Editing Chronic Pelvic Pain Syndrome & Prostatitis (section)

=== Pathogenesis ===

* '''<span style="color:#ff0000">Risk factors that allow bacterial colonization or infection of the prostate with potentially pathogenic bacteria include:</span>'''
** '''<span style="color:#ff0000">Intraprostatic ductal reflux</span>'''
** '''<span style="color:#ff0000">Phimosis</span>'''
** '''<span style="color:#ff0000">Specific blood groups</span>'''
** '''<span style="color:#ff0000">Unprotected penetrative anal rectal intercourse</span>'''
** '''<span style="color:#ff0000">UTI</span>'''
** '''<span style="color:#ff0000">Acute epididymitis</span>'''
** '''<span style="color:#ff0000">Indwelling urethral catheters and condom catheter drainage</span>'''
** '''<span style="color:#ff0000">Transurethral surgery, especially in men who have untreated, infected urine</span>'''
* Nonbacterial prostatitis and CPPS are caused by an interrelated cascade of inflammatory, immunologic, endocrine, muscular, neuropathic, and psychologic mechanisms that begin with an initiator in a genetically or anatomically susceptible man
** '''Intraprostatic ductal reflux'''
*** Reflux of urine and possibly bacteria into the prostatic ducts has been postulated as one of the causative mechanisms involved in the pathogenesis of chronic bacterial and non-bacterial prostatic inflammation in some individuals
*** '''Prostatic calculi are composed of substances found only in urine, not in prostatic secretions, further evidence that urinary intraprostatic reflux occurs''' and likely contributes to the formation of prostatic calculi.
**** If pathogenic bacteria reflux into the prostate gland, they may exist in protected aggregates within prostatic calculi themselves. This type of bacterial colonization in protective bacterial aggregates or biofilms associated with prostatic calculi may lead to recalcitrant CP and subsequent recurrent UTIs despite what seems to be adequate antibiotic therapy
** '''Chemically induced inflammation'''
*** Secondary to the noxious substances in the urine that have refluxed into the prostatic duct
** '''Dysfunctional voiding'''
*** Anatomic or neurophysiologic obstruction resulting in high-pressure dysfunctional flow patterns has been implicated in the pathogenesis of prostatitis syndrome.
** '''Pelvic floor muscle abnormalities'''
*** Sensory or motor disturbances or both consistent with neural dysregulation of the lower urinary tract may be a consequence of acquired abnormalities in the central nervous system (CNS). Certainly, extraprostatic tenderness is identified in many patients
** '''Neural sensitization'''
*** Altered autonomic nervous system responses may be responsible for the pain associated with CPPS
** '''Immunologic alterations'''
*** Non-infectious inflammation (non-bacterial prostatitis or CPPS) might also be secondary to immunologically mediated inflammation caused by some unknown antigen or perhaps even related to an autoimmune process
*** '''CPPS can exist through persistent immunologic mechanisms long after the bacteria have been eradicated.'''
*** Whatever the initiating event, the immunologic cascade appears to have an important role in the development of prostatitis or CPPS in patients who develop prostatic inflammation
** '''Pyschosocial associations'''
*** Psychological factors have always been considered to play an important role in the development or exacerbation of CP syndromes.