Journal of Periodontology; Copyright 2014

DOI: 10.1902/jop.2014.140229

Investigating the Association Between Obstructive Sleep Apnea (OSA) and Periodontitis Weiqiang Loke,* Thomas Girvan,† Paul Ingmundson,‡ Ronald Verrett,§ John Schoolfield,* Brian L. Mealey* * Department of Periodontics, University of Texas Health Science Center at San Antonio Dental School, San Antonio, TX. †



Sleep Clinic, South Texas Veterans Health Care System, Veterans Administration facility, San Antonio, TX.

Dental Clinic, South Texas Veterans Health Care System, Veterans Administration facility, San Antonio TX. §

Department of Comprehensive Dentistry, University of Texas Health Science Center at San Antonio Dental School, San Antonio, TX.

Purpose: Obstructive sleep apnea (OSA) is a sleep disorder characterized by disruptions of normal sleep architecture. Chronic periodontitis is a chronic disease of the periodontium that elicits a general inflammatory response to local dental plaque. It has been suggested that periodontal disease may increase in severity with increasingly severe OSA since both disease entities share common inflammatory pathways, acting synergistically to alter the host response. The aim of this study is to analyze the association between severity of OSA and prevalence/severity of periodontitis. Methods and Materials: 100 patients (normal=26, mild=21, moderate=19, severe=34) diagnosed with an overnight polysomnogram (PSG) underwent a comprehensive periodontal examination. Periodontal parameters measured included: mean periodontal pocket depth (PD), clinical attachment level (CAL), gingival recession (REC) and % of sites with bleeding on probing (BOP), plaque (Pl), PD ≥ 5mm & CAL ≥ 3mm. Results: 73% of the sampled population had moderate to severe periodontal disease. Chi-square analyses revealed no significant differences in the prevalence of periodontal disease between AHI groups, with a negligible Spearman’s correlation coefficient of 0.246 between AHI severity and periodontal disease severity categories. ANCOVA indicated significant association between AHI severity categories and % sites with plaque, after adjusting for age. Multivariable logistic regression analysis predicting moderate to severe periodontitis with AHI score, age, and smoking status indicated a significant association with age (p=0.028) but no significant association with the other two predictors. Conclusion: OSA was not significantly associated with the prevalence of moderate to severe periodontitis and all periodontal parameters, except for % plaque.

KEY WORDS: Periodontitis, Chronic; Sleep Apnea, Obstructive

Obstructive sleep apnea (OSA) is a sleep disorder characterized by periodic and repetitive partial or complete collapse of the upper airway during sleep, resulting in reduced ventilation (hypopnea) or absent ventilation (apnea) and consequently disruptions of normal sleep architecture and associated arterial desaturations.1, 2 OSA is currently diagnosed with an overnight sleep diagnostic test known as a polysomnogram (PSG), which remains the gold standard of diagnosis.3 The standard definition of an apneic event includes a minimum 10 second interval between breaths, with either a neurological arousal, a blood oxygen desaturation of 3-4% or greater, or both arousal and desaturation.4-6 Hypopnea is defined as an episode of shallow breathing (airflow reduced by at least 50%) during sleep, lasting for 10 seconds or longer and usually associated with a fall in blood oxygen saturation due to partial obstruction of the upper airway.1 1

