Background Association between periodontitis and prostate diseases of benign prostatic hyperplasia (BPH) and prostatitis is uncertain. Methods From the National Health Insurance Research Database of Taiwan, 5,510 patients with newly diagnosed chronic periodontitis and participated in therapies were selected from 2000 to 2015 as cohort 1. Matched with age and index year, 5,510 patients with periodontitis diagnosis without therapy were selected as cohort 2, and 5,510 participants without diagnosis were used as control. Cox proportional hazard and survival analysis were performed to compare the risks and the survival probabilities among cohorts. Results In two periodontitis cohorts, 636 and 638 participants compared with 550 in control (1,174 and 1,187 versus 989 per 100,000 person‐years) had prostate disorder. Difference was identified for prostatitis (n = 68, 70 versus 34; rate = 125, 130 versus 61 /100,000 person‐years; P <0.001) but not for BPH (n = 577, 575, versus 529; rate = 1,065, 1,070 versus 951 /100,000 person‐years, respectively). Different survival probabilities for prostate disorder and prostatitis, but not for BPH, were observed among cohorts. Periodontitis patients were more likely to develop prostate disorder after adjustment (adjusted hazard ratio [aHR] of 2.590 to 2.641 by competing model). With stratification, risks between two periodontitis cohorts exhibited no difference. When BPH cases were excluded, the aHRs for prostatitis were 4.611 to 4.798. Conclusions Despite treatment, the patients with periodontitis had higher risk of developing prostatitis than patients without periodontitis.

Two-way relationship between periodontitis and diabetes was advocated; however, bidirectional observation in general population is still inconclusive. Using the Taiwan Health Insurance Database (covering over 99% of the entire population),11,011 patients with severe periodontitis were recruited from 2000 to 2015.After matching by age, sex, and index date, 11,011 patients with mild periodontitis and 11,011 non-periodontitis controls were registered. The outcome of T2DM was traced. Conversely, the development of periodontitis was traced in 157,798 patients with T2DM, and 157,798 non-diabetic controls enrolled. The risks of T2DM significantly increased in groups with severe and mild periodontitis, with the adjusted hazard ratio (aHR) and 95% confidence interval (CI) being 1.94 (1.49–2.63, p < 0.01) and 1.72 (1.24–2.52, p < 0.01), respectively. Patients with severe periodontitis had a high risk of having diabetes compared to those with mild periodontitis [aHR, 1.17 (95% CI 1.04–1.26, p < 0.001)]. Conversely, the risk of periodontitis increased significantly in patients with T2DM [1.99 (1.42–2.48, p < 0.01)]. However, the high risk was not observed for the outcome of mild periodontitis [0.97 (0.38–1.57, p = 0.462)]. We, therefore, suggested the bi-direction is between diabetes and severe periodontitis, but not in mild type.

Objective Two-way relationship between periodontitis and diabetes was advocated. However, bidirectional epidemiological observation is still limited and inconsistent. Using the National Health Insurance Research Database of Taiwan (covering over 99% of the entire population), we estimate the development of diabetes in periodontitis patients or that of periodontitis in patients with type 2 diabetes mellitus (T2DM), respectively. Methods A total of 11,011 patients with severe periodontitis were recruited from 2000 to 2015. After matching by age, sex, and index date, 11,011 patients with mild periodontitis and 11,011 non-periodontitis controls were registered. Conversely, 157,798 patients with T2DM and 157,798 non-T2DM controls were enrolled, whereas the development of periodontitis was traced. Cox proportional hazards model was performed. Results Periodontitis patients tended to have a statistically high risk of having T2DM. Adjusted hazard ratio (aHR) was 1.94 (95% CI 1.49–2.63, p &lt; 0.01) and 1.72 (95% CI 1.24–2.52, p &lt; 0.01) for severe and mild periodontitis groups, respectively. Besides, the patients in severe periodontitis had a high risk of having T2DM compared to that in mild periodontitis [1.17 (95% CI 1.04–1.26, p &lt; 0.001)]. Conversely, the risk of periodontitis increased significantly in patients with T2DM [1.99 (95% CI,1.42–2.48, p &lt; 0.01)]. However, the high risk was observed for the outcome of severe periodontitis [2.08 (95% CI, 1.50–2.66, p &lt; 0.001)], not for that of mild periodontitis [0.97 (95% CI,0.38–1.57, p = 0.462)]. Conclusions We suggested the bi-direction is between T2DM and severe periodontitis, but not in mild type.

The aim of the study was to report our experiences in the treatment of chronic prostatitis using combination regimen including ciprofloxacin, doxazosin, allopurinol and biofeedback perineal massage. From May 2003 to April 2004, 7 patients with NIH Category II-chronic bacterial prostatitis and 7 patients with NIH Category IIIA-inflammatory chronic pelvic pain syndrome were treated. The NIH-Chronic Prostatitis Symptom Index (NIH-CPSI) was scored by the patient before and after the treatment, 6 months later. In Category II patients, the bacterial eradication rate was 71% after ciprofloxacin treatment during a follow-up of 6 months. The beneficial response rate to allopurinol, doxazosin and biofeedback perineal massage was 50%, 42% and 85%, respectively. In NIH Category IIIA patients, the individual beneficial response rate to ciprofloxacin, allopurinol, doxazosin and biofeedback perineal massage was 57%, 100%, 71% and 100%, respectively. Comparing pre-treatment and post-treatment results of the combination regimen, there was a statistically significant improvement in the 3 domains of pain score, urinary symptoms and quality of life impact of the NIH-CPSI. Combination regimen including ciprofloxacin, doxazosin allopurinol and biofeedback perineal massage in the treatment of chronic prostatitis is a safe and effective modality in our limited experience.