|Year : 2020 | Volume
| Issue : 1 | Page : 20-25
Types of bone destruction and its severity in chronic periodontitis patients with tobacco smoking habit using periapical radiographs and transgingival probing: A cross-sectional study
B J Janardhana Amaranath, Neelam Das, Ira Gupta, Rohit Gupta, Bijoy John, Munishwar Parvathi Devi
Department of Periodontology, Rama Dental College Hospital and Research Centre, Kanpur, Uttar Pradesh, India
|Date of Submission||01-Apr-2019|
|Date of Decision||16-Jun-2019|
|Date of Acceptance||24-Jun-2019|
|Date of Web Publication||04-Oct-2019|
Dr Neelam Das
H. No. 27c, Patel Nagar, P.O. Harjinder Nagar, Kanpur - 208 007, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Tobacco smoking is an independent risk factor for periodontal disease which increases periodontal pocketing, attachment loss, as well as bone loss leading to varied severity and bone destruction in the form of horizontal and vertical patterns. Aim: The aim of the present study is to determine and measure the types and severity of bone destruction in chronic periodontitis (CP) patients with tobacco smoking habit using intraoral periapical (IOPA) radiographs and transgingival probing. Materials and Methods: A total of 60 male participants with CP were included in the study. Group A comprised 30 heavy cigarette smokers and Group B comprised 30 nonsmokers. Clinical parameters such as plaque index (PI), probing pocket depth (PPD), and clinical attachment loss (CAL) were recorded. Amount and pattern of bone loss were assessed using IOPA and transgingival probing. Results: The mean values of PI, PPD, and CAL were 2.50 ± 0.28 mm, 9.33 ± 1.42 mm, and 10.2 ± 1.62 mm, respectively, for cigarette smokers, which were found to be higher and statistically significant as compared to nonsmokers. Cigarette smokers showed more bone destruction than nonsmokers in respect to maxillary molars 4.42 ± 1.31 mm and incisors 3.90 ± 1.10 mm as compared to nonsmokers. Types of bone destruction were more of vertical patterns (93.3%) in cigarette smokers. Conclusions: Tobacco smoking was associated with severe attachment loss. Tobacco smoking not only affects soft tissues but also hard tissues such as bone. Palatal sides of maxillary molars showed significantly higher bone loss and also had more percentage of vertical patterns of bone loss compared to nonsmokers. IOPA and transgingival probing may be used as noninvasive methods for the determination of types and severity of bone destruction in CP patients with or without tobacco smoking habit.
Keywords: Attachment loss, chronic periodontitis, horizontal bone loss, independent risk factor, pattern of bone destruction, tobacco smoking habit, transgingival probing, vertical bone loss
|How to cite this article:|
Amaranath B J, Das N, Gupta I, Gupta R, John B, Devi MP. Types of bone destruction and its severity in chronic periodontitis patients with tobacco smoking habit using periapical radiographs and transgingival probing: A cross-sectional study. J Indian Soc Periodontol 2020;24:20-5
|How to cite this URL:|
Amaranath B J, Das N, Gupta I, Gupta R, John B, Devi MP. Types of bone destruction and its severity in chronic periodontitis patients with tobacco smoking habit using periapical radiographs and transgingival probing: A cross-sectional study. J Indian Soc Periodontol [serial online] 2020 [cited 2020 Jun 5];24:20-5. Available from: http://www.jisponline.com/text.asp?2020/24/1/20/268610
| Introduction|| |
Habit of tobacco smoking is a most important environmental risk factor for destructive periodontal disease. It has a specific effect on the bony component of periodontal tissue support and increases the risk by 2–3-fold. The WHO (World Health Report, 2015) has reported that 1.3 billion people are cigarette smokers worldwide. Tobacco smoking is the practice of smoking and inhaling tobacco smoke by water pipes, cigars, bidis, and cigarettes. It affects pathogenesis of the periodontal disease in an individual and changes the periodontal disease patterns and affects periodontal therapy outcomes. Alveolar bone level measurement in periodontal disease is very important because it may affect planning of periodontal surgery, treatment response, and prognosis. Surgical approach is the most accurate procedure for obtaining this measurement, but it is an invasive procedure.
Hence, in this study, intraoral periapical (IOPA) and transgingival probing were used as relatively noninvasive methods for determination and measure the types and severity of bone destruction in chronic periodontitis (CP) patients with or without tobacco smoking habit.
