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Year : 2008  |  Volume : 19  |  Issue : 2  |  Page : 124-128
Study of the patterns of periodontal destruction in smokers with chronic periodontitis

Division of Periodontics, College of Dentistry, King Saud University, Post Box 60169, Riyadh 11545, Saudi Arabia

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Date of Submission10-May-2007
Date of Decision22-Oct-2007
Date of Acceptance22-Oct-2007


Cigarette smoking is a well-established risk factor for periodontitis and carries an increased risk for loss of periodontal attachment as well as for bone loss.
Aims: The purpose of the study was to investigate the pattern of the intraoral distribution of periodontal destruction among cigarette smokers with periodontitis by assessing the periodontal probing depth (PPD) and clinical attachment level (CAL).
Materials and Methods: Thirty smokers with chronic periodontitis were enrolled in the study. PPD, CAL, plaque index (PI), and bleeding on probing (BOP) were measured. The data was pooled for the anterior sextant and the posterior sextant as well as for the facial and lingual surfaces. The degree of periodontal destruction was compared in these sextants.
Statistical Analysis: Comparisons were made between maxillary anterior, maxillary posterior, mandibular anterior, and mandibular posterior using the one-way analysis of variance (ANOVA) test. When the overall ANOVA showed statistical significance, post hoc testing (Tukey-Kramer multiple comparisons test) was performed to explore the differences between any two groups. P -values <0.05 were considered significant.
Results: The maxillary anterior sextant showed significantly higher PPD and CAL loss than the other sextants. Similarly, the maxillary palatal area showed higher probing depth and clinical attachment loss than the facial sites and the mandibular regions.
Conclusions: From the results it can be concluded that there is variation in the periodontal tissue destruction in different areas of the oral cavity, with the maximum periodontal destruction in the maxillary palatal region. These observations emphasize the deleterious effects of smoking on the periodontal tissues.

Keywords: Attachment loss, bone loss, periodontitis, smoking

How to cite this article:
Anil S. Study of the patterns of periodontal destruction in smokers with chronic periodontitis. Indian J Dent Res 2008;19:124-8

How to cite this URL:
Anil S. Study of the patterns of periodontal destruction in smokers with chronic periodontitis. Indian J Dent Res [serial online] 2008 [cited 2022 Jan 20];19:124-8. Available from:
There is considerable evidence demonstrating the association of periodontal destruction with cigarette smoking. Cigarette smoking is an important risk factor for periodontal disease. [1],[2],[3] Cigarette smokers are five times more likely to develop severe periodontitis than nonsmokers. [4],[5] A meta-analysis of the effects of smoking on periodontal tissue confirmed smoking as a risk factor for periodontal disease with an odds ratio of 2.82. [6] Epidemiological data indicate that smokers have a greater incidence of tooth loss than nonsmokers. [7],[8] Furcation involvement in the molar teeth is also more frequent in smokers than in nonsmokers. [9],[10] These studies suggest that cigarette smoking increases the susceptibility to periodontal pathogens and to tissue destruction. [5],[6]

Cigarette smoking influences periodontal disease through a variety of systemic effects, for example, there is impaired chemotaxis, decreased phagocytosis by both oral and peripheral neutrophils, and reduced antibody production. [11],[12] A substantial body of evidence is available to demonstrate the local detrimental effects of smoking on periodontal health. These local effects include vasoconstriction caused by nicotine as well as decreased oxygen tension, which may create a favorable subgingival environment for colonization by anaerobic bacteria. [13] Although it is possible that the heat from cigarette smoking could have a local effect on the periodontium, there is hardly any scientific evidence to support such an effect. Some studies have reported differences in the pattern of periodontal destruction among smokers, which may imply a localized effect of smoking on maxillary palatal surfaces, especially in the anterior region. [4],[10],[14]

Smokers tend to have greater numbers of deeper periodontal pockets and greater mean periodontal probing depth (PPD). [15],[16],[17] Studies have also shown greater mean clinical attachment level (CAL) loss in smokers compared to nonsmokers. [10],[18] Haffajee and Socransky [19] found that the patterns of attachment loss in smokers and nonsmokers were different. Smokers had more clinical attachment loss and greater probing depth in all areas, with the highest values being in the palatal area. Baharin et al ., [20] in a retrospective comparative study showed that the proportion of sites with bone loss of 4.5 mm or greater was higher in smokers, with the greatest difference being observed in the upper anterior sites.

