Smokers lose 6 extra teeth: periodontitis = tooth loss

Smokers lose 6 extra teeth: periodontitis = tooth loss

JohnPolito
Joined: 11 Nov 2008, 19:22

12 Jan 2010, 05:22 #1

Smoking Related
Periodontitis & Tooth Loss

Smokers lose 6 extra teeth: smoking = periodontitis = tooth loss
A former three pack-a-day smoker who has been quit for ten years, last week I had two additional teeth pulled, bringing my total to six.  Oh, they were both dead, likely for a number of years.  You see, I had five root canals during my final two years of smoking.   A 2006 study found that the male ex-smoker's risk of smoking related tooth loss remained “significantly elevated for the first 9 years of abstinence but eventually dropped to the level of men who never smoked after 13 or more years.”

A 1998 study found that, unrelated to differences in oral hygiene, by age 35 the average smoker had 0.6 fewer teeth than the average non-smoker, by age 50 1.5 fewer, by age 65 they had 3.5 fewer and by age 75 the average smoker had 5.8 fewer teeth.  I'm 55 and heavy smoking (roughly 50 pack years) has accelerated my decline by 20 years.  But why?  Periodontitis.

Periodontitis (peri = around, odont = tooth, -itis = inflammation) refers to inflammatory diseases affecting the periodontium, the tissues surrounding and supporting our teeth. Periodontitis results in gradual loss of bone supporting our teeth, which eventually results in tooth loss. 

The exact cause of periodontitis in smokers is poorly understood.  Research suggest that it may have little to do with how well or often we brush.  Researchers suspect that it's likely associated with years of assaults by scores of smoked toxins.  The same double whammy effects of carbon monoxide and nicotine that make circulatory disease smoking's #1 cause of death deprives gums, bone and teeth of normal oxygen levels and blood flow. 

Read Joel's Smoking and Circulation article if you don't yet undestand why interrupted blood flow kills more smokers than lung cancer.  Smoking not only kills heart muscle via attacks and brain regions via strokes but teeth via disease. 

Most disturbing is that we can have rather serious periodontitis and not realize it.  As a vasoconstrictor nicotine  squeezes blood vessels, which often masks and hides gum bleeding until nicotine use ends.  Symptoms of periodontitis can include breath odor, gums that bleed easily, appear shiny or bright red, are swollen or tender when touched but otherwise painless, or loose teeth.  The primary treatment objective is to reduce inflamation. 

For me, my teeth seemed to all feel smoking's destructive effects about the same time.  I found myself living in my dentist's chair.  Having inflamed nerve roots ripped from five teeth was a real wake-up call.  The incidence of root canals in smokers is 70% higher.  What still bothers me is that my dentist never once mentioned the likely cause until setting in the chair during my final root canal.  It was clearly too late by then anyway as my smoking pack-years had caught up with me.  I guess he simply assumed I somehow knew that smoking destroys teeth.  I didn't.  Well, maybe deep down I did or at least should have.  But like that river in Egypt I was swimming in denial. 

"John, smoking is killing your teeth!"

The good news is that I've always been pretty good about brushing.  My remaining teeth don't look too bad, are mostly up front and form a nearly solid facade that fools most, until I begin talking.  The bad news is that I'll likely lose more.

What I'd like to do with this thread is share with you smoking related tooth and gum related research.  It's my hope that doing so might help you further appreciate the importance of the mission at hand ... no nicotine today!   But should you experience the worst dental nightmare imaginable, I sincerely hope you feel as I do.   I'll take toothlessness any day over ever going back to living as nicotine's slave!  Anyway, if at all concerned about relapse, what sense would relapse make if it means losing more teeth sooner?  

Knowledge and  understanding isn't just power but a quitting method.  We hope you'll continue reading at Freedom and WhyQuit, and become smarter than your addiction is strong.  Millions of words but just one rule ... no nicotine today!

Breathe deep, hug hard, live long,

John (Gold x10)  
Last edited by JohnPolito on 06 Aug 2017, 00:14, edited 14 times in total.
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JohnPolito
Joined: 11 Nov 2008, 19:22

12 Jan 2010, 05:33 #2

Study Title:
Risk of tooth loss after
cigarette smoking cessation


Journal: Preventing Chronic Disease, October 2006, Volume 3(4), Page A115. Epub 2006 Sep 15.

Study Authors: Krall EA, Dietrich T, Nunn ME, Garcia RI.
Department of Health Policy and Health Services Research, Boston University Goldman School of Dental Medicine, Veterans Affairs Normative Aging Study and Dental Longitudinal Study, VA Boston Healthcare System, Boston, Mass 02118, USA. [url=mailto:kralle@bu.edu]kralle@bu.edu[/url]

INTRODUCTION: Little is known about the effect of cigarette smoking cessation on risk of tooth loss. We examined how risk of tooth loss changed with longer periods of smoking abstinence in a prospective study of oral health in men.