The aim of this study is to determine and measure the types and severity of bone destruction in CP patients with tobacco smoking habit using IOPA and transgingival probing.
Objectives of the study
- To investigate the types of bone destruction in CP patients with tobacco smoking habit
- To assess the severity of bone destruction in CP patients with tobacco smoking habit
- To determine site predilection if any for severe bone loss in CP patients with tobacco smoking habit
- To compare the types and severity of bone destruction in CP patients with or without tobacco smoking habit.
| Materials and Methods|| |
A cross-sectional study was conducted on 60 male participants with CP aged between 30 and 50 years, who had visited the department of periodontology. Study groups comprised 30 heavy cigarette smokers (smoked ≥20 cigarettes/day) in Group A and 30 nonsmokers in Group B. Details of smoking habits were obtained through the prepared questionnaire about the duration and number of cigarettes per day. Written consent from the patients and ethical clearance was taken from the Institutional Ethical Committee.
Systemically healthy male patients with CP having minimum of 1 mm clinical attachment loss (CAL), aged between 30 and 50 years, who have been smoking a minimum of ≥20 cigarettes/day for more than 10 years were included in the study. Whereas, participants with abnormal tooth morphology, with the teeth having crown or restorations extending till or beyond cementoenamel junction (CEJ), significant medical history such as diabetes and viral, fungal/bacterial infections, patients who had received periodontal treatment in the past 6 months, or patients suffering from aggressive periodontitis/periodontal abscess/NUG/oral submucous fibrosis (limited mouth opening makes it difficult to check pockets in lingual and palatal surfaces), and past smokers were excluded from the study.
The clinical parameters recorded for all the study participants included plaque index (PI) by Silness J. and Loe H., probing pocket depth (PPD), CAL, and patterns of bone destruction, which were assessed through radiographic examination (IOPA) and transgingival probing.
PPD and CAL were recorded at six sites  – mesiobuccal, midbuccal, distobuccal, mesiolingual, midlingual, and distolingual areas per tooth using UNC-15 periodontal probe.
Radiographic evaluation to determine bone destruction and types of bone loss at interproximal areas was carried out with full-mouth intraoral periapical radiographs (14-IOPA) in CP patients with or without tobacco smoking habit using paralleling technique. All the radiographs were taken by single examiner using standard film holder and Kodak insight dental film size 1.3 cm × 4 cm. Exposure time was adjusted to 0.25 s, and the films were processed by automatic X-ray film processor (Velopex Intra-X automatic dental X-ray film processor). Interdental bone loss was measured by mounting IOPA on the X-ray viewer. The measurement of the distance between CEJ and alveolar bone crest (ABC) was calculated by Electronic Digital Vernier Caliper, calibrated to the nearest 0.5 mm, and magnifying lens was used to enhance accuracy of reading. There was a single examiner involved in recording the measurements from the radiographs. On each proximal site of radiographic image, the bone level was measured directly from CEJ to the ABC using Electronic Digital Vernier Caliper by placing one pointed beak of calipers at CEJ and another at the alveolar crest [Figure 1].
|Figure 1: Measurement of bone destruction from intraoral periapical radiograph using digital vernier caliper|
Click here to view
Interproximal bone loss is defined as “the distance between CEJ and ABC measured in millimeters.”
The landmarks for measuring interproximal bone loss was from CEJ to ABC. ABC is the most coronal level where the periodontal membrane retained its normal width. When an infrabony defect was present, the measurement was made to the apical border of the radiolucency, or when radiographic image indicated differing heights of ABC, the most apical level was chosen.
The following formula was used to calculate alveolar bone loss (ABL) on each proximal surface:
ABL = (Distance from CEJ to ABC) – 2 mm
Subtraction of 2 mm from the CEJ to ABC distance was adopted as a criterion in the formula used because the normal radiographic distance between CEJ and interproximal ABC is 2 mm.
ABL is considered to be radiographically imaged at the most cervical level along the proximal root surface, where periodontal ligament started to be of equal width.
Bone loss is considered to be horizontal, when bone loss is perpendicular to the long axis of tooth, along the whole length of the ABC, with the occurrence of resorption of the buccal and lingual cortical plates, including interproximal bone. Whereas, bone loss is considered to be vertical when it is occurring in a vertical or oblique direction as compared to the long axis of the tooth resulting in a hollowed-out trough within the bone, alongside of a root surface, while the base of the defect is located apical to the surrounding bone.