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The apnea-hypopnea index (AHI)4 is a commonly used index to categorize the severity of OSA, and it represents the average number of apneas and/or hypopneas per hour of recorded sleep. In adults, an AHI of less than 5 events per hour is considered normal. Mild OSA is defined as an AHI ≥5-15 events per hour, moderate OSA >15-30 events per hour, and severe OSA as >30 events per hour. The underlying mechanisms of OSA are largely associated with upper airway anatomy, dilator muscle dysfunction, lung volume or ventilatory control stability.7 Ongoing studies also suggest other possible pathophysiology pathways that include local and systemic inflammation8 and clock gene dysfunction9. Neuropsychiatric complications associated with OSA include daytime somnolence, cognitive dysfunction, depression and Alzheimer’s disease.10-12 OSA has been associated with an increased risk for development of vascular disorders such as coronary heart disease, hypertension, stroke, congestive cardiac failure, and atherosclerosis, as well as metabolic disorders such as impaired glucose tolerance and insulin resistance.11 Although the exact pathogenesis pathway of OSA leading to such complications is uncertain, studies have suggested the role of OSA in activation of various inflammatory processes through hypoxia and oxidative stress-induced reperfusion injury from intermittent hypoxia during apneic events in OSA.12, 13 Currently, treatment for OSA is confined to relief of the mechanical obstruction rather than focusing on the functional aspect of the disease.14 Better understanding of the underlying pathophysiology may bring about new and novel treatment strategies in the future.15 The biofilm derived from dental plaque in periodontitis is capable of adding to pre-existing systemic inflammatory burden through elevation of serum levels of C-reactive protein16 and a host of other important inflammatory cytokines and mediators.17-19 The resultant inflammatory response from periodontitis coupled with genetic and environmental risk factors could potentiate any existing inflammatory disease. A pilot study performed by Gunaratnam et al.20 found a higher prevalence of periodontitis among patients with OSA, suggesting a possible association between obstructive sleep apnea and periodontitis. Since treatment of periodontitis has been shown to improve systemic inflammation, metabolic control of glycemia, and parameters of vascular health 21, 22, treatment of periodontitis may prove to be one of the future novel ways in improving OSA. Epidemiologically, data from several OSA studies accomplished with PSG suggest that the prevalence of OSA is between 5-28% 23-27, with higher prevalence in males. Periodontitis is also a common chronic disease with a high prevalence. According to the most recent National Health and Nutrition Examination Survey 2009-2010 (NHANES), 47% of adults older than 30 years of age have chronic periodontitis, distributed as a prevalence 8.7%, 30% and 8.5% with mild, moderate and severe forms of periodontitis, respectively.28 The aim of this study was to determine whether OSA has any association with periodontitis. In particular, the association between OSA severity and the prevalence of periodontitis was investigated. In addition, the relationships between OSA severity and various clinical parameters of periodontal disease status were examined.

METHODS AND MATERIALS This cross-sectional study was conducted from June 2012 to August 2013 following approval by the Institutional Review Board of the University of Texas Health Science Center and the South Texas Veterans Health Care System, Veterans Administration facility, San Antonio Texas (Protocol number: HSC12-123H). All patients provided written informed consent prior to participation. Patients (N=100) were recruited by purposive consecutive sampling from the pool of patients who were scheduled for PSG‖ evaluation6 at the South Texas Veterans Health Care System facility, San Antonio Texas. A final total of 26 subjects in normal, 21 in mild, 19 in 2

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moderate and 34 in severe AHI groups were examined. The mean age was 52.6 (range: 28-79). Patient demographics are presented in Table 1. The population sampled at the VA hospital has a bias towards males, with males accounting for 91% of the data represented (Table 1). In terms of ethnicity, the distribution surveyed is representative of the U.S. population with a majority of the population sampled being Caucasian. A comprehensive periodontal evaluation was performed for each patient by a single examiner (WL) immediately prior to PSG; thus, the examiner was blinded to the patient’s OSA category. Following PSG, the patients diagnosed with varying degrees of OSA (test group) were stratified into the following categories: mild, moderate and severe according to AHI. At the same time, those patients whose PSG determined they did not have OSA acted as the control group. All patients had to have a minimum of 16 remaining natural teeth to be included in the study. Prior to periodontal examination, patient-level variables that are putative confounders such as BMI, diabetes and smoking history were recorded during the patient examination in detail as follows: • The body mass index (BMI) was calculated for each patient from data available in the chart. • If the patient had diabetes, the chart was reviewed to determine the last HbA1c (lab results had to be taken within the last 6 months prior to periodontal examination). •

Smoking history was determined by questioning of patients and categorized as:

o Non-smoker (never smoked) o Former smoker (smoked, but has quit prior to the study). Time since quit was determined in months. o Current smoker. Current smokers and former smokers who quit within the past 6 months were excluded from the study. The inclusion criteria for the OSA patients were: •

Mild OSA (AHI between ≥5-15/hr), Moderate (AHI >15-30 /hr), Severe (AHI >30/hr)



