Etiology and Morphology of Anal Ulcers
Anal ulcers (also known as anorectal ulcers or anal erosions) represent mucosal defects developing under the influence of a broad spectrum of factors.
Infectious agents play a significant role in ulcer development. Among sexually transmitted infections (STIs), chlamydia and lymphogranuloma venereum are the most frequent causes, while syphilis and gonorrhea are less common. Specific infections can be caused by Mycobacterium tuberculosis: anal canal tuberculosis may progress and lead to the formation of an anal fistula. Viral infections, particularly herpes simplex virus, typically cause ulcers in immunocompromised individuals.
Non-infectious causes include:
- Inflammatory Bowel Disease (IBD): Crohn's disease provokes ulcers in 50% of cases, and ulcerative colitis in 18%. Histological tissue changes are typically non-specific.
- Traumatic and mechanical factors: A classic example is solitary rectal ulcer syndrome, which is closely associated with trauma and mucosal prolapse.
- Iatrogenic (drug-induced) factors: Mucosal defects may arise from prolonged local application of rectal suppositories (e.g., containing indomethacin).
- Systemic diseases: Ulcers accompany mucocutaneous syndromes (Stevens-Johnson syndrome, Behçet's disease) and various atrophic skin conditions.
Anal Fissure: Characteristics and Causes
Anal fissures (acute or chronic) morphologically present as non-specific linear ulcers. Their typical localization is the distal anal canal, with the defect crossing the dentate line.
In cases with an undetermined cause, a traumatic etiology is most likely. The mechanism involves severe stretching of the distal anal canal during the passage of stool. The primary triggering factor is the presence of coarse plant fibers in the stool.
The second most frequent group of causes is iatrogenic postoperative complications. Fissures very frequently form during the recovery period following surgical removal of hemorrhoids (hemorrhoidectomy). Furthermore, chronic inflammatory bowel diseases consistently lead to the development of anal fissures.
Viral Infections: CMV and HPV
Viral pathogens cause specific tissue changes in the anogenital region that require careful microscopic analysis.
Cytomegalovirus (CMV) Infection Develops predominantly in the setting of severe immunodeficiency, including AIDS. Macroscopically, the infection manifests as proctitis and perianal ulceration. These ulcers are frequently covered with pseudomembranes and carry a high risk of bowel wall perforation. Microscopic examination reveals viral cytomegaly: specific inclusions form within epithelial and endothelial cells, known as the "owl's eye" phenomenon.
Condyloma Acuminata (Anogenital Warts) Caused by human papillomavirus (HPV types 6, 11, 16, and 18, with type 6 dominating in the perianal region). The disease affects the urogenital tract and anal canal (statistically more common in men who have sex with men). Macroscopically, the process begins as papules that transform into vegetative growths.
The histological picture of HPV infection includes:
- Marked acanthosis and papillomatosis.
- Hyperkeratosis of the anal canal epithelium.
- Basal cell hyperplasia.
- Koilocytic atypia of Malpighian layer cells (perinuclear vacuolization).
- Multinucleated cells, eosinophilic inclusions, and dyskeratosis.
- Subepithelial inflammatory infiltration.
Important: The detection of nuclear hyperchromasia, marked cellular pleomorphism, and high mitotic activity indicates malignant transformation—the development of intraepithelial neoplasia or carcinoma in situ.
Specific Bacterial Infections
This group of lesions includes gonococcal infection, chlamydial infection, and syphilitic proctitis. The primary route of transmission for these pathogens is sexual (primarily reported in men who have sex with men). The morphological picture in the anal canal tissues for these diseases fully corresponds to the characteristic systemic and tissue features of these specific infections.