Transgingival probing to assess bone loss facially and lingually was done as per method described by Greenberg. The bone sounding procedure was performed with an adequate local anesthesia, and UNC-15 periodontal probe attached with rubber stopper was used to measure the distance from CEJ to ABC on buccal and lingual sides of a tooth, at midbuccal, mesiobuccal, distobuccal, mesiolingual, distolingual, and mid-lingual areas. The probe was placed in a coronoapical direction, held against the tooth, and advanced apically so that the rubber stop would stay at the buccal/lingual edge of the occlusal surface while the probe was advanced beyond the gingival crest into the sulcus until osseous tissue was felt and this distance was recorded. Thus, recorded measurement indicates the distance from the occlusal surface to the estimated location of the bony crest [Figure 2]a and [Figure 2]b.
|Figure 2: (a) Transgingival probing to assess bone destruction facially and lingually; (b) usage of digital vernier caliper to measure the distance obtained in the probe through transgingival probing|
Click here to view
ABL by transgingival probing (TGP) on the facial and lingual surface was calculated using the following formula:
ABL = (Distance measured from Occlusal edge to alveolar bone crest – Distance measured from Occlusal edge to CEJ) – 2 mm (Biologic width)
Two milliliters was subtracted because it corresponds to Biological width, in periodontally healthy teeth. It is the histological distance from the top of ABC to the bottom of gingival sulcus.
The IBM SPSS Statistics 21.0, United states was used to analyze the data collected. It included calculation of means, standard deviation, and percentages. Comparison of continuous variables between cigarette smokers and nonsmokers was made using the Student's unpaired t-test, whereas for paired observations between related groups, paired t-test was used. Chi-square test was used to analyze the difference between categorical variables. All values were considered as statistically significant for a value of P ≤ 0.05. Sample size has taken from previous studies of this topic, i.e., 60 sample size, 30 participants in each group that sample size is estimated 5% α error and 85% power of the test.
| Results|| |
The mean plaque score was found to be 2.50 ± 0.28 and 1.42 ± 0.30 in cigarette smokers and nonsmokers, respectively [Table 1]. In maxillary teeth, mean PPD score for cigarette smokers and nonsmokers was 4.95 ± 0.72 mm and 3.91 ± 1.05 mm, whereas in mandibular teeth, mean PPD score for cigarette smokers and nonsmokers was 4.38 ± 0.70 mm and 3.54 ± 1.40 mm, respectively [Table 2]. The mean CAL score in maxillary teeth for cigarette smokers and nonsmokers was 5.50 ± 0.90 mm and 4.63 ± 1.01 mm, whereas mean CAL score in mandibular teeth for cigarette smokers and nonsmokers was 4.65 ± 0.72 mm and 4.04 ± 0.71 mm, respectively [Table 3]. In maxillary teeth, mean values of interproximal bone loss for cigarette smokers and nonsmokers were 3.70 ± 0.96 mm and 3.05 ± 1.04 mm, whereas in mandibular teeth, mean values of interproximal bone loss for cigarette smokers and nonsmokers were 2.67 ± 0.66 mm and 2.20 ± 0.63 mm, respectively. Whereas, maxillary molars were associated with highest interproximal bone loss 4.42 ± 1.31 mm compared to other teeth [Table 4]. The mean values of facial and palatal bone loss in maxillary teeth for cigarette smokers and nonsmokers were 3.16 ± 0.89 mm and 2.45 ± 0.89 mm, whereas in mandibular teeth, mean values of facial and palatal bone loss for cigarette smokers and nonsmokers were 2.24 ± 0.61 mm and 1.81 ± 0.63 mm, respectively. Whereas, palatal side of maxillary molars was associated with the highest bone loss of 3.68 ± 1.11 mm compared to buccal sides of other teeth [Table 5]. While comparing interproximal bone loss pattern among cigarette smokers and nonsmokers, cigarette smokers had 93.3% of vertical bone defects and 6.7% of horizontal bone defects, whereas nonsmokers had 40.0% vertical defects and 60.0% of horizontal defects [Figure 3]a and [Figure 3]b. Overall, the mean score values for PI, PPD, CAL, and bone loss scores by transgingival probing and radiographic examination were found to be higher in cigarette smokers as compared to nonsmokers and were statistically significant (P ≤ 0.05).
