Chronic prostatitis is a complex concept. The current research believes that it is not an independent disease, but a syndrome or syndrome with their own unique forms. This syndrome has its own unique etiology, clinical characteristics, and outcome.
Although the etiology of prostatitis started late, it also went through a complicated and tortuous process. In the late 19th century, it was considered that chronic prostatitis was related to vaginal trauma, masturbation, and overindulgence; in the early 20th century, due to the in-depth study of bacteriology and infectious diseases, microbiologists regarded bacterial infection as the cause of prostatitis; Neisseria gonorrhoeae was once considered as the main infectious pathogen of prostatitis.
In the 1950s, it was recognized that inflammation of the prostate could be mediated by no bacteria. In the following decades, there has been no breakthrough in the etiology of prostatitis.
In recent years, due to the rapid development of molecular biology and other disciplines, the pathogenesis of prostatitis has been paid more attention. However, the etiology of the prostate is very complex, so it is necessary to broaden the research field of prostatitis, pay attention to interdisciplinary research, and promote the in-depth study of prostate etiology.
1. Etiology
As early as the 20th century, bacteria and prostatitis have been linked. At present, many mathematicians still think that it may be related to bacterial infection. But it is undeniable that the vast majority of prostatitis is chronic nonbacterial prostatitis (NBP).
2. Urine reflux
In recent years, many scholars at home and abroad have found that there is urine reflux in patients with prostatitis, which may be of great significance to the pathogenesis of various types of prostatitis.
3. Abnormal immune function
Some scholars think that the inflammatory response of chronic prostatitis is the expression of low systemic immune function, but the local immune function of the prostate usually shows abnormal enhancement, and cell and humoral immune response are involved in the immune response process of chronic prostatitis.
4. Lower urinary tract epithelial dysfunction
After the damage of the lower urinary tract epithelium, the permeability of the cells increased. As a result, the potentially toxic substances (mainly potassium ions, etc.) in the urine entered the bladder muscle, depolarizing the sensory nerve cells, causing clinical symptoms such as frequency of urination and urgency of urination, and the symptoms continued to progress and increased with time.
5. Genetic susceptibility
The occurrence of chronic prostatitis may also be related to genetic susceptibility. Riley et al. (2002) suggested that chronic prostatitis also has gene susceptibility. Further study on the genetic characteristics of chronic prostatitis will help to find the causes of chronic prostatitis and lay a foundation for gene prevention and treatment of prostatitis.
6. Comprehensive effects of various factors
There are many etiology hypotheses of chronic prostatitis, and a single pathogenesis can not explain the complex clinical manifestations of prostatitis, which may be the result of the interaction of multiple factors. How to find some key regulation points in the pathogenesis of chronic prostatitis is a challenge for urologists and andrologists.