Montaser N. Al-Qutub*
How to CITE:
J Pak Dent Assoc.2011; 20 (2): 83-88
To estimate the pattern of alveolar bone loss among smokers and non smokers.
One hundred and forty medically healthy male patients aged 30 to 55 years participated in the study. Parameters such as periodontal pocket depth (PPD), clinical attachment loss (CAL), bleeding on probing (BOP), and plaque index (PI) were measured clinically and bone loss was measured radiographically using Scion Image Analysis Software. Statistical analysis was performed with the SPSS version 17.0 (Statistical Package for Social Sciences for Windows, SPSS Inc., Chicago, IL USA). P values <0.05 were considered significant.
Clinical parameters such as PPD, attachment loss, BOP, and PI were significantly high among smokers. Radiographically, bone loss for smokers was higher than that observed in nonsmokers (p < 0.05). The maxillary anterior teeth showed significantly higher PPD and CAL than the posterior sextant in smokers when compared to nonsmokers. Percentage of sites with probing depth greater than or equal to 4 mm was high among the smoker group. Higher probing depth and CAL were noticed in the maxillary palatal area than in the facial sites and the mandibular regions. Alveolar bone loss was higher among the smoker group.
The results of the present study indicate that smokers seem to have a greater bone loss compared to nonsmokers. Cigarette smoking may aggravate bone loss resulting from periodontitis.
Periodontitis; Attachment Loss, Bone Loss, Pocket Depth; Radiography; Smoking.
Periodontitis is a local chronic inflammation in the supporting tissues of the teeth leading to bone loss and progressive loss of tooth support 1. This could be the result of alteration in the homeostatic balance between the periodontal bacteria and the host response to these microorganisms2, 3. The primary feature of periodontitis includes marginal inflammation, periodontal pocket formation, attachment loss, and alveolar bone loss 4. Bone loss in one tooth tends to be accompanied by loss in the adjacent tooth, especially due to improper maintenance 5. Radiographs taken from proximal sites suggestive of mild bone loss have demonstrated a progression of the defect one year later 6. Vertical bone loss is regarded as an important symptom of traumatic occlusion or deficient root cementum 7
Smoking is one of the most potential factors in the initiation and progression of destructive periodontal disease 8-11. In addition to smoking, socioeconomic status, behavior, and stress have been identified as potential risk factors for periodontitis 10, 12. Smoking is considered to be an important public health problem in Saudi Arabia. 13
Studies from Saudi Arabia have reported the prevalence of cigarette smoking to be between 8% and 60% 14, 15. The relationship between smoking and periodontal disease has been reported in several published literatures even from the mid-20th century. A study by Arno et al. 16 found a significant relationship between smoking and periodontal diseases. Later, another study by the same author reported a greater bone loss among smokers on examining radiographically 17. Smoking not only affects the periodontal disease patterns but also influences the outcome of periodontal therapy 18.
Excellent periodontal diagnostic procedures will provide the doctor relevant information regarding the type, severity, and location of the periodontal disease. The periodontal probe and intra-oral radiographs are the most commonly used tools for clinical diagnosis of periodontal disease as well as for monitoring the efficacy of the treatment 19. Details on the hard tissue changes can be obtained from the radiographic assessment; it shows the cumulative changes over a period of time. Oral radiological examination of marginal bone level is one way to study the progression of periodontal diseases. But it has also been observed that the amount of bone loss tends to be underestimated by radiographic assessment4, 20, 21. Several studies using different means of diagnostic measures for assessing bone loss such as radiographs, periodontal pocket depth (PPD), and attachment loss measures have supported a pathogenic relation between smoking and periodontitis among different population10, 22- 25. The published literatures provide good evidence to support the fact that a higher level of periodontal disease as well as bone loss is noticed among smokers when compared to nonsmokers 9, 26, 27. Smoking makes the oral tissue more vulnerable to periodontal pathogens, thereby leading 28 to greater bone loss, 9, 10 attachment loss 10, 29, and mean probing depth 9, 24.