|Table 2: Intra and intergroup comparison of probing pocket depth for cigarette smokers and nonsmokers|
Click here to view
|Table 3: Intra and intergroup comparison of clinical attachment loss for cigarette smokers and nonsmokers|
Click here to view
|Table 4: Intra and intergroup comparison of interproximal bone destruction as assessed by intraoral periapical radiograph for cigarette smokers and nonsmokers|
Click here to view
|Table 5: Intra and intergroup comparison of buccal and lingual/palatal bone destruction as assessed by transgingival probing for cigarette smokers and nonsmokers|
Click here to view
|Figure 3: (a) Comparison of interproximal bone destruction pattern among cigarette smokers; (b) comparison of interproximal bone destruction pattern among nonsmokers|
Click here to view
| Discussion|| |
This study was conducted to determine and compare the types and severity of bone destruction between cigarette smokers and nonsmokers with CP. Higher scores of PPD and CAL were associated with maxillary teeth of cigarette smokers compared to nonsmokers. Similar findings were observed in the studies of Rosa Griffiths Martel.
Periodontal tissue destruction in cigarette smokers is attributed to nicotine-induced toxic effects. Several literature reviewed the effect of nicotine on bone resorption. Tobacco smoke is a complex mixture of chemicals and consists of cytotoxic substances such as nicotine. Nicotine is one of the chemicals with pharmacological and toxicological negative effects on human health. The nicotine is on an average 8–9 mg in one cigarette of tobacco. Cigarette smokers absorb 1 mg of nicotine per cigarette which produces vasoconstriction, reducing blood flow and edema, which leads to the activation of the sympathetic nervous system, acceleration of heart rate and increased blood pressure, as well as masking of the early signs of periodontal inflammation such as gingival inflammation, redness, and bleeding. Tobacco contains alkaloid nicotine that exerts cytotoxic effects on periodontal fibroblast function, which is critical for the maintenance of periodontal tissues and wound healing. Nicotine exaggerates the response of interleukin-6 and tissue necrosis factor-alpha in osteoclasts. Nicotine also aggravates the bone resorption by activating tissue-type plasminogen activator, prostaglandin E2, and matrix metalloproteinase. Another mechanism of bone loss in cigarette smokers is due to suppression of osteoprotegerin production and change in RANKL/OPG ratio. Tobacco smoking also impaired the numbers of T-helper lymphocytes, which are essential to B-cell activation and antibodies production. The combined effect of alternation in microbial profile and host mechanisms is responsible for drastic periodontal tissue destruction in cigarette smokers.,,,
In this study, interproximal bone loss was found to be more in maxillary teeth of cigarette smokers, compared to mandibular teeth, and palatal sides also showed significant bone destruction; these findings are in accordance with the several earlier studies, which demonstrated that the palatal surfaces of maxillary teeth are more subjected to periodontal destruction due to the localized and direct effects of tobacco smoking. Similar findings were observed in Bergström  who found the higher mean distance between CEJ and ABC in molars and incisors of maxillary teeth compared to mandibular teeth.
Ramli and Taiyeb Ali  and Schuller and Holst  stated that the greater loss of alveolar bone in the maxillary region may indicate that the tobacco smoking affects maxillary more than the mandibular region. The difference of CEJ-ABC distance in maxilla and mandible can be explained by the difference in bone density between the two arches and also the direct effect of tobacco smoking on maxillary rather than mandibular teeth. In the present study, palatal aspects of maxillary molars showed significantly higher bone loss and also had more percentage of vertical bone defects compared to nonsmokers. This is in contrary with a few studies where the greatest difference in attachment loss was found in the anterior maxillary region by Haber and Kent, Haffajee and Socransky, and van der Weijden et al.
Cigarette smokers had more percentage of vertical bone loss compared to nonsmokers in this study. These findings were similar to the observations of Norderyd and Hugoson, Norderyd et al., and Bergström. They found that the occurrence of vertical defects was about 2–3 fold elevated in cigarette smokers compared to nonsmokers, suggesting that the impact of tobacco smoking on the periodontal bone was within the range of that reported earlier regarding the effect of tobacco smoking on periodontal bone destruction.
| Conclusions|| |
It is concluded that cigarette smokers were presented with severe CP. Palatal aspects of maxillary molars showed significantly higher bone loss and also had more percentage of vertical bone defects compared to nonsmokers. Tobacco smoking definitely affects the periodontium negatively. IOPA along with transgingival probing may be used as relatively noninvasive methods for determination of types and severity of bone destruction in CP patients with or without tobacco smoking habit.