Aged 30 yrs old and above



Non-smokers, or former smokers who quit at least 6 months prior to examination



No history of acute coronary syndrome



ASA classification I or II

• Patients with diabetes were only included if glycemic control was good to moderate (documented HbA1c within last 6 months was < 8%). Periodontal examination included a full periodontal charting at 6 points per tooth (MF, F, DF, DL, L, ML), excluding third molars, recording probing depth (PD), recession (REC) and clinical attachment level (CAL). Bleeding on probing was assessed at 6 points per tooth and recorded as either present or absent within 15 seconds of probing. Presence of visible plaque was evaluated at 4 sites per tooth (M, F, D, L) and recorded as present or absent. Periodontal variables were examined for differences across all 4 different categories of OSA (none, mild OSA, moderate OSA and severe OSA). Following comprehensive clinical periodontal examination, the periodontal variables were assessed for both the test and control groups to determine relationships with sleep apnea and recorded as follows for each patient: 1. Mean periodontal pocket depth (PD) 3

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2. Mean clinical attachment level (CAL) 3. Mean gingival recession (REC) 4. % of sites with bleeding on probing (BOP) as a measure of gingival inflammation 5. % of sites with plaque 6. % of sites with PD > 5mm 7. % of sites with CAL > 3mm The definitions of periodontitis used in this study are the AAP/CDC definitions of periodontal disease as described by Eke et al.:29 • Mild periodontitis was defined as 2 or more inter-proximal sites with ≥ 3 mm AL and ≥ 2 interproximal sites with ≥ 4mm PD (not on the same tooth) or 1 site with ≥5mm. • Moderate periodontitis was defined as 2 or more interproximal sites with ≥ 4 mm clinical AL (not on the same tooth) or 2 or more interproximal sites with PD ≥ 5 mm, also not on the same tooth. • Severe periodontitis was defined as 2 or more interproximal sites with ≥ 6 mm AL (not on the same tooth) and 1 or more interproximal site(s) with ≥ 5 mm PD. Statistical Analysis The association between OSA and periodontal disease was analyzed using statistical methods that treated OSA as an exposure factor and periodontal diagnosis as outcome. Since OSA was represented by both ordinal (AHI classification) and continuous (observed AHI count) measures, while periodontal diagnosis was represented by dichotomous, ordinal, and continuous measures, several statistical methods were used. For the purposes of a priori power analysis, a one-way ANOVA comparing means for a continuous value periodontal index across the four classifications of OSA severity was considered. Based on equal sample sizes of 25 patients per group, the proposed total sample of 100 patients achieves 91% power to reject the null hypothesis of equal means using an F test with a 0.05 significance level if the population effect size is 0.39 or more. To achieve this effect size, the standard deviation of the 4 group means needs to be at least 39% of the common standard deviation within groups. This effect size requires a clinically significant mean difference of one common standard deviation to be present for the sample population between the control group and at least one of the OSA severity groups. Statistical analyses to assess associations between OSA severity represented as an ordinal grouping variable (normal, mild, moderate, severe) and demographic and periodontal variables were performed using chi-square tests for categorical measures, Spearman rank correlations for ordinal and continuous measures, and ANCOVAs for periodontal indices with age as a covariate. When small expected frequencies were observed, Fisher’s exact tests were substituted for chisquare tests. If the F-test for the main effect for OSA severity was significant for ANCOVA, then age-adjusted mean comparisons were performed for the severe group vs. the normal, mild and moderate OSA groups. Additional analyses were performed to assess associations between continuous AHI scores and demographic and periodontal variables using Spearman rank correlations for ordinal and continuous measures and multivariable logistic regressions predicting moderate to severe periodontitis using 10 unit increments for AHI. Hosmer-Lemeshow goodness-of-fit tests were performed to verify the validity of multivariable logistic regression models. The number of predictors for logistic regression was limited to the smaller number of patients between negatives 4

