Yuhan Huang1, Dominique S Michaud2, Jiayun Lu1, H Ballentine Carter3,4, Elizabeth A Platz5,6,7. 1. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Room E6132, 615 N Wolfe St, Baltimore, MD, 21205, USA. 2. Department of Public Health and Community Medicine, Tufts University School of Medicine, Boston, USA. 3. Department of Urology and the James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 4. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA. 5. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Room E6132, 615 N Wolfe St, Baltimore, MD, 21205, USA. eplatz1@jhu.edu. 6. Department of Urology and the James Buchanan Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA. eplatz1@jhu.edu. 7. Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD, USA. eplatz1@jhu.edu.
Abstract
PURPOSE: We evaluated the association between clinically assessed periodontal disease and serum prostate-specific antigen (PSA) concentration in men without a prostate cancer diagnosis in a US nationally representative sample of non-institutionalized men. METHODS: Included were 1263 men aged ≥ 40 years who participated in the National Health and Nutrition Examination Survey in 2009-2010. Measurements of periodontal health and tooth count were used to define periodontal disease severity (no, mild, moderate, severe) and edentulism. Linear and logistic regressions were used to estimate the association of periodontal disease severity and edentulism with PSA concentration and elevated PSA, respectively. RESULTS: Adjusting for age and other factors including race, body mass index, and education, the natural logarithm of PSA concentration did not change with increasing severity (mild - 0.20, 95% confidence interval [CI] - 0.34 to - 0.05; moderate - 0.12, 95% CI - 0.26 to 0.01; severe - 0.16, 95% CI - 0.43 to 0.12; edentulism - 0.16, 95% CI - 0.35 to 0.04; P-trend 0.13) compared with dentate men without periodontal disease. Although the multivariable-adjusted ORs of elevated PSA were not statistically significant, participants with more severe periodontal disease were less likely to have PSA > 2.0 and > 2.5 ng/mL, but more likely to have PSA > 4.0 ng/mL, compared to dentate men without periodontal disease. Similar non-significant associations with PSA were observed when comparing edentulous men to dentate men without periodontal disease. CONCLUSIONS: In this US nationally representative sample, men with periodontal disease did not have higher serum PSA and were not more likely to have clinically elevated PSA after taking into account age and other factors, contrary to the hypothesis. This study suggests that periodontal disease does not notably affect the specificity of PSA for prostate cancer screening.
PURPOSE: We evaluated the association between clinically assessed periodontal disease and serum prostate-specific antigen (PSA) concentration in men without a prostate cancer diagnosis in a US nationally representative sample of non-institutionalized men. METHODS: Included were 1263 men aged ≥ 40 years who participated in the National Health and Nutrition Examination Survey in 2009-2010. Measurements of periodontal health and tooth count were used to define periodontal disease severity (no, mild, moderate, severe) and edentulism. Linear and logistic regressions were used to estimate the association of periodontal disease severity and edentulism with PSA concentration and elevated PSA, respectively. RESULTS: Adjusting for age and other factors including race, body mass index, and education, the natural logarithm of PSA concentration did not change with increasing severity (mild - 0.20, 95% confidence interval [CI] - 0.34 to - 0.05; moderate - 0.12, 95% CI - 0.26 to 0.01; severe - 0.16, 95% CI - 0.43 to 0.12; edentulism - 0.16, 95% CI - 0.35 to 0.04; P-trend 0.13) compared with dentate men without periodontal disease. Although the multivariable-adjusted ORs of elevated PSA were not statistically significant, participants with more severe periodontal disease were less likely to have PSA > 2.0 and > 2.5 ng/mL, but more likely to have PSA > 4.0 ng/mL, compared to dentate men without periodontal disease. Similar non-significant associations with PSA were observed when comparing edentulous men to dentate men without periodontal disease. CONCLUSIONS: In this US nationally representative sample, men with periodontal disease did not have higher serum PSA and were not more likely to have clinically elevated PSA after taking into account age and other factors, contrary to the hypothesis. This study suggests that periodontal disease does not notably affect the specificity of PSA for prostate cancer screening.
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