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1. Investigating the Association Between Obstructive Sleep Apnea and Periodontitis Weiqiang Loke,* Thomas Girvan, Paul Ingmundson, Ronald Verrett, John Schooleld,* and Brian L. Mealey* Background: Obstructive sleep apnea (OSA) is a sleep dis- order characterized by disruptions of normal sleep archit- ecture. Chronic periodontitis is a chronic disease of the periodontium that elicits a general inammatory response to local dental plaque. It has been suggested that periodontal dis- ease may increase in severity with increasingly severe OSA because both disease entities share common inammatory pathways, acting synergistically to alter the host response. The aim of this study is to analyze the association between se- verity of OSA and the prevalence/severity of periodontitis. Methods: One hundred patients from a large veterans ad- ministration sleep study center (n = 26 normal, n = 21 mild, n = 19 moderate, n = 34 severe) diagnosed with an overnight polysomnogram underwent a comprehensive periodontal ex- amination. Periodontal parameters measured included the fol- lowing: 1) mean periodontal probing depth (PD); 2) clinical attachment level (CAL); 3) gingival recession; and 4) percent- age of sites with bleeding on probing, plaque, PD 5 mm, and CAL 3 mm. Results: Seventy-three percent of the sampled population had moderate/severe periodontal disease. x2 analyses revealed no signicant differences in the prevalence of peri- odontal disease between the apneahypopnea index (AHI) groups, with a negligible Spearman correlation coefcient of 0.246 between AHI severity and periodontal disease severity categories. Analysis of covariance indicated a signicant asso- ciation between AHI severity categories and percentage of sites with plaque, after adjusting for age. Multivariable logis- tic regression analysis predicting moderate/severe peri- odontitis with AHI score, age, and smoking status indicated a signicant association with age (P = 0.028) but no signi- cant association with the other two predictors. Conclusion: OSA was not signicantly associated with the prevalence of moderate/severe periodontitis and the peri- odontal parameters examined, except percentage plaque. J Periodontol 2015;86:232-243. KEY WORDS Chronic periodontitis; sleep apnea, obstructive. O bstructive sleep apnea (OSA) is a sleep disorder characterized by periodic and repetitive par- tial or complete collapse of the upper airway during sleep, resulting in reduced ventilation (hypopnea) or absent venti- lation (apnea) and, consequently, disrup- tions of normal sleep architecture and associated arterial desaturations.1,2 OSA is currently diagnosed with an overnight sleep diagnostic test known as a poly- somnogram (PSG), which remains the gold standard of diagnosis.3 The stan- dard denition of an apneic event in- cludes a minimum 10-second interval between breaths, with a neurologic arousal, a blood oxygen desaturation of 3% to 4% or greater, or both arousal and de- saturation.4-6 Hypopnea is dened as an episode of shallow breathing (air- ow reduced by 50%) during sleep, lasting for 10 seconds and usually associated with a fall in blood oxygen saturation attributable to partial ob- struction of the upper airway.1 The apneahypopnea 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 ve events per hour is considered normal. Mild OSA is dened as an AHI of at least ve to 15 events per hour, moderate OSA as >15 to 30 events per hour, and se- vere OSA as >30 events per hour. The underlying mechanisms of OSA are primarily associated with upper airway * 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. Department of Comprehensive Dentistry, University of Texas Health Science Center at San Antonio Dental School. doi: 10.1902/jop.2014.140229 Volume 86 Number 2 232 2. anatomy, dilator muscle dysfunction, lung volume, or ventilatory control stability.7 Ongoing studies also suggest other possible pathophysiology path- ways that include local and systemic inammation8 and clock gene dysfunction.9 Neuropsychiatric com- plications associated with OSA include daytime somnolence, cognitive dysfunction, depression, and Alzheimers disease.10-12 OSA has been associated with an increased risk for development of vascular disorders, such as coronary heart disease, hyperten- sion, stroke, congestive cardiac failure, and ath- erosclerosis, 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 inammatory processes through hypoxia and oxidative stress-induced