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and positives for moderate to severe periodontitis divided by 10. For statistical tests, p3mm with AHI classification, these relationships were further evaluated by analysis of covariance (ANCOVA) (Table 3). The significant relationship between AHI class and % plaque was confirmed by ANCOVA (p=0.037), with the age-adjusted Severe group mean significantly greater than the age-adjusted Mild group mean (mean difference of 21.7% with 95% CI of [7.0%, 36.3%], p=0.004). The age covariate was also significantly associated with % plaque (p=0.001). However, ANCOVA revealed no significant relationship between AHI class and %BOP (p=0.126) or % sites with CAL >3mm (p=0.842). The age covariate was significantly associated with %BOP (p=0.025) but not significantly associated with %CAL >3mm (p=0.266). Analyzing Periodontal Disease as a Categorical Variable The relationship between periodontitis classification as a categorical variable (ADA/CDC-mild, moderate, severe) and other patient-level variables was separately analyzed using Fisher’s exact tests. The analysis showed no statistically significant relationship between periodontitis classification and ethnicity (p=0.086) or gender (p=0.902). However, periodontal classification was significantly related to diabetes (p15-30 /hr), Severe OSA (AHI >30/hr)] and as continuous variables based on the absolute AHI values. Because the prevalence of moderate to severe periodontitis was higher in this study population than originally expected, a post-hoc power analysis was performed to determine the sample size needed to detect significant AHI group differences in percentages for moderate to severe periodontitis for a population with a very high prevalence of moderate to severe disease. The sample size would need to be doubled in such a population (N=200) to attain a sample size sufficient to detect AHI group differences by chi-square test at the 0.05 level with power of 84%. This study found no meaningful association between OSA and the prevalence of moderate/severe periodontitis. Furthermore, there was a negligible correlation between AHI severity and periodontal disease severity categories. We conclude that the relationship between the severity of OSA and periodontal status, if any, was weak in this specific patient population. Caution should be exercised when extrapolating the results of this study to the general population as the high prevalence of periodontitis recorded in this study differs from the prevalence found in the U.S. population as a whole.28,29 The high percentage of patients with moderate to severe periodontitis makes evaluation of differences in AHI severity between groups with no, mild, moderate and severe periodontitis more difficult. However, this patient population was selected from consecutively treated VA sleep center patients, without regard to their periodontal status, and periodontal examination was performed prior to the PSG study. Future studies should 7

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evaluate larger sleep study patient populations to provide a greater number of patients with little or no periodontitis. A summary of the various study designs, definitions and limitations of the previous studies are found in Table 5. The findings of this study are in disagreement with previous studies which examined the relationship between OSA and periodontal disease20, 31-33. The difference in study outcomes has several possible explanations. First, this study used 6-point comprehensive full mouth periodontal examination on all teeth that were present. One of the other studies32 used partial mouth charting, which may lead to an underestimation of the prevalence of periodontal disease. Second, the definitions of periodontal disease used in the previous studies were different from the current study. Some of the definitions may have underestimated32 the prevalence of periodontal disease, while others may have overestimated31 the prevalence of periodontal disease, relative to the CDC/AAP definition employed in this study.28 Third, the clinical diagnosis of OSA in one of the previous studies33 did not utilize the PSG sleep test, instead using a questionnaire meant for screening patients undergoing general anesthesia. Fourth, most of the previous studies either collapsed all the OSA groups into a dichotomous definition of presence or absence of sleep apnea,10 or had a stratification of three OSA groups (< 5, 5–10 and >10 events/hr),32 or obtained the diagnosis from ICD-9 databases.31 This may mask the inherent differences in prevalence of periodontal disease based on the AHI-defined severity groups from detection. The current study provides the most rigorous OSA classification of any study published to date, employing the current accepted stratification of the AHI groups into non-OSA (AHI 15-30 /hr), and severe OSA (AHI >30/hr).4 Finally, some studies20,31 examined the periodontal status of OSA patients only, comparing the prevalence of periodontitis in the OSA study population with that found in populations outside the study group such as national demographic dental databases20 or insurance databases.31 The current study examined both OSA and non-OSA patients, newly diagnosed with a PSG gold standard test within the Veterans Administration-eligible population. In other studies demonstrating an association between OSA and periodontal disease, the association as measured by odds ratio was relatively weak (1.75-1.84).31,32 In the current study, the odds ratio for AHI and prevalence of periodontitis was not statistically significant (O.R.= 1.057; 95% CI = [0.896-1.248]; p=0.511) and, coupled with the negligible correlation between AHI and periodontal disease severity categories suggests that there is no dose-response relationship between AHI severity and prevalence of periodontitis. This was confirmed statistically when AHI was expressed as an absolute value and treated as a continuous variable (rho=0.191; 95% CI = [-0.006 0.373]). In addition, the clinical parameters providing information on periodontitis severity and extent – mean PD, mean CAL, % of site with CAL >3mm, and % of sites with PD >5mm – were not significantly correlated with AHI severity.