We are thankful to all the study participants for their cooperation in completing this study.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Newman MG, Takei H, Klokkevold PR, Carranza FA. Smoking and periodontal disease. Carranza's Clinical Periodontology. 12th
ed. University of London: Elsevier Health Sciences; 2015. p. 404-13.
Haber J. Smoking is a major risk factor for periodontitis. Curr Opin Periodontol 1994;6:12-8.
Pejcic A, Obradovic R, Keric L, Kojovic D. Smoking and periodontal disease – A review. Biol Med 2007;14:53-9.
Abolfazli N, Lafzi A, Eskandari A, Saleh Saber F, Shirmohamadi A. Diagnostic value of bone sounding technique for estimation of bone level in periodontal defects. Shiraz Univ Dent J 2008;9:120-6.
Anil S. Study of the patterns of periodontal destruction in smokers with chronic periodontitis. Indian J Dent Res 2008;19:124-8.
] [Full text]
Jeffcoat MK. Radiographic methods for the detection of progressive alveolar bone loss. J Periodontol 1992;63 Suppl 4S: 367-72.
Björn H, Halling A, Thyberg H. Radiographic assessment of marginal bone loss. Odontol Revy 1969;20:165-79.
Suomi JD, West JD, Chang JJ, McClendon BJ. The effect of controlled oral hygiene procedures on the progression of periodontal disease in adults: Radiographic findings. J Periodontol 1971;42:562-4.
Pepelassi EA, Diamanti-Kipioti A. Selection of the most accurate method of conventional radiography for the assessment of periodontal osseous destruction. J Clin Periodontol 1997;24:557-67.
Fukuda CT, Carneiro SR, Alves VT, Pustiglioni FE, De Micheli G. Radiographic alveolar bone loss in patients undergoing periodontal maintenance. Bull Tokyo Dent Coll 2008;49:99-106.
Glickman I. Bone loss and patterns of bone destruction in periodontal disease. Clinical Periodontology. 6th
ed. New Delhi, Philadelphia: W.B. Saunders Co.; 1984. p. 234-7.
Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6.
Greenberg J, Laster L, Listgarten MA. Transgingival probing as a potential estimator of alveolar bone level. J Periodontol 1976;47:514-7.
Rosa GM, Lucas GQ, Lucas ON. Cigarette smoking and alveolar bone in young adults: A study using digitized radiographs. J Periodontol 2008;79:232-44.
Malhotra R, Kapoor A, Grover V, Kaushal S. Nicotine and periodontal tissues. J Indian Soc Periodontol 2010;14:72-9.
] [Full text]
Al-Tayeb D. The effects of smoking on the periodontal condition of young adult Saudi population. Egypt Dent J 2008;54:1-11.
Feldman RS, Bravacos JS, Rose CL. Association between smoking different tobacco products and periodontal disease indexes. J Periodontol 1983;54:481-7.
Katono T, Kawato T, Tanabe N, Suzuki N, Yamanaka K, Oka H, et al.
Nicotine treatment induces expression of matrix metalloproteinases in human osteoblastic saos-2 cells. Acta Biochim Biophys Sin (Shanghai) 2006;38:874-82.
Bergström J. Influence of tobacco smoking on periodontal bone height. Long-term observations and a hypothesis. J Clin Periodontol 2004;31:260-6.
Ramli J, Taiyeb Ali TB. Association between smoking and periodontal disease. Ann Dent UM 1999;6:21-6.
Schuller AA, Holst D. Testing the consistency of measurements of the distance between the cemento-enamel junction and the alveolar bone crest on bitewing radiographs. J Clin Periodontol 1996;23:977-81.
Haber J, Kent RL. Cigarette smoking in a periodontal practice. J Periodontol 1992;63:100-6.
Haffajee AD, Socransky SS. Relationship of cigarette smoking to attachment level profiles. J Clin Periodontol 2001;28:283-95.
van der Weijden GA, de Slegte C, Timmerman MF, van der Velden U. Periodontitis in smokers and non-smokers: Intra-oral distribution of pockets. J Clin Periodontol 2001;28:955-60.
Norderyd O, Hugoson A. Risk of severe periodontal disease in a Swedish adult population. A cross-sectional study. J Clin Periodontol 1998;25:1022-8.
Norderyd O, Hugoson A, Grusovin G. Risk of severe periodontal disease in a Swedish adult population. A longitudinal study. J Clin Periodontol 1999;26:608-15.
Bergström J. Tobacco smoking and risk for periodontal disease. J Clin Periodontol 2003;30:107-13.
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]