The pathophysiologic mechanism of<unk> s is unknown and debated. Some researchers suggest it may be the bladder's response to prolonged periods of underfilling. Another possible mechanism of<unk>  is over expression of angiogenic growth factors in the bladder. It has been shown that<unk> s are also presented under hydrodistension procedures. During the filling portion of hydrodistension, one can see white fibrous bundles as the bladder is stretched. When stretched, blood flow is interrupted in these fibrous bundles. After this stretching phase, the emptying phase allows blood flow to resume. This is where one can see bleeding from capillaries. In relation to interstitial cystitis, when noxious stimuli are present, it causes injury to the bladder mucosa resulting in recruitment of inflammatory cells. Disruption of glycosaminoglycan (GAG) layer along with the increased presence of mast cells, T cells, and B cells causes the bladder epithelium to become more permeable. Injury to the GAG layer may lead to increased release of adhesion factors that bind to angiogenic molecules, which generally have little presence under normal conditions, to promote wound healing. Ultimately, increased adhesion factors and overproduction of angiogenic factors from mast cells and disruption of the GAG layer results in tissue fibrosis. As mentioned above, the technique of hydrodistention is one method used to diagnose interstitial cystitis, in which the atrophic bladder is filled and emptied and thus, the stretch of the bladder wall is one possible mechanism of<unk> s.
Glomerulation
Moist desquamation
Reticular formation
Granulation
Craterization
Hydrodilatation
Infibulation
Ossification