To examine the relationship between chronic periodontal disease (CPD) and erectile dysfunction (ED), the interview sheet including the CPD self-checklist (CPD score) and the 5-item version of the International Index of Erectile Function (IIEF-5) was distributed to 300 adult men who received a comprehensive dental examination. Statistical analyses were performed by the Spearman's rank correlation coefficient and other methods. Statistical significance was accepted at the level of P<0.05. The interview sheets were collected from 88 men (response rate 29.3%, 50.9 ± 16.6 years old). There was a statistically significant correlation between the CPD score and the presence of ED (P=0.0415). The results in the present study suggest that ED is related to the damage caused by endothelial dysfunction and the systematic inflammatory changes associated with CPD. The present study also suggests that dental health is important as a preventive medicine for ED.

What's known on the subject? and What does the study add?There is known to be an association between overactive bladder (OAB) and irritable bowel syndrome (IBS).The study investigates the association between OAB and IBS using an internet-based survey in Japan. It is the first to investigate the prevalence and severity of OAB in the general population using the OAB symptom score questionnaire.ObjectiveTo investigate the association between overactive bladder (OAB) and irritable bowel syndrome (IBS) by using an internet-based survey in Japan.Subjects and MethodsQuestionnaires were sent via the internet to Japanese adults.The overactive bladder symptom score was used for screening OAB, and the Japanese version of the Rome III criteria for the diagnosis of IBS was used for screening this syndrome.ResultsThe overall prevalence of OAB and IBS was 9.3% and 21.2%, respectively.Among the subjects with OAB, 33.3% had concurrent IBS.The prevalence of OAB among men was 9.7% and among women it was 8.9%, while 18.6% of men and 23.9% of women had IBS.Concurrent IBS was noted in 32.0% of men and 34.8% of women with OAB.ConclusionTaking into account a high rate of concurrent IBS in patients with OAB, it seems to be important for physicians to assess the defaecation habits of patients when diagnosing and treating OAB.

In this study, we investigated the effects of bladder outlet obstruction (BOO) on the expression and function of large conductance (BK) and small conductance (SK) Ca(2+)-activated K(+) channels in detrusor smooth muscle. The bladder from adult female Sprague-Dawley rats with 6-wk BOO were used. The mRNA expression of the BK channel alpha-subunit, beta1-, beta2-, and beta4-subunits and SK1, SK2, and SK3 channels were investigated using real-time RT-PCR. All subunits except for the BK-beta2, SK2, and SK3 channels were predominantly expressed in the detrusor smooth muscle rather than in the mucosa. The mRNA expression of the BK channel alpha-subunit was not significantly changed in obstructed bladders. However, the expression of the BK channel beta1-subunit and the SK3 channel was remarkably increased in obstructed bladders. On the other hand, the expression of the BK channel beta4-subunit was decreased as the severity of BOO-induced bladder overactivity progressed. In detrusor smooth muscle strips from obstructed bladders, blockade of BK channels by iberiotoxin (IbTx) or charybdotoxin (CTx) and blockade of SK channels by apamin increased the amplitude of spontaneous contractions. These blockers also increased the contractility and affinity of these strips for carbachol during cumulative applications. The facilitatory effects elicited by these K(+) channel blockers were larger in the strips from obstructed bladders compared with control bladders. These results suggest that long-term exposure to BOO for 6 wk enhances the function of both BK and SK types of Ca(2+)-activated K(+) channels in the detrusor smooth muscle to induce an inhibition of bladder contractility, which might be a compensatory mechanism to reduce BOO-induced bladder overactivity.

Purpose In this study, we evaluated the role of M2 and M3 mAChR subtypes in activation of bladder afferent pathways in rats with chronic spinal cord injury (SCI). Materials and Methods Adult female Sprague-Dawley rats were spinalized at the Th9 level. Continuous cystometry was performed under an awake condition 2 or 4 weeks after SCI. The effects of intravesical administration of an mAChR agonist (oxotremorine-M; Oxo-M), a non-selective antagonist (atropine), an M2-selective antagonist (methoctramine) and an M3-selective antagonist (darifenacin) were examined. After cystometry, the bladder was removed and separated into mucosa and detrusor, and M2 and M3 mAChR mRNA expression in the mucosa was determined with real time quantitative PCR. Results At 2 and 4 weeks after SCI, intravesical administration of a non-selective mAChR agonist (25μM Oxo-M) increased the area under the curve of non-voiding contractions (NVCs) although intercontraction interval (ICI) of voiding contractions and maximum voiding pressure (MVP) did not change. This effect was blocked by atropine and methoctramine (10μM), but not by darifenacin (50μM). However, mAChR antagonists alone (50μM) had no effect on cystometric parameters. M2 mAChR mRNA expression was increased in mucosa of SCI rats compared to normal rats. Conclusions Our results suggest that the M2 mAChR subtype plays an important role in bladder afferent activation that enhances detrusor overactivity in SCI rats. However, because mAChR antagonists alone did not affect any cystometric parameters, the muscarinic mechanism controlling bladder afferent activity may not be involved in the emergence of detrusor overactivity in SCI.