorable effects on healing and maintenance of periodontal health. Dentists can play an important role in smoking cessation and also help the patients to maintain good periodontal health during maintenance phase of periodontal therapy.  


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