Even though a few studies have reported that the periodontal destruction pattern may vary in different areas of the oral cavity among smokers, further studies were recommended to prove the relationship. Hence, the present study was undertaken to investigate the intraoral distribution of periodontal destruction pattern among cigarette smokers with periodontitis by studying the PPD and CAL.

   Materials and Methods Top

Study population

A total of 30 systemically healthy smokers aged 25-55 years old were enrolled in the study. They were selected from among the patients who were referred to the periodontology clinic between September 2005 to February 2006 for diagnosis and treatment of periodontitis. Approval of the ethics committee was obtained from the College of Dentistry Research Center (CDRC), King Saud University. Periodontal status of the patients were assessed according the classification of the American Academy of Periodontology. [21] Smoking status was determined based on the daily consumption of cigarettes. [22]

Subjects with a PPD of ≥4 mm in at least 30% of the teeth, and who had smoked a minimum of 20 cigarettes per day for not less than five years, were included in the present study. The following criteria were also used to exclude subjects from the study: (1) age less than 25 or more than 55 years; (2) persons suffering from any chronic medical condition, including diabetes and viral, fungal, or bacterial infections; (3) persons suffering from aggressive periodontitis, periodontal abscess, or necrotizing ulcerative gingivitis or periodontitis; (4) persons who had received periodontal treatment or antibiotics within the preceding three months.

Clinical periodontal examination

An extensive medical history was taken with the help of a printed questionnaire and by interview of 20 to 30 min duration. All clinical measurements were performed by the same examiner. Calibration exercises for probing measurements were performed in five patients before the actual study. The patients' details were masked so that the examiner was blind to the patients' information.

PPD and CAL were measured with a calibrated probe (Williams markings) at the mesio-buccal, mid-buccal, disto-buccal, mesio-lingual, mid-lingual, and disto-lingual aspect of each tooth. The data was pooled for the anterior sextants and posterior sextants for comparison. Further comparison of the PPD and CAL of the facial and lingual surfaces of these sextants were also done. The smoking history was assessed through a standardized interview and a questionnaire. The smoking exposure was expressed in terms of consumption (number of cigarette per day) and duration (in years).

Statistical analysis

Mean PPD and CAL were calculated for the entire mouth, for the upper jaw, the lower jaw, the buccal aspect, the lingual aspect, the anterior teeth, and the posterior teeth. Comparisons were made between upper anterior, upper posterior, lower anterior, and lower posterior using the one-way analysis of variance (ANOVA) test. When the overall ANOVA showed statistical significance, post hoc testing (Tukey-Kramer multiple comparisons test) was performed to explore the differences between any two groups. P-values <0.05 were considered as significant.

   Results Top

[Table - 1] presents the mean percentage of teeth remaining in each region of the mouth. [Table - 2] shows the mean plaque index (PI) and bleeding on probing (BOP) for the four sextants studied. The PI and BOP did not show any statistically significant variations between the maxillary and mandibular anterior and posterior areas of the mouth.

The mean PPD and clinical attachment loss for all regions are presented in [Table - 3] [Figure - 1]. The maxillary anterior teeth had significantly deeper pockets than the posterior teeth and the mandibular region ( P < 0.05) [Figure - 2].

The differences between the lingual and facial sites are presented in [Table - 4]. It was only statistically significant for the palatal sites in the maxilla, with upper anterior palatal sites showing greater probing depth difference ( P < 0.001) than the maxillary anterior facial sites, maxillary posterior buccal sites, palatal sites, lower anterior facial and lingual sites, and lower posterior buccal and lingual sites.

The maxillary anterior palatal sites showed greater mean attachment loss ( P < 0.05) than the maxillary anterior facial sites, the maxillary posterior palatal sites, and the maxillary posterior buccal sites. However, the mandibular sites showed lower mean attachment level loss than the maxillary sites ( P < 0.001).