METHODS: Research subjects were 789 men who participated in the Veterans Administration Dental Longitudinal Study from 1968 to 2004. Tooth status and smoking status were determined at examinations performed every 3 years, for a maximum follow-up time of 35 years. Risk of tooth loss subsequent to smoking cessation was assessed sequentially at 1-year intervals with multivariate proportional hazards regression models. Men who never smoked cigarettes, cigars, or pipes formed the reference group. Hazard ratios were adjusted for age, education, total pack-years of cigarette exposure, frequency of brushing, and use of floss.

RESULTS: The hazard ratio for tooth loss was 2.1 (95% confidence interval [CI], 1.5-3.1) among men who smoked cigarettes during all or part of follow-up. Risk of tooth loss among men who quit smoking declined as time after smoking cessation increased, from 2.0 (95% CI, 1.4-2.9) after 1 year of abstinence to 1.0 (95% CI, 0.5-2.2) after 15 years of abstinence. The risk remained significantly elevated for the first 9 years of abstinence but eventually dropped to the level of men who never smoked after 13 or more years.

CONCLUSION: These results indicate that smoking cessation is beneficial for tooth retention, but long-term abstinence is required to reduce the risk to the level of people who have never smoked.

PMID: 16978490 [PubMed - indexed for MEDLINE]

Link to Free Full Text Copy of Study: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779279
Last edited by JohnPolito on 12 Jan 2010, 13:50, edited 1 time in total.
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JohnPolito
Joined: 11 Nov 2008, 19:22

12 Jan 2010, 05:56 #3

Study Title:
Relationship between smoking and
dental status in 35-, 50-, 65-,
and 75-year-old individuals.

Journal: Jounal of Clinical Periodontology; April 1998, Volume 25(4); Pages 297-305.

Study Authors: Axelsson P, Paulander J, Lindhe J.
Department of Periodontology, Faculty of Odontology, Göteborg University, Sweden.

The aim of the present study was to examine the dental status and smoking habits in randomized samples of 35-, 50-, 65-, and 75-year-old subjects (n = 1093), recruited for a cross-sectional epidemiological study in the County of Värmland, Sweden. The following clinical variables were recorded by 4 well-calibrated dentists: number of edentuolous subjects, number of missing teeth, probing attachment level, furcation involvement, CPITN scores, DMF surfaces, plaque and stimulated salivary secretion rate (SSSR). In addition, the subjects reported in a questionnaire their tobacco habits, oral hygiene habits, dietary habits etc.

The percentage of smokers in 35-, 50-, 65-, and 75-year-olds was 35%, 35%, 24% and 12%, respectively. In 75-year-olds, 41% of the smokers were edentulous compared to 35% of non-smokers. The difference in number of missing teeth between smokers and non-smokers was 0.6 (p=0.15), 1.5 (p=0.013), 3.5 (p=0.0007) and 5.8 (p=0.005) in the 4 age groups.
Smokers had the largest mean probing attachment loss in all age groups. The differences between smokers and non-smokers in mean attachment level were 0.37 (p=0.001), 0.88 (p=0.001), 0.85 (p=0.001) and 1.33 mm (p=0.002) in the 35-, 50-, 65-, and 75-year-olds, respectively. Treatment need assessed by CPITN was in all age groups greatest among smokers. The number of intact tooth surfaces was fewer in 35-, 50-, and 75-year-old smokers than in non-smokers. The number of missing surfaces (MS) was higher in 50-, 65-, and 75-year-old smokers than in non-smokers. In addition, 35-year-old smokers exhibited a significantly larger number of decayed and filled tooth surfaces (DFS) than non-smokers. Male smokers had significantly higher SSSR than non-smoking males (p=0.012). Plaque index and oral hygiene were similar in smokers and non-smokers. Smokers reported a more frequent intake of sugar containing soft drinks (p=0.000) and snacks (p=0.003) than non-smokers. The opposite was reported for consumption of fruit (p=0.003).

It was concluded that smoking is a significant risk indicator for tooth loss, probing attachment loss and dental caries.

PMID: 9565280 [PubMed - indexed for MEDLINE]

Link to PubMed study abstract (summary): http://www.ncbi.nlm.nih.gov/pubmed/9565280
Last edited by JohnPolito on 12 Jan 2010, 13:55, edited 1 time in total.
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JohnPolito
Joined: 11 Nov 2008, 19:22

12 Jan 2010, 06:16 #4

Periodontitis (peri = around, odont = tooth, -itis = inflammation) refers to a number of inflammatory diseases affecting the periodontium - that is, the tissues that surround and support the teeth. Periodontitis involves progressive loss of the alveolar bone around the teeth, and if left untreated, can lead to the loosening and subsequent loss of teeth. Periodontitis is caused by microorganisms that adhere to and grow on the tooth's surfaces, along with an overly aggressive immune response against these microorganism. A diagnosis of periodontitis is established by inspecting the soft gum tissues around the teeth with a probe and x-ray films by visual analysis, to determine the amount of bone loss around the teeth. Specialists in the treatment of periodontitis are periodontists; their field is known as "periodontology" or "periodontics".

Source: Wikipedia



Study Title:
Smoking and periodontal disease:
clinical evidence for an association
Journal: Oral Health & Preventive Dentistry, 2009, Volume 7(4), Pages 369-376.

