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Inflammatory Diseases of the Prostate and Penis

Prostatitis (in the context of the male urogenital system)

For medical students2 min readUpdated 2026-10-10

The provided material examines prostate functions in conjunction with the physiology of the male reproductive system. The primary focus among non-neoplastic inflammatory pathologies is placed on penile lesions: balanoposthitis and cavernositis.

Prostatic secretionContains proteins, citric acid, and prostaglandins to ensure ejaculate properties.
BalanoposthitisA frequent pathology caused by staphylococci, streptococci, fungi, and trichomonads.
Gangrenous balanoposthitisAn outcome of a purulent-ulcerative process with massive necrosis of penile tissues.
CavernositisCan develop via hematogenous spread during tonsillitis, sepsis, or osteomyelitis.

Physiology of the Prostate Gland

The prostate gland plays a key role in the formation of fully functional seminal fluid. Its secretion is rich in specific proteins, citric acid, and prostaglandins. This fluid not only provides the necessary volume of ejaculate but also imparts the biological properties required for fertilization.

In addition to its exocrine role, the gland performs important auxiliary tasks. It actively participates in the metabolism of male sex hormones, exerts a regulatory effect on spermatogenesis, and influences the activity of the hypothalamic-pituitary axis.

Inflammatory Diseases of the Penis

Among non-neoplastic pathologies of the male genitalia, inflammatory processes occupy a leading position. The most clinically significant forms are balanoposthitis and cavernositis.

Balanoposthitis

This is a combined inflammation of the glans penis skin and the inner mucosal layer of the prepuce (foreskin). Development of the disease is promoted by predisposing factors: diabetes mellitus, chronic infections, or immunodeficiencies (frequently associated with purulent urethritis).

Classification of acute forms:

Chronic balanoposthitis is dangerous due to scarring of the prepuce, which inevitably leads to phimosis—a pathological narrowing that prevents retraction of the glans.

Cavernositis

This is significantly less common and represents inflammation of the corpora cavernosa. Infection may spread via:

  1. Hematogenous route (against the background of tonsillitis, osteomyelitis, sepsis).
  2. Direct organ trauma.
  3. Intracavernosal medication injections.
  4. Complication of acute purulent urethritis.

Hormonal Regulation of the Reproductive System

To understand the pathogenesis of these diseases, it is important to consider the hormonal axis regulated by the hypothalamus. The arcuate nucleus secretes stimulatory gonadotropin-releasing hormone (GnRH) and inhibitory factors.

In response, the pituitary gland secretes:

Combined testosterone and androgen-binding protein initiate spermatogenesis. The system operates via a negative feedback loop: excess testosterone suppresses the pituitary and hypothalamus.

Complications and Fibrotic Changes

Chronic inflammations can lead to fibrotic changes. For instance, long-standing balanoposthitis causes phimosis. Conversely, attempting forceful retraction of the glans in the presence of phimosis can lead to paraphimosis—acute entrapment of the glans by the stenotic preputial ring.

Severe sclerotic processes within the corpora cavernosa (cavernous fibrosis) most commonly result from prolonged priapism (pathological erection lasting over 3 days) or previous inflammation. This condition leads to partial or complete loss of erectile function.

Mnemonic

To remember testicular cells: Leydig — Luteinizing hormone (both start with L) → make testosterone. Sertoli — FSH (stimulate Spermatogenesis and Secrete protein).

Frequently asked questions

What inflammatory non-neoplastic diseases of the male reproductive system are distinguished in pathology?

Pathology distinguishes inflammatory diseases of various organs of the male reproductive system. The main nosologies include:

  • Balanoposthitis — inflammation of the skin of the glans penis and the inner leaf of the prepuce.
  • Cavernositis — inflammation of the corpora cavernosa of the penis.
  • Orchitis — inflammation of the testicular parenchyma (including acute infectious and specific orchitis).
  • Epididymitis — inflammation of the epididymis.
  • Prostatitis — inflammation of the prostate gland (acute and chronic).
  • Vesiculitis — inflammation of the seminal vesicles.
What are the main pathways of infection entry into the prostate gland in prostatitis?

The main pathways of infection entry into the prostate during the development of prostatitis involve three mechanisms:

  • Urogenital route — reflux of infected urine into the prostatic ducts (usually as a consequence of lower urinary tract infection).
  • Lymphogenic spread — transport of infection via lymphatic vessels from the rectum.
  • Hematogenous dissemination — penetration of the pathogen via the bloodstream during bacteremia.
What morphological forms of acute prostatitis are distinguished in pathology?

Based on the depth and extent of morphological changes, three forms of acute prostatitis are distinguished:

  • Catarrhal form — pronounced neutrophilic infiltration of the prostatic ducts against a background of vascular congestion and stromal edema.
  • Follicular form — addition of foci of inflammatory infiltration in the secretory units of the prostate to the ductal changes.
  • Parenchymatous form — formation of diffuse neutrophil infiltrates, abscesses, and granulation tissue foci.
What microscopic changes are characteristic of parenchymatous prostatitis?

Parenchymatous prostatitis is characterized by:

  • Diffuse infiltrates consisting predominantly of neutrophils.
  • Abscesses.
  • Foci of granulation tissue.
What cellular elements form the basis of the inflammatory infiltrate in chronic nonspecific prostatitis?

The inflammatory infiltrate in chronic prostatitis is based on mononuclear cells and neutrophils, depending on the form. The cellular composition includes:

  • Lymphocytes — infiltrating the stroma and adjacent glandular tissue.
  • Plasma cells — present in inflammatory foci of the stroma.
  • Macrophages — found in the stroma, and in non-bacterial prostatitis, lipid-laden macrophages are found in the lumens of the glands.
  • Neutrophils — filling dilated glands in chronic non-bacterial prostatitis.
What types of specific granulomatous prostatitis occur in clinical practice?

Specific granulomatous prostatitis includes forms associated with:

  • Tuberculosis.
  • Syphilis.
  • Fungal infections.

Tuberculous prostatitis is characterized by the formation of epithelioid cell granulomas with foci of caseous necrosis.

What are the possible local complications of acute purulent prostatitis?

Possible local complications and morphological manifestations of acute purulent prostatitis include:

  • Urinary retention.
  • In the parenchymatous form — abscess formation and granulation tissue foci.
What morphological outcomes are characteristic of long-standing chronic prostatitis?

Long-standing chronic prostatitis is characterized by sclerotic changes in the organ tissue and stone formation. The main morphological outcomes include:

  • Fibrosis — frequently revealed by proliferation of granulation and fibrous tissue in the prostate stroma, leading to its induration and deformation.
  • Lithiasis (stone formation) — formation of intraprostatic calculi (prostatic stones), which serve as a reservoir for pathogens.
What is the difference between phimosis and paraphimosis?

Phimosis is the narrowing of the prepuce making it impossible to uncover the glans penis. Paraphimosis is an acute complication where the narrowed prepuce traps the retracted glans, impairing blood circulation.

What do Sertoli cells produce besides stimulating spermatogenesis?

They possess endocrine functions: synthesizing estrogens, androgen-binding protein, and inhibin, which acts on the pituitary via negative feedback.

What are the main pathogens of ordinary balanoposthitis?

The pathology is most frequently caused by staphylococci, streptococci, trichomonads, and fungal infections.

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