(A) Type I prostatitis
The main causative factor is pathogenic infection. The actual fact is that the actual body’s resistance is low, the more virulent bacteria or other pathogens infect the prostate and rapidly grow and multiply, mostly bloodstream infection, retrograde infection via the urethra. The pathogens are mainly Escherichia coli, followed by Staphylococcus aureus, Klebsiella pneumoniae, Aspergillus, Pseudomonas spp. The majority of these are single pathogen infections.
(B) Type II prostatitis
The pathogenic factors are also mainly pathogenic infections, but the body is more resistant and/or the pathogens are less virulent, with retrograde infections being the main pathogens, mainly Staphylococcus spp, followed by Escherichia coli, Corynebacterium spp and Enterococcus spp. Prostate stones and urinary reflux may be important reasons for the persistence of pathogens and recurrence of infection.
(C) Type III prostatitis
The etiology is complex and widely debated: it may be caused by a single initiating factor, or it may be multifactorial from the beginning, with one or more of them playing a key role; or it may be a number of different diseases that are difficult to identify but have the same or similar clinical manifestations; or even these diseases may have been cured and the damage and pathological changes caused by them continue to act independently. Most scholars believe that its main etiology may be the result of a combination of pathogenic infection, inflammation and abnormal pelvic floor neuromuscular and immune abnormalities.
1. Pathogenic infection
Although routine bacterial examination fails to isolate pathogens in patients with this type, they may still be associated with some specific pathogens: such as anaerobic bacteria, L-type Aspergillus, nanobacteria, or Chlamydia trachomatis, mycoplasma, and other infections. It is also possible to detect up to 77% of local prokaryotic DNA in this type of patient; some clinical “aseptic” prostatitis with chronic inflammation, recurrent or aggravated, may be related to these pathogens. The other pathogens such as parasites, fungi, viruses, trichomonas, and Mycobacterium tuberculosis may also be important causative factors for this type, but the lack of reliable evidence has not yet led to a unified opinion.
2. Urinary dysfunction
Many patients with prostatitis have a variety of urodynamic changes, such as reduced urinary flow rate, functional urinary tract obstruction, and dysfunction of the detrusor-urethral sphincter synergy. These functional abnormalities may only be a clinical phenomenon, and their nature may be related to various underlying pathogenic factors.
3.Psychological factors
The study shows that more than half of the patients with untreated prostatitis have significant psycho-psychological factors and personality traits changes, such as: anxiety, depression, hypochondria, hysteria, and even suicidal tendencies. These changes in mental and psychological factors can cause autonomic dysfunction, resulting in posterior urethral neuromuscular dysfunction, leading to pain in the pelvic region and dysfunctional urination; or cause changes in hypothalamic-pituitary-gonadal axis function and affect sexual function, further aggravating symptoms, eliminating mental tension can lead to symptom relief or healing. However, it is not clear whether the psychosomatic changes are the direct cause or secondary.
4, neuroendocrine factors
Patients with prostate pain are often prone to fluctuations in heart rate and blood pressure, indicating that they may be related to autonomic responses. The local pathological stimulation of the prostate and urethra triggers spinal reflexes through the afferent nerves of the prostate, activates astrocytes in the lumbar and sacral medulla, and nerve impulses are transmitted through the genitofemoral nerve and iliogastric nerve, and sympathetic nerve endings release norepinephrine, prostaglandins, calcitonin gene-related peptides, and substance P, causing vesicourethral dysfunction, and cause abnormal activity of the perineum and pelvic floor muscles, and persistent pain and involvement pain in the corresponding areas other than the prostate.
5. Abnormal immune response
Studies this year have shown that immune factors play a very important role in the development and evolution of type III prostatitis. Changes in the levels of certain cytokines, such as IL-2, IL-6, IL-8, IL-10, TNF-α and MCP-1, can occur in the prostatic fluid and/or seminal plasma and/or tissues and/or blood of patients, and the level of IL-10 plays a role in The level of IL-10 was positively correlated with the pain symptoms in patients with type III prostatitis, and the application of immunosuppressive therapy had some effect. This suggests that type III prostatitis may be an allergic inflammatory response or an autoimmune disease, a chain reaction mediated by cytokines. Inflammation under the action of initiating factors such as: certain seminal plasma protein antigens produced by the prostate such as PSA can act as autoantigenic substances; residual fragments of pathogens or necrotic tissues can also act as antigens, which in turn leads to the production of pro-inflammatory cytokines by the organism, these cytokines can upregulate the expression of chemokines, and the expression products affect the organism through their respective mechanisms of local immune response in the prostate.
6, the theory of oxidative stress
Under normal circumstances, the body’s oxygen free radical production, utilization and removal in a dynamic balance. The prostatitis patient oxygen free radical production and (or) the role of the free radical scavenging system is relatively reduced, so that the body’s ability to respond to oxidative stress is reduced, oxidative stress products and (or) by-products increase, may also be one of the pathogenesis.
7, pelvic related disease factors
The actual fact that some prostatitis patients often have dilated prostate peripheral plexus, hemorrhoids, and varicose veins suggests that some chronic prostatitis patients’ symptoms may be related to pelvic venous congestion and blood stagnation, which may also be one of the reasons for the persistent treatment. The reason for this is the fact that some patients with a clinical diagnosis of chronic prostatitis may also be due to interstitial cystitis.
(iv) Type IV prostatitis
The reason for this is the lack of research data on the pathogenesis of the disease because there are no clinical symptoms and it is often detected during the examination of other related diseases, which may be partly the same as the etiology and pathogenesis of type III prostatitis.
(E) Triggering factors of prostatitis
The important triggers for the onset of prostatitis include: smoking, alcohol, spicy food, inappropriate sexual activity, prolonged congestion of the prostate caused by sedentary and long-term chronic extrusion of the pelvic floor muscles, cold, fatigue, etc. resulting in a decrease in body resistance or idiosyncratic constitution.