Authors: Moimaz SA, Zina LG, Saliba O, Garbin CA.

Purpose: The aim of the present study was to assess the periodontal condition and smoking status, according to dose and duration information, and to estimate the percentage of subjects with periodontitis attributable to cigarette smoking in a representative adult rural population in southern Brazil.

Materials and Methods: Bivariate statistical analysis was used to evaluate the association of smoking status with periodontitis in a cross-sectional study comprising 165 dentate individuals, aged 35 to 66 years, subjected to oral clinical examination of six sites per tooth in all sextants.

Results: The prevalence of periodontitis (having >/= 1 pocket of >/= 4 mm around the index teeth) in the population was 35.2%. Overall, 13.9% had a cumulative loss of attachment > 4 mm; 35.7% of subjects were current smokers, classified as heavy (average 25.3 pack years), moderate (average 14.6 pack years) and light smokers (average 3.1 pack years). Statistical analysis showed that current smokers had an 11 times (95% confidence interval [CI] = 4.69 to 26.62) and former smokers had a nine times (95% CI = 3.29 to 25.96) greater probability of having established periodontitis compared with non-smokers. The number of pack years (P = 0.0004) and years of smoking exposure (P = 0.0013) were associated with an increased prevalence of periodontitis. The number of current smokers with periodontitis might be reduced by 80%, had they not smoked cigarettes. Of the subjects with periodontitis, 64% could be prevented among current smokers by eliminating tobacco consumption.

Conclusions: Cigarette smoking was strongly associated with periodontitis, and there was a relationship with dose and duration of smoking. These findings contributed to the evidence of smoking as a risk factor for periodontal disease and support the importance of dose-response analysis on determining the strength of this association.

PMID: 20011755 [PubMed - in process]

Link to PubMed study abstract: http://www.ncbi.nlm.nih.gov/pubmed/20011755



Title:
Tobacco smoking and chronic
destructive periodontal disease.


Journal: Odontology. 2004 September; Volume 92(1), Pages 1-8.

Author: Bergström J.
Karolinska Institutet, Stockholm, Alfred Nobels allé 8, Box 4064, S141 04 Huddinge, Sweden. [url=mailto:Jan.Bergstrom@ofa.ki.se]Jan.Bergstrom@ofa.ki.se[/url].

Tobacco smoking is the main risk factor associated with chronic destructive periodontal disease. No other known factor can match the strength of smoking in causing harm to the periodontium. The harmful effects manifest themselves by interfering with vascular and immunologic reactions, as well as by undermining the supportive functions of the periodontal tissues.

The typical characteristic of smoking-associated periodontal disease is the destruction of the supporting tissues of the teeth, with the ensuing clinical symptoms of bone loss, attachment loss, pocket formation, and eventually tooth loss. A review of the international literature that has accumulated over the past 20 years offers convincing evidence that smokers exhibit greater bone loss and attachment loss, as well as more pronounced frequencies of periodontal pockets, than non-smokers do. In addition, tooth loss is more extensive in smokers.

Smoking, thus, considerably increases the risk for destructive periodontal disease. Depending on the definition of disease and the exposure to smoking, the risk is 5- to 20-fold elevated for a smoker compared to a never-smoker. For a smoker exposed to heavy long-life smoking, the risk of attracting destructive periodontal disease is equivalent to that of attracting lung cancer. The outcome of periodontal treatment is less favorable or even unfavorable in smokers.

Although long-term studies are rare, available studies unanimously agree that treatment failures and relapse of disease are predominantly seen in smokers. This contention is valid irrespective of treatment modality, suggesting that smoking will interfere with an expected normal outcome following commonplace periodontal therapies.

The majority of available studies agree that the subgingival microflora of smokers and non-smokers are no different given other conditions. As a consequence, the elevated morbidity in smokers does not depend on particular microflora. The mechanisms behind the destructive effects of smoking on the periodontal tissues, however, are not well understood. It has been speculated that interference with vascular and inflammatory phenomena may be one potential mechanism. Nicotine and carbon monoxide in tobacco smoke negatively influence wound healing.

Smoking research over the past two decades has brought new knowledge into the domains of periodontology. Even more so, it has called into question the prevailing paradigm that the disease is primarily related to intraoral factors such as supra- and subgingival infection. Smoking research has revealed that environmental and lifestyle factors are involved in the onset and progression of the disease.

Being the result of smoking, destructive periodontal disease shares a common feature with some 40 other diseases or disorders. As a consequence, periodontal disease should be regarded as a systemic disease in the same way as heart disease or lung disease. Thus, chronic destructive periodontal disease in smokers is initiated and driven by smoking. Its progression may or may not be amplified by unavoidable microbial colonization.

PubMed source link: http://www.ncbi.nlm.nih.gov/pubmed/15490298
Last edited by JohnPolito on 12 Jan 2010, 13:57, edited 2 times in total.
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JohnPolito
Joined: 11 Nov 2008, 19:22

12 Jan 2010, 06:40 #5

Title:
Nicotine effects on alveolar bone
changes induced by occlusal trauma:
a histometric study in rats.

