Kaumudi J Joshipura1, Francisco J Muñoz-Torres2, Bruce A Dye3, Brian G Leroux4, Margarita Ramírez-Vick5, Cynthia M Pérez6. 1. Center for Clinical Research and Health Promotion, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, United States; Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, United States. Electronic address: kaumudi.joshipura@upr.edu. 2. Center for Clinical Research and Health Promotion, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, United States. 3. National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, MD, United States. 4. School of Dentistry, University of Washington, Seattle, WA, United States. 5. Department of Medicine, Endocrinology, Diabetes and Metabolism Section, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico, United States. 6. Department of Biostatistics and Epidemiology, Graduate School of Public Health, University of Puerto Rico, Medical Sciences Campus, San Juan, Puerto Rico, United States.
Abstract
BACKGROUND: Clinical trials have shown very modest short-term improvements in glycemic control among participants with diabetes after periodontitis treatment. Few longitudinal studies suggest that periodontitis may be related to prediabetes/diabetes risk. METHODS: We evaluated 1206 diabetes free participants in the San Juan Overweight Adults Longitudinal Study (SOALS) and 941 with complete 3-year follow-up data were included. The National Health and Nutrition Examination Survey (NHANES) methods were used to assess periodontitis. Diabetes and prediabetes were classified using American Diabetes Association cutoffs for fasting and 2-hour post-load glucose and HbA1c. We used Poisson regression adjusting for baseline age, gender, smoking, education, family history of diabetes, physical activity, waist circumference, and alcohol intake. RESULTS: Over the 3-year follow-up, 69 (7.3%) of the 941 individuals developed type 2 diabetes, and 142 (34.9%) of the 407 with normal glycemia at baseline developed prediabetes. In multivariable models, greater mean pocket depth and mean attachment loss at baseline were associated with lower risk of developing prediabetes/diabetes over the follow-up (IRR = 0.81; 95% CI: 0.67-0.99, and IRR = 0.86; 95% CI: 0.74-0.99, respectively). Increase in periodontal attachment loss from baseline to follow-up was associated with higher prediabetes/diabetes risk (multivariate IRR = 1.25; 95% CI: 1.09-1.42), and increase in pocket depth was associated with >20% fasting glucose increase (multivariate IRR = 1.43; 95% CI: 1.14-1.79). The inverse associations persisted after additionally adjusting for baseline income, sugar-sweetened beverages, number of teeth, oral hygiene, glycemia, or previous periodontal therapy. CONCLUSIONS: There is no association between periodontitis and risk of prediabetes/diabetes in this longitudinal study.
BACKGROUND: Clinical trials have shown very modest short-term improvements in glycemic control among participants with diabetes after periodontitis treatment. Few longitudinal studies suggest that periodontitis may be related to prediabetes/diabetes risk. METHODS: We evaluated 1206 diabetes free participants in the San Juan Overweight Adults Longitudinal Study (SOALS) and 941 with complete 3-year follow-up data were included. The National Health and Nutrition Examination Survey (NHANES) methods were used to assess periodontitis. Diabetes and prediabetes were classified using American Diabetes Association cutoffs for fasting and 2-hour post-load glucose and HbA1c. We used Poisson regression adjusting for baseline age, gender, smoking, education, family history of diabetes, physical activity, waist circumference, and alcohol intake. RESULTS: Over the 3-year follow-up, 69 (7.3%) of the 941 individuals developed type 2 diabetes, and 142 (34.9%) of the 407 with normal glycemia at baseline developed prediabetes. In multivariable models, greater mean pocket depth and mean attachment loss at baseline were associated with lower risk of developing prediabetes/diabetes over the follow-up (IRR = 0.81; 95% CI: 0.67-0.99, and IRR = 0.86; 95% CI: 0.74-0.99, respectively). Increase in periodontal attachment loss from baseline to follow-up was associated with higher prediabetes/diabetes risk (multivariate IRR = 1.25; 95% CI: 1.09-1.42), and increase in pocket depth was associated with >20% fasting glucose increase (multivariate IRR = 1.43; 95% CI: 1.14-1.79). The inverse associations persisted after additionally adjusting for baseline income, sugar-sweetened beverages, number of teeth, oral hygiene, glycemia, or previous periodontal therapy. CONCLUSIONS: There is no association between periodontitis and risk of prediabetes/diabetes in this longitudinal study.
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