CONCLUSIONS In conclusion, this is the first cross-sectional study showing that OSA, when defined in AHI severity categories, is not significantly associated with the prevalence of periodontitis in this specific VA population. Furthermore, none of the clinical periodontal parameters except for % plaque were significantly related to severity of OSA. In addition, when AHI was expressed in absolute values, there was no correlation with any periodontal parameters measured. ACKNOWLEDGMENTS The authors would like to thank the sleep technicians Amy McHenry and Larry Tho for their support in the recruitment of patients at the Audie L. Murphy Memorial Sleep Lab. The authors report no conflicts of interest related to this study. 8

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DISCLAIMERS: None

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Eckert DJ, Malhotra A, Jordan AS. Mechanisms of apnea. Prog Cardiovasc Dis 2009;51:313-323.

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Antonopoulou S, Loukides S, Papatheodorou G, Roussos C, Alchanatis M. Airway inflammation in obstructive sleep apnea: is leptin the missing link? Respir Med 2008;102:1399-1405.

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Burioka N, Koyanagi S, Endo M, et al. Clock gene dysfunction in patients with obstructive sleep apnoea syndrome. Eur Respir J 2008;32:105-112.

10. Even mild sleep apnea increases heart risk. Research shows that minimally symptomatic obstructive sleep apnea can increase arterial stiffness. Heart Advis 2009;12:4. 11. Arter J, Chi D, M G, Fitzgerald S, Guha B, Krishnaswamy G. Obstructive sleep apnea, inflammation, and cardiopulmonary disease. Front Biosci 2004;9:2892-2900. 12. Atkeson A, Jelic S. Mechanisms of endothelial dysfunction in obstructive sleep apnea. Vasc Health Risk Manag 2008;4:1327-1335. 13. Alam I, Lewis K, Stephens JW, Baxter JN. Obesity, metabolic syndrome and sleep apnoea: all proinflammatory states. Obes Rev 2007;8:119-127. 14. Abad VC, Guilleminault C. Treatment options for obstructive sleep apnea. Curr Treat Options Neurol 2009;11:358-367. 15. Owens RL, Eckert DJ, Yeh SY, Malhotra A. Upper airway function in the pathogenesis of obstructive sleep apnea: a review of the current literature. Curr Opin Pulm Med 2008;14:519-524. 16. Schenkein HA, Loos BG. Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases. J Periodontol 2013;84:S51-69. 17. Buhlin K, Hultin M, Norderyd O, et al. Risk factors for atherosclerosis in cases with severe periodontitis. J Clin Periodontol 2009;36:541-549. 18. Ebersole J, Machen R, Steffen M, Willmann D. Systemic acute-phase reactants, C-reactive protein and haptoglobin, in adult periodontitis. Clin Exp Immunol 1997;107:347-352. 19. Ebersole J, Cappelli D, Mathys E, et al. Periodontitis in humans and non-human primates: oral-systemic linkage inducing acute phase proteins. Ann Periodontol 2002;7:102-111. 20. Gunaratnam K, Taylor B, Curtis B, Cistulli P. Obstructive sleep apnoea and periodontitis: a novel association? Sleep Breath 2009;13:233-239. 21. Blum A, Front E, Peleg A. Periodontal care may improve systemic inflammation. Clin Invest Med 2007;30:E114-117.

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22. Vidal F, Figueredo C, Cordovil I, Fischer R. Periodontal therapy reduces plasma levels of interleukin-6, Creactive protein, and fibrinogen in patients with severe periodontitis and refractory arterial hypertension. J Periodontol 2009;80:786-791. 23. Lee W, Nagubadi S, Kryger MH, Mokhlesi B. Epidemiology of Obstructive Sleep Apnea: a Population-based Perspective. Expert Rev Respir Med 2008;2:349-364. 24. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med 2002;165:1217-1239. 25. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993;328:1230-1235. 26. Bixler EO, Vgontzas AN, Lin HM, et al. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Respir Crit Care Med 2001;163:608-613. 27. Durán J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep apnea-hypopnea and related clinical features in a population-based sample of subjects aged 30 to 70 yr. Am J Respir Crit Care Med 2001;163:685-689. 28. Eke PI, Dye BA, Wei L, Thornton-Evans GO, Genco RJ, Cdc Periodontal Disease Surveillance workgroup: James Beck GDRP. Prevalence of periodontitis in adults in the United States: 2009 and 2010. J Dent Res 2012;91:914-920. 29. Eke PI, Thornton-Evans G, Dye B, Genco R. Advances in surveillance of periodontitis: the Centers for Disease Control and Prevention periodontal disease surveillance project. J Periodontol 2012;83:1337-1342. 30. Hinkle DE, Wiersma W, Jurs SG. Applied statistics for the behavioral sciences. In. Boston: Houghton Mifflin, 2003. 31. Keller JJ, Wu CS, Chen YH, Lin HC. Association between obstructive sleep apnoea and chronic periodontitis: a population-based study. J Clin Periodontol 2013;40:111-117. 32. Seo WH, Cho ER, Thomas RJ, et al. The association between periodontitis and obstructive sleep apnea: a preliminary study. J Periodontal Res 2013;48:500-506. 33. Ahmad NE, Sanders AE, Sheats R, Brame JL, Essick GK. Obstructive sleep apnea in association with periodontitis: a case-control study. J Dent Hyg 2013;87:188-199.