Journal: Journal of Periodontology, March 2004, Volume 75(3), Pages 348-352.

Authors: Nogueira-Filho GR, Fróes Neto EB, Casati MZ, Reis SR, Tunes RS, Tunes UR, Sallum EA, Nociti FH Jr, Sallum AW.
Department of Periodontics, School of Dentistry, Bahia Science Foundation (FDC), Bahia, Brazil. [url=mailto:get_nogueira@uol.com.br]get_nogueira@uol.com.br[/url]

BACKGROUND: The aim of the present study was to verify nicotine effects on alveolar bone changes induced by occlusal trauma during a periodontitis experimental model in rats.

METHODS: Thirty adult male rats were used. The animals were randomly assigned to one of three groups receiving daily intraperitoneal injections: A, nicotine solution (0.44 mg/ml) and occlusal overload; B, saline solution and occlusal overload; or C, saline solution. Rats from groups A and B underwent bilateral amputation of the second and third molar cusps to simulate an occlusal overload. The first molars were then randomly assigned to receive a cotton ligature in the sulcular area, while the contralateral tooth was left unligated. The animals were sacrificed 30 days later. The resected mandibles were processed, and histomorphometric measurements were performed in the alveolar bone adjacent to the furcation area of the first molars.

RESULTS: Nicotine enhanced the bone loss induced by occlusal trauma (P<0.001) on the ligated teeth of group A (12.27 4.4 mm2), when compared to groups B (8.43 3.51 mm2) and C (4.43 2.17 mm2). Alveolar bone loss (P<0.01) was also observed in the contralateral teeth of groups A (nicotine + trauma) and B (saline + trauma), when compared to group C (saline only).

CONCLUSION: Within the limits of the study, it is concluded that nicotine may influence the alveolar bone changes induced by occlusal trauma by enhancing bone loss.

PMID: 15088871 [PubMed - indexed for MEDLINE]

PubMed source link: http://www.ncbi.nlm.nih.gov/pubmed/15088871

But this bone repair study leaves us with somewhat
conflicting results as to nicotine's role, alone, in periodontitis:

Title: Smoking affects the self-healing
capacity of periodontal tissues.
A histological study in the rat


Journal: European Journal of Oral Science, 2005, Volume 113, Pages 400-403

Authors: Bruno Braga Benatti, João Batista César-Neto, Patrícia Furtado Gonçalves, Enílson Antônio Sallum, Francisco Humberto Nociti Jr


Department of Prosthodontics and Periodontics, Division of Periodontics, School of Dentistry at Piracicaba, UNICAMP, Piracicaba, São Paulo, Brazil Correspondence to Dr Francisco H. Nociti Jr, Faculdade de Odontologia de Piracicaba, Unicamp, Avenida Limeira 901, Bairro Areião 13414-903, Piracicaba, S.P., Brazil

Telefax: + 55-19-34125301
E-mail: [url=mailto:]nociti@fop.unicamp.br[/url]

Copyright 2005 Eur J Oral Sci


KEYWORDS
cigarette smoke • nicotine • rats • periodontal regeneration

Benatti BB, Cèsar-Neto JB, Gonçalves PF, Sallum EA, Nociti FH Jr. Smoking affects the self-healing capacity of periodontal tissues. A histologic study in the rat. Eur J Oral Sci 2005; 113: 400-403.© Eur J Oral Sci, 2005
ABSTRACT
This study aimed to evaluate in rats the impact of cigarette smoke inhalation (CSI) and nicotine administration (NA) on a periodontal healing model in the absence of a plaque biofilm. Wistar rats (n = 42) were assigned to three groups: Group 1, control (n = 14); Group 2, NA (3 mg kg−1) (n = 14); and Group 3, CSI (n = 14). Thirty days after CSI and NA exposure, fenestration defects were created buccally to the distal root of the first mandibular molar. The animals were killed 21 d later and their mandibles were processed for histological examination. The percentage of bone fill and the density of newly formed bone were assessed histometrically. Intergroup analysis demonstrated that compared to the control and NA groups, CSI was associated with a reduced rate of bone repair. No new cementum had been formed along the root surface in any of the three groups. It is concluded that cigarette smoke reduces the self-healing capacity of periodontal tissues.



Accepted for publication July 2005


DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1600-0722.2005.00240.x About DOI
Last edited by JohnPolito on 13 Jan 2010, 13:58, edited 2 times in total.
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JohnPolito
Joined: 11 Nov 2008, 19:22

13 Jan 2010, 16:36 #6

Dent Res. Author manuscript; available in PMC 2008 February 4.
Published in final edited form as:
J Dent Res. 2006 April; 85(4): 313-317.
PMCID: PMC2225991
NIHMSID: NIHMS38032
Copyright notice and Disclaimer

Study Title:
Cigarette Smoking Increases
the Risk of Root Canal Treatment

Journal: Journal of Dental Research, April 2006, Volume 85(4), Page 313-317

Study Authors
: E.A. Krall,1,2* C. Abreu Sosa,3 C. Garcia,2 M.E. Nunn,2 D.J. Caplan,4 and R.I. Garcia1,2
1VA Dental Longitudinal Study, VA Boston Healthcare System
2Department of Health Policy & Health Services Research, Boston University Goldman School of Dental Medicine, 715 Albany Street, 560, Room 338, Boston, MA 02118, USA
3University of Puerto Rico School of Dentistry
4Department of Dental Ecology, University of North Carolina School of Dentistry
*corresponding author, Email: [url=mailto:kralle@bu.edu]kralle@bu.edu[/url]
Image The publisher's final edited version of this article is available at J Dent Res.
Image See other articles in PMC that cite the published article.