The pattern of bone loss in the oral cavity is not clear. Data from some studies suggest that the maximum effect of smoking is noticed in the anterior region. This can be related to the localized effect of smoking on the palatal surface of the oral cavity 8, 29, 30. A similar study conducted by Anil 31 on the same population reported statistical difference in the pattern of tissue destruction in different areas of the oral cavity, with the maximum periodontal destruction demonstrated in the maxillary palatal region. A study by Natto 32 to examine the association between tobacco smoking and periodontal health in Saudi Arabia found that the prevalence of periodontal diseases was significantly greater in water pipe smokers and cigarette smokers compared to nonsmokers. A wide variation in periodontal destruction exists among the different tooth groups. Cross-sectional studies have indicated that some areas of the teeth are more severely affected by periodontal break-down than others, the severity of which increases with age 33, 34. The objective of this study was to estimate the pattern of alveolar bone loss among smokers and nonsmokers.
As many as 140 medically healthy male patients aged 30 to 55 years participated in our study. They were selected between April 2010 and December 2010 from the department of periodontology clinic. Ethical clearance was obtained from the College of Dentistry Research Center (CDRC), King Saud University. The periodontal status of the patients was assessed according to the classification of the American Academy of Periodontology 35. Smoking status was determined based on the daily consumption of cigarettes. Individuals with a PPD of ≥4 mm in at least 30% of the teeth were included in the study. Patients who consumed at least 10 cigarettes per day for a period of over 10 years were included in the smoking group. A Comparative group consisted of nonsmokers (those who had never smoked). Patients suffering from diabetes, aggressive periodontitis, periodontal abscess, or necrotizing ulcerative gingivitis or periodontitis and those who had received periodontal treatment or antibiotics during the preceding three months were excluded from the study. Those who had viral, fungal, or bacterial infections were also excluded from the study. Questionnaires were provided to collect the medical and smoking history. The smoking exposure was expressed in terms of consumption (number of cigarette per day) and duration (in years). All clinical measurements were performed by a single examiner. Calibration exercises for probing measurements were performed in five patients before the actual study. The patients personal information was masked to avoid bias. PPD and CAL were measured at the mesio-buccal, mid-buccal, disto-buccal, mesio-lingual, mid-lingual, and disto-lingual aspect of each tooth using a calibrated probe (Williams markings). In this cross-sectional study 140 sets (one of each patient) comprising of 16 periapical radiographs were analyzed before the start of the treatment. For measuring the alveolar bone loss, the cemento-enamel junction (CEJ) and the alveolar bone crest (ABC) were used as references.
Radiographs were obtained by the paralleling technique by the same operator and machine. An X-ray holder or cone positioner was used during the X-ray exposure. This device enabled the film to be parallel to the long axis of the tooth and the X-ray tube head was aimed at right angles to both tooth and film, enhancing the paralleling technique. Radiographs were digitized with a 5,490 C Hewlett Packard scanner (Hewlett Packard Company, CA, USA) using an XPA device for the digitization of negatives so that no black mask adaptation was necessary. The scanning area was standardized for all films to ensure a higher reliability of digitization. The Radiographs were analyzed using Scion Image for Windows (Scion Corporation, Frederick, MD, USA). The distortion factor was calculated from the known dimensions of the tooth based on the inbuilt feature of Scion Image Analysis Software. The distance between the CEJ and ABC, and between the ABC and AP, measured along the root surface was used to determine the presence or absence of normal alveolar bone, with bone loss thus being defined in relation to root length (Fig. 1). Each image was calibrated. The reference for the calibration of the digitized image was the natural size of the radiographic film (Kodak DF58) of 31 X 41 mm.
Radiographs were excluded according to the following criteria:
a)Visibility of the anatomical landmarks, cemento- enamel junction (CEJ), alveolar bone crest (ABC), or tooth apex (AP) was not clear;
b)Visibility of the CEJ was compromised by the presence of restorations, prostheses, overlapping images, or incomplete X-ray image of teeth;
c)Only one proximal site (mesial and distal) was measurable compromising the “unit of analysis”, that is, teeth.
Statistical analysis was performed with the SPSS version 17.0 (Statistical Package for Social Sciences for Windows, SPSS Inc., Chicago, ILvUSA). P-values <0.05 were considered as significant.
The mean age of the study participants was 35.5 + 5 years (smokers: 39.0 + 3 years and nonsmokers: 32.5 + 3). Of the total participants in the study, 60.71% were smokers and 39.29% were nonsmokers. The mean plaque index (PI) (Table 1) in the anterior sextant of the maxillary arch for the smoker group was higher than that of the nonsmokers (65.65 + 6.73 and 53.23 + 3.67, respectively). Similar observations were noticed in the mandibular arch where the mean PI of the posterior sextant was higher than the anterior sextant in both smokers and nonsmokers.