Corresponding author: Dr. Brian L. Mealey, UTHSCSA Dept of Periodontics - MSC 7894, 7703 Floyd Curl Drive, San Antonio, Texas 78229-3900, Phone: (210) 567-3567, Fax: (210) 5673761, [email protected] Submitted April 16, 2014; accepted for publication September 3, 2014. Figure 1. Box plot analysis of AHI category and periodontal variables: A. Mean probing depth (PD); B. Mean recession (REC); C. Mean clinical attachment level (CAL); D. % sites with bleeding on probing (BOP); E. % sites with plaque (Pl); F. % sites with PD ≥5mm; G. % sites with CAL ≥3mm Table 1. Frequency table on patient characteristics (AHI) Normal Ethnicity African American 4 Caucasian 16 Hispanic 6 Other 0 Gender Female 4 Male 22 Smoking history Former smoker 6 Non-smoker 20 Diabetes

Mild

Moderate

Severe

Grand Total

2 13 3 3

1 13 5 0

8 16 10 0

15 58 24 3

3 18

2 17

0 34

9 91

2 19

6 13

11 23

25 75

10

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17 4 21

13 6 19

22 12 34

76 24 100

Table 2. Pearson Chi Square test for AHI classification and presence or absence of moderate to severe periodontitis Periodontal Disease (Moderate/Severe) AHI classification Total No Yes Normal 11 (42.3%) 15 (57.7%) 26 (100.0%) Mild 5 (23.8%) 16 (76.2%) 21 (100.0%) Moderate 6 (31.6%) 13 (68.4%) 19 (100.0%) Severe 5 (14.7%) 29 (85.3%) 34 (100.0%) Total Count 27 (27.0%) 73 (73.0%) 100 (100.0%) p=0.111 Table 3. ANCOVA analysis of % sites with BOP, % sites with plaque, % sites with CAL >3mm (means unadjusted for the age covariate) AHI Class N % BOP + SD* % plaque + SD** % sites CAL >3mm + SD*** Normal 26 13.1 + 12.4 34.0 + 27.6 42.5 + 20.7 Mild 21 11.3 + 9.4 31.5 + 20.5 44.4 + 23.7 Moderate 19 14.9 + 9.0 47.2 + 28.7 44.0 + 27.8 Severe 34 19.8 + 19.0 52.3 + 31.5 48.4 + 22.6 Total 100 15.3 + 14.2 42.2 + 29.0 45.2 + 23.2 * % BOP: F= 1.952; p=0.126 ** % plaque: F= 2.938; p=0.037 *** % sites CAL >3mm: F= 0.276; p=0.842 Table 4. Logistic regression model for periodontal disease prevalence and AHI Logistic regression model with age and smoking history included in the model Variable O.R. 95% C.I. P value AHI 10-unit increments 1.044 0.883 – 1.234 0.615 Age 10-year increments 1.523 1.047 – 2.216 0.028 Smoking History (Y/N) 3.492 0.918 – 13.279 0.067

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Table 5. Summary of cross-sectional studies on periodontal disease-OSA relationships Study Sample size Mean Age, Definition Definitions of BMI, AHI and periodontitis diagnosis of OSA 66 (54 men and 12 Mean age: (AHI) >5/h CDC/AAP: Gunaratnam, women), Australia 54.9 years 200920 (±12.8)

Seo, 201332

OSA group: AHI>5/h

Mean BMI: 30.5 kg/m2 (range 18.351.2 kg/m2)

No control group for non OSA patients, used national health survey data

Mean AHI 36.55 ± 25.77),

687 (460 men and 227 women), Korea

Mean age: 55.85 years (±6.63)

Presence of two or more interproximal sites with ≥4 mm CAL, not on the same tooth, or two or more interproximal sites with PD ≥5 mm, not on the same tooth. At least one periodontal pocket with a probing depth of 4 mm or more and CAL ≥3 mm at the same site on a tooth.