Abstract



Few studies have investigated smoking as a risk factor for root canal treatment. We studied the effect of smoking on the incidence of root canal treatment, controlling for recognized risk factors, in 811 dentate male participants in the VA Dental Longitudinal Study. Participants were not VA patients. Follow-up ranged from 2 to 28 years. Root canal treatment was verified on radiographs and evaluated with proportional hazards regression models. Compared with never-smokers, current cigarette smokers were 1.7 times as likely to have root canal treatment (p < 0.001), but cigar and/or pipe use was not significantly associated with root canal treatment. The risk among cigarette smokers increased with more years of exposure and decreased with length of abstinence. These findings suggest that there is a dose-response relationship between cigarette smoking and the risk of root canal treatment.
Keywords: smoking, tobacco, endodontics, root canal treatment


INTRODUCTION



Root canal treatment is often indicated when the dental pulp becomes infected by bacteria. Caries lesions, dental procedures, and tooth fracture increase the likelihood of bacterial access. Factors that alter the host response to inflammation, such as smoking, may also indirectly influence the risk of infection and its subsequent treatment. Little research has been conducted on the association between smoking and root canal treatment. Bergström et al. (2004) reported that current smokers had a higher prevalence of endodontic treatment and a higher percentage of treated roots than did non-smokers, but, after adjustment for age, the differences were not statistically significant. An important limitation of that study was its cross-sectional design (Garcia, 2005).


Smoking impairs the body's responses to infection (Das, 1985; Tracy et al., 1997; Frohlich et al., 2003), exacerbates bone loss in the systemic skeleton (Krall and Dawson-Hughes, 1991) and oral cavity (Krall et al., 1999), decreases the blood's oxygen-carrying capacity (Ijzerman et al., 2003), and causes vascular dysfunction (Pittilo, 1990). Any one of these pathophysiologic pathways can potentially affect the health of the tooth pulp and surrounding bone tissues and result in a higher incidence of root canal treatment in smokers than in non-smokers. We investigated this hypothesis in a cohort of adult men who have been followed for three decades in the VA Dental Longitudinal Study.


MATERIALS & METHODS



Subjects


The VA Dental Longitudinal Study (DLS) is a closed-panel prospective study of oral health and aging in men (Kapur et al., 1972). At the study baseline in 1968-73, the DLS enrolled 1231 medically healthy men, ages 21 to 84 yrs, who concurrently participated in the Normative Aging Study (Bell et al., 1966). The men were not patients of the VA healthcare system, but received dental and medical care from the private sector. Participants returned to the study site every three years to receive clinical and radiographic dental examinations and complete questionnaires (see APPENDIX). Up to 28 yrs of follow-up are included in this analysis. The study was reviewed and approved by the Department of Veterans Affairs Subcommittee on Human Studies and the Boston University Medical Center Institutional Review Board. All participants gave written informed consent.



Examinations


At each examination, the number of teeth remaining was counted, and each tooth was evaluated for restorations, caries, periodontal probing at six sites, and clinical assessments of tooth mobility and calculus. Probing pocket depth, mobility, and calculus were recorded as ordinal scores. Pocket depth scores ranged from 0 (≤ 2 mm) to 3 (≥ 5 mm); mobility scores from 0 (none) to 4 (depressability); and calculus scores from 0 (none) to 3 (circumferential band around tooth). Alveolar bone loss was measured from periapical radiographs on the distal and mesial sites of each tooth by a modified Schei ruler method (Schei et al., 1959), which expresses the reduction in alveolar bone height as the percent of the total distance between the cemento-enamel junction and the root apex. The maximum probing depth and bone loss scores per tooth were used in analyses. Radiographic caries was also assessed.


Of the 1231 men initially enrolled in the DLS, 1058 were potentially eligible for this analysis, on the basis of having 2 or more teeth at baseline. Over a period of 1 yr, two Boston University endodontic residents, each trained and calibrated, reviewed serial periapical radiographs from a randomly ordered sample of those eligible (n = 852) to determine the presence or absence of root canal treatment and periradicular radiolucency. The final dataset consisted of 811 men with at least one follow-up examination and complete smoking information, and 18,893 teeth that were free of root canal treatment at baseline. Because the exact date of root canal treatment was not known, the date of onset was systematically computed as the midpoint between the DLS examination date at which the root canal treatment first appeared on radiograph and the examination date that immediately preceded it. The endodontists each independently reviewed 576 radiographs, and the kappa for inter-examiner agreement for the presence/absence of root canal treatment was 1.00.


