Symptomatic inflammatory conditions of the prostate are quite common, accounting for about 2 million outpatient visits annually in the United States. These visits are evenly split between primary care and urology.  Prostatitis is clinically divided into acute bacterial prostatitis and various types of chronic prostatic infectious and inflammatory conditions, including chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) in men. This review will cover all such symptomatic prostatic conditions except acute bacterial prostatitis (NIH Category I), which will be described separately. (See our companion Statpearls reference article on "Acute Bacterial Prostatitis.") Chronic prostatitis is the most common urological diagnosis in men younger than 50 and the third most commonly diagnosed male urological condition. This condition accounts for up to 25% of all outpatient urology consults and outpatient visits and is estimated to have affected 5% of all men aged 20 to 50 years. The term "prostatodynia" is not encouraged or recommended in current practice, as it carries the negative historical connotation of being a "wastebasket" designation for a melange of symptoms. Chronic prostatitis has a significant negative impact on quality of life and, in this respect, is comparable with other major long-term health conditions (eg, ischemic heart disease and diabetes mellitus). Despite being common in clinical practice, chronic prostatitis is often misdiagnosed, misclassified, and poorly managed, resulting in significant morbidity, prolonged symptoms, and overall patient dissatisfaction. Understanding the classification, presentation, evaluation, and optimal management of the various types of chronic prostatitis is necessary at all levels to improve outcomes. Early recognition and the correct clinical classification of the condition with prompt and appropriate treatment improves outcomes and minimizes patient morbidity.

Chronic pelvic pain syndrome (CPPS) is a common complication of prostatitis, which was associated with the pathological depolarization of macrophage and the neuroinflammation. However, its underlying reason is far from clear and few effective treatments is applicable. In this study, we tested the effect of obacunone (Oba), a highly oxygenated triterpenoid, on CPPS. The experimental autoimmune prostatitis (EAP) was induced by subcutaneous injection of heterologous prostate homogenate in mice. We found that EAP led to prostatodynia, neuronal activation of spinal dorsal horn, and the pro-inflammatory depolarization of macrophage within prostate, which was significantly alleviated by oral administration of Oba in a dose-dependent manner. Mechanistically, EAP-induced production of IL-6 on prostatic macrophage was suppressed by Oba. Moreover, co-administration of Oba and MIF inhibitor ISO-1 did not lead to additive effect when compared with either alone. In summary, we conclude that Oba prevents the production of macrophage-derived pro-inflammatory factors by inhibiting MIF, which eventually alleviates CPPS after prostatitis.

There is considerable circumstantial evidence linking tissue pleomorphic forms of unknown origin with idiopathic chronic inflammatory, collagen, lymphoproliferative, nephro-urological (including interstitial cystitis and prostatodynia), and neoplastic diseases. Although these forms have been observed in stained tissue histopathologic specimens for many decades, most are ignored and generally regarded as diagnostically insignificant staining artifacts or debris. It is hypothesized that these pleomorphic forms are not staining artifacts/cellular debris, but instead represent various stages in the life cycle of stressed bacteria: cell wall-deficient/defective (often called L-forms) that are difficult-to-culture or nonculturable. Essential to the thesis is that small, electron dense, non-vesiculated L-forms are the central (core) element in bacterial persistence. Depending on the stimulus received, these dense forms might be considered as undifferentiated cells, with the capacity to develop along several different routes. Hence, these altered forms created in vivo take up intracellular and/or extracellular residence; possibly establishing a sort of immune protected parasitic relationship, resisting/surviving phagocytic action, and creating subtle pathologic changes in the host during a prolonged period of tissue persistence. This might translate into an etiology for chronic inflammatory diseases, when the stressed bacteria increase in numbers and overwhelm the normal biological functions of the host. In the last few decades, an increasing percentage of the population has become immunosuppressed. Some mechanisms for this increase are aging; autoimmunity; congenital, metabolic and degenerative disorders; and AIDS. The life of a patient so affected is prolonged by therapy with hormones, antimicrobials, and immunosuppressants. It is therefore not surprising that pleomorphic, dormant, and mutant bacterial populations arise in vivo when bacteria are exposed to agents that interfere with structural components and metabolic processes necessary to survival of the microbe. Recent provocative, microbiological data lend credence to the hypothesis and corroborate the multiplicity of pleomorphic forms that develop during reproduction of L forms in vitro. It is proposed that in vivo persistence of these bacterial elements escape immune surveillance partially, completely, or may integrate with host cell organelles to create bacteria-host-cell-antigen complexes which could provoke immunopathologic consequences. Highly relevant, newly published data on modifications of gene expression, modes of division for stressed bacteria, and the paradoxical finding of peptidoglycan in L-forms are pertinent to the hypothesis that atypical, pleomorphic bacteria are the organisms operative in persistence and expression of pathology over a wide spectrum of diagnostically troublesome human diseases.