   Discussion Top

Clinical studies have shown clear associations between smoking and alveolar bone loss, loss of periodontal attachment, and tooth loss. [2],[3],[7],[19] The increased risk of tooth loss may be attributable to the direct effect of tobacco smoking on periodontal tissues. [15] In other words, smokers are assumed to have more periodontal destruction than nonsmokers. Mahuca and colleagues [23] evaluated the degree of periodontal disease and its relationship to smoking habits. They reported higher probing depths and attachment loss in smokers. Smokers diagnosed with severe forms of periodontitis were shown to have more affected teeth and a higher mean loss of periodontal attachment than nonsmokers with these conditions. [18],[24] A number of clinical investigations have reported that cigarette smokers with periodontitis have more extensive periodontal destruction in the maxillary region. However, in this study, significant effects were mainly seen in the palatal anterior region. [25]

The difference in patterns of periodontal destruction in smokers as studied by Haber and Kent [26] was suggestive of a local effect of smoking. Preber and Bergstrom [27] suggested that higher local exposure to cigarette smoke of the palatal maxillary surfaces, as compared to the other areas, could lead to a significant increase in probing depth. Van der Weijden et al . [14] reported that the palatal surfaces of the maxillary anterior teeth showed the highest probing depth and they attributed it to a possible local effect of smoking. Haffajee and Socransky [19] have also reported a difference in pocket depth and attachment level profiles at the palatal maxillary sites. Smokers showed the greatest numerical difference in the mean proportion of sites probing 4 mm and above on the upper anterior palatal surfaces. [20] However, it must be stressed that probing depth proportion cannot be equated with attachment loss, and CAL measurements should also be taken into account for a reliable assessment of periodontal destruction.

The results of the present study were different, in that the mean of periodontal probing depth and attachment loss differ in almost all regions. Data were pooled by maxillary and mandibular regions and facial and lingual surfaces. In the maxilla, the anterior palatal region showed the highest variation from the other segments. These findings were in agreement with previous reports showing maximum periodontal destruction in the maxillary palatal region. [20],[24]

The evidence for the systemic effects of smoking on the periodontium is overwhelming and has been proposed as the most important factor. [12],[28] However, the possibility of an additional local effect of tobacco use cannot be ruled out. The present data suggest that there might be a local effect of cigarette smoking in addition to a systemic effect. Cigarette smoke is more likely to come in contact with the lingual surface of the maxilla, the area where the differences in attachment level and pocket depth values were the greatest. Clearly, there is little controversy regarding the effect of cigarette smoking on the clinical parameters of periodontal disease. What is less clear is the mechanism by which cigarette smoking causes its harmful effects. One of the mechanisms might be an alteration of the subgingival microbiota due to smoking. [22] The reduced gingival crevicular fluid flow reported in smokers means that antibodies and other protective substances derived from the serum will be reduced in quantity. These factors may influence the host defense, increasing the vulnerability to subgingival microbiota at these sites. [29] In addition, smoking may affect the vasculature, the humoral immune system, and the cellular and soluble inflammatory system and may also have effects throughout the cytokine and adhesion molecule network. [30],[31] The importance of these smoking-related alterations and their precise mode of action in increasing the risk of periodontal disease remain to be elucidated.

There is considerable evidence for the role of smoking in the etiology of periodontal disease as well as for its adverse influence on the treatment of periodontitis. In the treatment of periodontal disease in smokers, caution should be exercised in planning advanced periodontal treatment procedures such as regenerative surgery. Smoking influences healing; therefore, the capacity for regeneration, particularly of bone regeneration, may be impeded. [32],[33] The effects of smoking on the outcome of non-surgical periodontal therapy may manifest as less gingivitis resolution, less probing depth reduction, and less attachment gain in smokers. [34] The longer-term effects are evidenced by the fact that 80-90% of periodontal treatment failures occur in smokers. [29],[35]

   Acknowledgment Top

The author wishes to acknowledge Dr. Hamdan Al-Ghamdi for the technical assistance in the compilation of the data.

   References Top

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Correspondence Address:
Sukumaran Anil
Division of Periodontics, College of Dentistry, King Saud University, Post Box 60169, Riyadh 11545
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0970-9290.40466

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  [Table - 1], [Table - 2], [Table - 3], [Table - 4]

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