Education, frequency of toothbrushing and flossing, and smoking history were obtained by interviewer-administered questionnaires. At baseline, cigarette status and duration were assessed by these questions: "Have you ever smoked cigarettes?", "Have you smoked in the last year?", "How long have you been smoking cigarettes?", "How long has it been since you quit smoking?", and "For how many years were you a cigarette smoker?" Smoking duration and time since quitting prior to baseline were asked only at baseline. Cigarette status and dose were updated, at each follow-up examination between 1971 and 1985, with "Do you use tobacco?" and "If yes, how many packs of cigarettes per day?". The questions were changed to "Do you smoke at all?", "If yes, do you smoke cigarettes?", and "How many cigarettes in an average day (½, 1, 1½, or 2+ packs/day)" at follow-up examinations after 1985. Similar questions at all examinations assessed cigar- and pipe-smoking information.



Statistical Analysis


Participants were categorized on the basis of smoking status during follow-up: never-smoker, former cigarette smoker (quit prior to the DLS baseline examination), current cigarette smoker (for any part of follow-up), or current cigar and/or pipe smoker. Men who smoked cigarettes in combination with either pipes or cigars were classified as cigarette smokers.


Characteristics of the men by smoking status were compared with parametric or non-parametric analysis of variance (continuous variables) or chi-square statistic (categorical variables). In participant-level analyses, risk of any incident root canal treatment was estimated with proportional hazards regression. Current cigarette- and cigar/pipe-smoking status at each examination was treated as a time-dependent covariate. In addition, the risks of incident root canal treatment by current cigarette status, number of years smoked, and number of years since last smoked were estimated at the tooth level with multivariate proportional hazards regression to account for multiple root canal treatments within individual participants. All analyses were performed with never-smokers (n = 230) as the reference group, and again with never and former cigarette smokers (n = 440) as the reference group. Since the results were not substantially different, only the risks relative to never-smokers are presented. Differences were considered statistically significant at p < 0.05. Hazards ratios (HR) and 95% confidence intervals (95%CI) are presented.



RESULTS



The participants were 48 ± 9 (mean ± SD) yrs old at baseline and had 24 ± 6 teeth remaining. Table 1 shows characteristics by smoking status. Current cigarette smokers were younger, had fewer teeth remaining, the highest percentages of teeth with calculus, alveolar bone loss > 20%, and probing pocket depth > 3 mm, and had lost more teeth than never-smokers, former cigarette smokers, or current cigar/pipe smokers.

Image
Table 1 Characteristics of Men in Root Canal Incidence Study, by Smoking Status




Incidence of Root Canal Treatment


Incident root canal treatments were observed in 998 teeth among 385 participants. Teeth that had incident root canal treatment were more likely, at the examination prior to root canal treatment, to be crowned (21 vs. 4%), have periradicular radiolucency (8 vs. 0%), mobility ≥ 0.5 mm (5 vs. 2%), alveolar bone loss > 20% (27 vs. 12%), probing pocket depth > 3 mm (28 vs. 16%), any coronal caries (30 vs. 19%), any fillings (75 vs. 56%), and fillings on all 5 surfaces (5 vs. 2%) relative to teeth that were never treated (all p < 0.001).


The age-adjusted risk of incident root canal treatment was significantly greater in current cigarette smokers, relative to never-smokers, but not in cigar or pipe smokers (Table 2). The hazards ratio attributable to cigarette smoking was similar, but remained statistically significant, in models that also controlled for number of teeth present, any teeth with periradicular radiolucency, and percentages of teeth with crowns, coronal caries, and alveolar bone loss > 20%. The results were not changed when education, brushing, or flossing was included in the models. Multivariate analyses of root canal treatment risk at the tooth level yielded similar hazards ratios when controlled for age, presence of a crown, any coronal caries, radiolucency, and alveolar bone loss level (HR and 95%CI for current cigarette use = 1.9, 1.4 to 2.5; for current cigar/pipe use = 1.3, 0.9 to 1.7).

Image Table 2 Smoking Status and the Risk of Root Canal Treatment Relative to Never-smokers: Hazards Ratios and 95% Confidence Intervals for Cigarette Smokers and Cigar/Pipe Smokers Relative to Never-smokers




The association of root canal treatment risk varies with length of time since last smoked (Fig 1Image). Relative to never-smokers, the hazards ratio was elevated for the teeth of men who had quit 9 or fewer years prior to baseline (HR = 1.9, 95%CI = 1.3 to 2.8). But among men who had quit more than 9 yrs previously, the hazards ratio was similar to that in never-smokers (HR = 1.0, 95%CI = 0.7 to 1.5).

Image Image

Figure 1 Hazards ratios (■) and 95% confidence intervals (error bars) for risk of root canal treatment among former cigarette smokers (smoked prior to study baseline, but remained abstinent during follow-up), by length of time since last smoked. The median (more ...)