reperfusion injury from intermittent hypoxia during apneic events in OSA.12,13 Currently, treatment for OSA is conned to relief of the mechanical obstruction rather than focusing on the functional aspect of the disease.14 Better understanding of the underlying pathophys- iology may bring about new and novel treatment strategies in the future.15 The biolm derived from dental plaque in peri- odontitis is capable of adding to pre-existing sys- temic inammatory burden through elevation of serum levels of C-reactive protein16 and a host of other important inammatory cytokines and medi- ators.17-19 The resultant inammatory response from periodontitis coupled with genetic and environ- mental risk factors could potentiate any existing inammatory 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 OSA and periodontitis. Because treatment of periodontitis has been shown to improve systemic inammation, metabolic control of glycemia, and parameters of vascular health,21,22 treatment of periodontitis may prove to be one of the future, novel ways to improve OSA. Epidemiologically, data from several OSA stud- ies accomplished with PSG suggest that the prev- alence of OSA is between 5% and 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 to 2010, 47% of adults aged >30 years have chronic periodontitis (CP), distributed as a prevalence of 8.7%, 30%, and 8.5% with mild, moderate, and severe forms of peri- odontitis, respectively.28 The aim of this study is to determine whether OSA has any association with periodontitis. In par- ticular, the association between OSA severity and the prevalence of periodontitis was investigated. In addition, the relations between OSA severity and various clinical parameters of periodontal disease status were examined. MATERIALS AND METHODS This cross-sectional study was conducted from June 2012 to August 2013 after approval by the Institutional Review Board of the University of Texas Health Science Center and the South Texas Veterans Health Care System, Veterans Administration (VA) facility, San Antonio, Texas (protocol no. HSC12-123H). All patients provided written informed consent be- fore participation. Patients (n = 100) were recruited by purposive consecutive sampling from the pool of patients who were scheduled for PSGi evaluation6 at the South Texas Veterans Health Care System facility, San Antonio, Texas. The participants included 91 males and 9 females, aged 28 to 79 years; mean age: 52.6 years), with a nal total of 26 individuals in the normal, 21 in the mild, 19 in the moderate, and 34 in the severe AHI groups examined. Addi- tional patient demographics are presented in Table 1. The population sampled at the VA hospital has a bias toward males, with males accounting for 91% of the data represented (Table 1). In terms of eth- nicity, the distribution surveyed is representative of the U.S. population, with a majority of the pop- ulation sampled being white. A comprehensive periodontal evaluation was per- formed for each patient by a single examiner (WL) immediately before the PSG; thus, the examiner was masked to the patients OSA category. After PSG, the patients diagnosed with varying degrees of OSA (test group) were stratied into the following categories: mild, moderate, and severe according to the AHI. At the same time, those patients whose PSG determined that they did not have OSA acted as the control group. All patients had to have a minimum of 16 remaining natural teeth to be in- cluded in the study. Before the periodontal examination, patient-level variables that are putative confounders, such as body mass index (BMI), diabetes, and smoking history, were recorded during the patient examination in detail as follows. The BMI was calculated for each patient from data available in the chart. If the pa- tient had diabetes, the chart was reviewed to de- termine the most recent hemoglobin A1c (HbA1c) (laboratory results had to be taken within the 6 months before the periodontal examination). Smok- ing history was determined by questioning patients and categorized as follows: 1) non-smoker (never smoked); 2) former smoker (smoked but quit before i Easy III PSG System, Cadwell Laboratories, Kennewick, WA. J Periodontol February 2015 Loke, Girvan, Ingmundson, Verrett, Schooleld, Mealey 233 3. the study; time since quitting was determined in months); and 3) 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 as follows: 1) mild (AHI of at least ve to 15 per hour), moderate (AHI >15 to 30 per hour), and severe (AHI >30 per hou