On analyzing, the mean bleeding on probing (BOP) (Table 1) score was found to be higher among the smoker group than the nonsmoker group. But when compared within the smoker group the PI and BOP did not show any statistically significant variations between the maxillary and the mandibular anterior and posterior region of the mouth. The ANOVA test was performed to analyze the mean PPD and CAL between the two groups. The mean PPD as well as the CAL was significantly higher among smokers compared to nonsmokers (Table II).
Looking at the pattern of distribution among smokers, it was observed that the maxillary anterior teeth had significantly deeper pockets than the posterior teeth and the mandibular region. On analyzing the percentage of sites with probing depth greater than or equal to 4 mm, it was observed that the group of smokers showed a higher percentage in almost all regions when compared to nonsmokers (Table III). The mean PPD (Table IV) in the smoker group was statistically significant for the palatal sites in the maxilla. The upper anterior palatal sites showed the maximum probing depth (P < 0.05) compared to the maxillary anterior facial sites, maxillary posterior buccal sites, palatal sites, lower anterior facial and lingual sites, and lower posterior buccal and lingual sites. Also, when the CAL (Table IV) was observed the maxillary anterior palatal sites in the smoker group showed a greater mean attachment loss (P < 0.05) than the maxillary anterior facial sites, the maxillary posterior palatal sites, and the maxillary posterior buccal sites.
On analyzing the radiographs, a significant difference (p < 0.05) was observed in the bone loss between smokers and nonsmokers. The mean bone loss was 4.55 ± 2.04 mm and 3.04 ± 0.98 mm in smokers and nonsmokers, respectively. There was a significant difference (p < 0.01) in the bone loss between groups of teeth (Table V). There was also a significant difference in the bone loss around incisors (p < 0.01) between smokers and nonsmokers. Regarding the dental arches, it was observed a higher mean alveolar bone loss in the upper arch, but the difference between the lower and upper arch was not significant.
The objective of this study was to measure the bone loss in smokers and nonsmokers. The results of the present study indicate that smokers seem to have a greater bone loss compared to nonsmokers. This clearly shows that cigarette smoking acts as an aggravating factor in periodontitis. This study supports the results of other studies which showed a greater bone loss among smokers when compared to nonsmokers both clinically and radiographically 36, 37. Although the reason for it is unknown, it could be hypothesized that nicotine present in tobacco smoke exerts a vasoactive action on the local tissues.
A higher level of bone loss was observed in incisors than in molars. These results are in accordance with previous studies by Haber and Kent 24 who showed that smoking was associated with more severe and widespread disease as current smokers possessed more affected sites per subject and a higher proportion of deeper sites than nonsmokers. The results of this study show a statistically significant increase in the PPD as well as the CAL among the group of smokers compared to the non-smokers. Grossi et al. 10 have reported a higher likelihood of a more severe attachment loss in smokers compared to nonsmokers and light smokers. The mean periodontal probing depth and attachment loss were different in almost all regions. The BOP and PI were higher for smokers when compared to nonsmokers. This contradicts the findings of Darby et al. 38 who found that the BOP was lower for smokers compared to nonsmokers. However, the study by Preber and Bergstrom 39, 40 reported a lower BOP but a higher PI among smokers. Thus, according to the present results, it can be stated that smoking is an independent risk factor for bone loss and periodontitis. It may also be mentioned here that the immunosuppressive effects of smoking have been well-documented. Smoking causes a reduction in the functional activity of leucocytes and macrophages in the saliva and the crevicular fluid as well as a decrease in the chemotaxis and phagocytosis of blood and tissue PMNs. It modifies the local and systemic host resistance and favours the proliferation of anaerobic bacteria, thus predisposing the periodontal structures to disease progression. Though this study is an additional evidence of smoking having an adverse effect on periodontal bone loss, its effects on the periodontal health of two-thirds of the world population in developing countries needs to be further investigated using well- organized representative samples.
One of the limitations of the study is that the non- standardized radiographs were used to assess the extent of alveolar bone loss. Within the limits of this study it may be concluded that cigarette smoking may aggravate bone loss resulting from periodontitis. It leads to deeper periodontal pockets and also plays an important role in the intra-oral distribution suggesting a local effect. The implications are that smoking cessation efforts should be considered in the treatment of periodontitis.
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