Among current cigarette smokers, the hazards ratio for root canal treatment increased from 1.2 (95%CI = 0.7 to 1.9) for teeth in men who smoked a total of ≤ 4 yrs, to 2.0 (95%CI = 1.2 to 3.3) in those who smoked from 5 to 12 yrs, and 2.2 (95%CI = 1.5 to 3.3) in those who smoked > 12 yrs (Fig. 2Image).
Image Image

Figure 2 Hazards ratios (■) and 95% confidence interval (error bars) for risk of root canal treatment among current cigarette smokers, by total yrs smoked. Numbers in each interval are 48 participants/1347 teeth with ≤ 4 yrs, 78 participants/1782 (more ...)








DISCUSSION



To our knowledge, this is the first longitudinal analysis that describes smoking as a risk factor for root canal treatment. The outcome in our study, root-canal-treated teeth, is a surrogate for periapical periodontitis and underestimates the true incidence of such lesions. Caplan (2004) reviewed community-based studies of periapical periodontitis and root canal treatment and found the prevalence of non-root-filled teeth with periapical periodontitis to be low (from 0.1 to 5%). Similarly, Bergström et al. (2004) reported that a small percentage, approximately 1-3%, of teeth had untreated lesions. However, a more important consideration is that root canal treatment is only one possible outcome of teeth with periapical periodontitis; another is tooth extraction, which is more prevalent in smokers than in non-smokers and results in an unknown proportion of potentially root-canal-treated teeth being lost to follow-up.


Conclusions from the few cross-sectional studies on smoking and periapical periodontitis are inconsistent. Bergström et al. (2004), in a study of 241 individuals, found no evidence that smoking increased the risk of periapical lesions. Although the prevalence of periapical periodontitis was higher in current and former smokers than in non-smokers, the unadjusted odds ratio (1.6) was not statistically significant and was further reduced in multiple logistic regression analyses. However, the authors focused on current endodontic disease and did not include past treatment as an outcome (Garcia, 2005). Smokers had 30% more endodontically treated roots, but the difference was not significant after adjustment for age. In a study of 613 individuals, Kirkevang and Wenzel (2003) also reported an odds ratio of 1.6 for smoking and periapical periodontitis, which was significant in multiple logistic regression models.


The most common means of bacterial entry to the pulp cavity are caries lesions on the coronal or root surfaces. Secondary caries, inadequate coronal restorations, and root caries were each associated with increased odds of periapical periodontitis (Kirkevang and Wenzel, 2003). In our study, adequacy of restoration was not assessed, and root caries was not noted separately in the first several examination cycles, but crowns and coronal caries each increased the risk of root canal treatment. Prospective studies suggest that smokers tend to have more decayed or filled coronal (Drake et al., 1997) and root surfaces (Locker, 1996) than do non-smokers.


Smokers have impaired responses to infection. The functions of polymorphonuclear leukocytes, macrophages, T-cell lymphocytes, antibodies, and immunoglobulins A, G, and M are suppressed in smokers (Holt, 1987). Smokers have elevated levels of mediators of acute-phase inflammatory response, such as TNF-α (Tappia et al., 1995) and IL-6 (de Maat and Kluft, 2002), that are capable of inflicting damage to tissues. Smoking also induces a chronic systemic inflammatory response that may persist even after smoking has actively ceased. C-reactive protein (CRP) levels in serum were higher in current smokers than in non-smokers (Frohlich et al., 2003), particularly among heavy smokers of more than 1 pack per day (Das, 1985). In addition, CRP levels were greatest among those with longer duration of smoking and more pack-years, and were inversely correlated with duration of abstinence (Frohlich et al., 2003).

Peripheral leukocyte counts are also higher in current smokers than in non-smokers and exhibit dose-response relationships (Sparrow et al., 1984; Schwartz and Weiss, 1991; Tracy et al., 1997), although, as noted above, their function is impaired. These observations suggest that once bacterial infection begins in the pulp and surrounding tissues, smokers are less likely than non-smokers to be able to limit the destruction.


Another underlying explanation for our findings is impaired oxygen delivery and damage to the circulatory system inside the tooth. Levels of carboxyhemoglobin in the blood are elevated in smokers, resulting in a decreased oxygen-carrying capability. In addition, smoking is associated with impaired microvascular function and endothelial cell injury in blood vessels, possibly due to free-radicals found in tobacco smoke (Ijzerman et al., 2003). Blood vessels in the healthy gingiva constrict in reaction to environmental agents that induce stress, a response identical to that in the extremities (Giddon, 1966; Zelechowski et al., 1969). Because components in cigarette smoke induce stress (Giddon, 1966) and reduce blood flow volume, vessels that serve the tooth root are likely to show signs of vascular dysfunction that restrict nutrient supply and impede cellular repair. This suggests that smoking may be a factor that contributes to early tissue death within the pulp cavity.


There may also be residual confounding factors that contribute to the increased root canal treatment risk we observed in current cigarette smokers. Smoking is inversely correlated with socio-economic status and may be a marker for poor dental hygiene or lack of dental care (USDHHS, 2000). In our study, current cigarette smokers tended to have less education, although adjustment for this characteristic did not change the risk estimates. There may be differences between smokers and non-smokers in addition to oral hygiene practices and education that we were unable to measure adequately, but that could further attenuate the observed association between smoking and root canal treatment.


