The exact pathophysiology of hemorrhoidal development is poorly understood. For years the theory of varicose veins, which postulated that hemorrhoids were caused by varicose veins in the anal canal, had been popular but now it is obsolete because hemorrhoids and anorectal varices are proven to be distinct entities. In fact, patients with portal hypertension and varices do not have an increased incidence of hemorrhoids.
Today, the theory of sliding anal canal lining is widely accepted. This proposes that hemorrhoids develop when the supporting tissues of the anal cushions disintegrate or deteriorate. Hemorrhoids are therefore the pathological term to describe the abnormal downward displacement of the anal cushions causing venous dilatation. There are typically three major anal cushions, located in the right anterior, right posterior and left lateral aspect of the anal canal, and various numbers of minor cushions lying between them. The anal cushions of patients with hemorrhoids show significant pathological changes. These changes include abnormal venous dilatation, vascular thrombosis, degenerative process in the collagen fibers and fibroelastic tissues, distortion and rupture of the anal subepithelial muscle. In addition to the above findings, a severe inflammatory reaction involving the vascular wall and surrounding connective tissue has been demonstrated in hemorrhoidal specimens, with associated mucosal ulceration, ischemia, and thrombosis.
Several enzymes or mediators involving the degradation of supporting tissues in the anal cushions have been studied. Among these, matrix metalloproteinase (MMP), a zinc-dependent proteinase, is one of the most potent enzymes, being capable of degrading extracellular proteins such as elastin, fibronectin, and collagen. MMP-9 was found to be over-expressed in hemorrhoids, in association with the breakdown of elastic fibers. Activation of MMP-2 and MMP-9 by thrombin, plasmin, or other proteinases resulted in the disruption of the capillary bed and promotion of angioproliferative activity of transforming growth factor β (TGF-β).
Recently, increased microvascular density was found in hemorrhoidal tissue, suggesting that neovascularization might be another important phenomenon of hemorrhoidal disease. Moreover, these workers found that microvascular density increased in hemorrhoidal tissue especially when thrombosis and stromal vascular endothelial growth factors (VEGF) were present.
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