Prostatitis, one of the most common urological infections afflicting adult men, has recently been divided into 4 different categories based on the National Institutes of Health consensus classification: acute bacterial prostatitis, chronic bacterial prostatitis, chronic nonbacterial prostatitis and pelvic pain syndrome, and asymptomatic inflammatory prostatitis. Most patients with prostatitis are found to have either nonbacterial prostatitis or prostatodynia. Prostatitis poses an international health problem, with epidemiologic studies suggesting a worldwide prevalence of more than 10%. This article reviews current modes of diagnosis and therapy for acute and chronic prostatitis.

Painful bladder syndrome or urologic chronic pelvic pain syndrome is a chronic condition that presents with lower urinary tract symptoms that include dysuria, urgency, frequent urination, and chronic pelvic pain. Diagnoses included in the painful bladder syndrome are interstitial cystitis and prostatodynia. The history, physical examination, and laboratory evaluation of patients with lower urinary tract symptoms are important in ruling out other diagnoses. Treatment options that are US Food and Drug Administration approved and evidence based are limited; however, many symptom-based treatment options can reduce symptoms and improve quality of life.

The first time in Scandinavia we present a case report of a pure primary low-grade neuroendocrine carcinoma (carcinoid tumor) of the prostate. Our patient is a 34-year-old male with a long history of symptomatic chronic prostatitis/prostatodynia. After developing severe obstructive uropathy, a transurethral resection was performed. An unexpected diagnosis of a low-grade neuroendocrine carcinoma was made. Subsequently, in radical prostatovesiculectomy, we noted metastases to both seminal vesicles and two inguinal lymph nodes. Follow up is ongoing.

Chronic idiopathic prostatitis, sometimes called prostatodynia or abacterial prostatitis, is a commonly diagnosed and poorly treated urological syndrome. Clinically, this condition frustrates the patient and physician due to its chronicity and resistance to therapy. Recent studies suggest that the etiology of chronic idiopathic prostatitis may be of bacterial origin. Three types of provocative data have demonstrated bacterial presence from prostatic specimens (tissue and secretions) that were negative by traditional clinical microbiologic tests: (i) presence of bacterial gene sequences in prostatic tissue encoding 16S rRNA and tetracycline resistance (tetM-tetO-tetS); (ii) controlled cultural findings showing coagulase-negative staphylococci as the most common isolates (68%) in prostatodynia (chronic idiopathic prostatitis); and (iii) culture of difficult-to-grow coryneforms in expressed prostatic secretions (EPS) on enriched culture media and direct microscopic observation of these pleomorphic bacteria in EPS. Additionally, earlier experimental studies in a rat model support the concept that antibiotic therapy in chronic bacterial prostatitis may not be due to altered antibiotic pharmacokinetics in the chronically inflamed prostate gland. Rather, ineffective antimicrobial eradication might result from protected bacterial micro-colonies within an infection-induced altered micro-environment deep within the prostate gland. We postulate that extracellular slime substances produced by bacteria that are buried in prostatic tissues could impair host defenses by their anti-phagocytic and anti-chemotactic properties that affect neutrophils as well as anti-proliferative characteristics that affect lymphocytes. These extracellular slime substances could also have cytoprotective properties which can conceal bacteria from otherwise bactericidal levels of antibiotics and lead to recrudescent infections resistant to therapy. Persistence of bacterial antigens might initiate a cascade of cellular immunologic events resulting in chronic inflammation of the prostate gland.