Cigar and pipe use is related to periodontal disease (Krall et al., 1999) and tooth loss (Krall et al., 1997) in this cohort, but not to root canal treatment risk. This finding may be due to the small number of cigar and pipe smokers, or to our difficulty in quantifying the amount smoked. Among cigarette smokers, risk estimates suggested a threshold effect around 5 yrs of exposure. Since cigar smokers tend to initiate the habit at a later age than do cigarette smokers (Gerlach et al., 1998), their total tobacco exposure may be limited. It is possible that a relationship exists between root canal treatment and cigars and pipes, but we did not have a sufficiently large sample size or exposure high enough to detect it.


Another limitation of the study is the gender and ethnic composition of the participant population. The DLS is a closed-panel prospective study that did not include women at its inception and has less than 5% minority participants. We would expect to see an association between smoking and root canal treatment risk in women and other ethnic groups as well, although absolute risk levels may differ and might be more closely related to cigarette exposure than to demographic characteristics.


Important strengths of the current study that differentiate it from previous studies are the large number of participants, the prospective design with long follow-up time, the frequent intervals at which radiographs were taken, control for caries and restorations, and the findings of dose-response relationships with years of exposure and duration of abstinence. The results suggest that smoking may have a causal role in the development of lesions that result in root canal treatment, and, conversely, that smoking prevention and cessation are critical strategies to reducing the risk of root canal treatment.




Supplementary Material



A supplemental appendix to this article is published electronically only at http://www.dentalresearch.org.
Click here to view.(29K, pdf)





Acknowledgments



This study was supported by a US Dept. of Veterans Affairs Epidemiology Merit Review grant and by the Massachusetts Veterans Epidemiology Research and Information Center, and by NIH grants R01 DE 013807, T35 DE07268, R01 DA10073, R15 DE12644, M01 RR 000533, and K24 DE00419. We thank Dr. Joel Chasen and Dr. Ryan Yamanaka for data collection on endodontic treatment status. Parts of the information in this manuscript were presented at the 2004 annual meeting of the Society for Research on Nicotine and Tobacco, Scottsdale, AZ, February, 2004.



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Last edited by JohnPolito on 13 Jan 2010, 16:39, edited 1 time in total.
Reply

NemoToid
Joined: 03 Jan 2011, 21:36

08 Feb 2011, 23:35 #7

John I have to thank you for your post on periodontal disease. I am 56, but at the age of 18 (I'd been a smoker for 3 years by then) my gums were inflamed and bleeding and I didn't know why. I went to a Dentist (he was a relative of mine) who thought I was "bad" for smoking, etc. Anyway, he neglected to tell me smoking was harming my mouth and teeth, so the next 20 years I carried on. I have had 2 teeth pulled in the last 6 months. These teeth were fine - no cavities, no breakage, but the bone in my jaws couldn't support them any longer. I have about 3 teeth left on top, plus a bridge for my front teeth. I don't smile much.
Reply

josnewlife
Joined: 13 Oct 2011, 19:30

15 Oct 2011, 07:20 #8

Thanks John for this info, I just quit 5 days ago and one of my teeth just broke off at the gum last night!Interesting reading that this was probably caused by smoking.
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JohnPolito
Joined: 11 Nov 2008, 19:22

17 Oct 2011, 17:49 #9

josnewlife wrote: Thanks John for this info, I just quit 5 days ago and one of my teeth just broke off at the gum last night! Interesting reading that this was probably caused by smoking.
Yes, I was just reading your journal which led me here.   Your comment about, if smoking was doing this to my teeth then what has it done inside my body, really hits the mark.   If we could only see what we've already done to our lungs, how super toxins have eaten away brain gray and white matter, or how nicotine and carbon monoxide have built and hardened plaque within our arteries.  

Jo, you don't want to do to your teeth what I've done to mine, as my three packs a day claimed six teeth, while damaging most that remain.  This mouth, like these badly damaged lungs, is an utter mess.  What I didn't appreciate is that each tooth lost means that our remaining teeth have to work that much harder and wear down that much sooner.  But I did this to myself.  

I love life here on the free side of the bars.   I only wish I could have arrived a decade sooner before losing any teeth, before that first root canal ever.   It's where you and so many others here clearly have me beat.  I do hope you'll continue to keep your day #1 commitment alive and strong.  As you know, Jo, there was always only one rule ... no nicotine today!

Breathe deep, hug hard, live long,

John - Gold x12
Reply

josnewlife
Joined: 13 Oct 2011, 19:30

07 Oct 2012, 20:15 #10

I've come back to this thread as I've had more tooth related problems. My almost 20 pack years have taken their toll on my teeth obviously. The destructive power of smoking doesn't surprise me any more!Image

 But I'm happy to report that in 2 days I'll be GOLD so whatever is happening with my teeth, I hate smoking and I'll never go back to it. Image

John, I hope your teeth aren't causing you too much trouble at the mo!


Jo
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