AHI was stratified only by 10

At least four teeth with one or more interproximal sites with a probing pocket depth of >4mm and CAL >6mm at the same site on a tooth.

AHI score of ≥ 5 was

Teeth examined

O.R. Perio-OSA

Limitation

All 6 sites at all existing teeth

Prevalence of periodontitis was 77–79% depending on definitions used, 4X higher than the reported prevalence in Australia.

No concurrent control group, used prevalence data from national demographic study as comparison to OSA group Whether control Patients had diagnosed or occult OSA is unknown

PD, CAL, REC and bleeding on probing (BOP)

Lobene modified gingival index (GI)

Silness and Loe plaque index (PI) All existing Ramfjord index teeth (#3, 9, 12, 19, 25, 28)

Bleeding on probing, probing

12

The periodontal examiner was not blinded to the study hypothesis. Hence, the potential for overdiagnosis of periodontitis Small sample size Overall, OSA was positively associated with periodontitis [odds ratio (OR) = 1.84, CI = 1.18–2.87] Probing pocket depth (OR =

Partial mouth examination. Not all teeth were examined, underestimation of disease

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the cut-off used to indicate the presence of OSA

Keller, 201331

Ahmad, 2013 33

7321 OSA patients, 21,963 non-OSA control patients (1:3 case: control ratio matched in terms of sex, age in intervals of 10-years, urbanization level and index year), Taiwan) over 62% were males.

Mean age: 47.6 years (±15.4)

154

Mean age: 61 years

(104 cases with

pocket depth, gingival recession, clinical attachment level (CAL), Silness and Loe plaque index and gingival index

Received a first-time diagnosis of OSA (ICD9-CM codes in the Longitudinal Health Insurance Database 2000)

Depth of 3 mm or greater constituted a diagnosis of periodontal disease, confirmed with mobility, bleeding, radiographic alveolar bone loss

Defined using a 4 item

ADA case type definitions: Moderate periodontitis

13

Full mouth 6 site probing

Full mouth periodontal exam with PD, CAL at 6

2.22, 95% CI = 1.30–3.77) CAL (OR = 1.86, 95% CI = 1.07–3.21) (OR = 2.51, 95% CI = 1.37–4.62) significant only in Patients ≥55 years of age, but not in Patients < 55 years of age. After adjusting for socioeconomic factors, OR=1.75 (95% CI = 1.68– 1.88) OR for prior CP among males was 1.81 (95% CI = 1.67–1.95; p < 0.001); among females was 1.62 (95% CI = 1.48– 1.78)

Cases were 4.1X more likely to be have OSA than

No concurrent control group, used historical data from insurance database

Multiple examiners Used samples with “prior diagnosis of chronic periodontitis’ They were unable to adjust for a number of confounding factors that were not included in the administrative data set analyzed in this study. Some of these factors included family history, cigarette smoking and occupational exposures. Utilization of questionnaire falls short of a clinical

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moderate/severe periodontitis, 50 controls with gingivitis,) 61 males, 93 female

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“STOP” OSA screening questionnair e

Type III:

Moderate alveolar bone loss and attachment loss 5-6mm PDs, 3-4mm CAL, mobility, furcation involvement is possible Severe Periodontitis Type IV: Severe alveolar bone loss and attachment loss, >7mm PDs, ≥5mm CAL, mobility and furcation involvement is possible

‖Cadwell Easy III PSG System (Cadwell Laboratories, Kennewick, WA) ¶SPSS 20.0 (IBM SPSS Inc., Chicago, IL).

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sites. Based primarily on the patients charts and reported severity of attachment loss; patients were classified according to the ADA case types.

controls (95% CI: 1.9, 11.4) (p=0.007)

diagnosis of OSA, with uncertain sensitivity or specificity; may misclassify the patients with/without OSA.

Journal of Periodontology; Copyright 2014

DOI: 10.1902/jop.2014.140229

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Investigating the association between obstructive sleep apnea and periodontitis.

Obstructive sleep apnea (OSA) is a sleep disorder characterized by disruptions of normal sleep architecture. Chronic periodontitis is a chronic diseas...
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