The causes of IC/BPS are still not known. The possible explanations are the dysfunction of the related nerves, autoimmune problems, allergic reactions, and stress. Hereditary factors may take part, too. Nevertheless, none of these hypotheses have been proven scientifically.
The condition itself, on the other hand, has been well described. The symptoms occur because of the inadequate status of the mucosa of the bladder and the upper part of the urethra. The healthy superficial mucus layer of the mucosa – which consists of glucose-amino-glycan or GAG – prevents salts, acids and other metabolic products (being present in the urine naturally) getting into the deeper layers of the bladder wall, and irritating the sub-mucosal pain receptors. In IC/BPS, this GAG-layer is damaged and enables the compounds described above to reach the receptors. This results in a sterile inflammation – in which there is no bacteria present – which can spread to the deeper layers of the bladder wall, too, and leads to an increased amount of mast cells. These cells produce histamine, which increases the pain. The constant irritation raises the number of pain receptors, which makes the symptoms worse. If the inflammation persists for years, other elements of the connective tissues build up in the edematous tissue, which makes the bladder wall lose its elastic properties. At the end of this process, an end-stage bladder can develop (a rigid bladder with very low capacity), which is an irreversible condition. The thick and rigid bladder wall slowly compresses the ureters, and as a consequence, kidney failure may appear.
Since the cause of the GAG-layer loss is not known, it is impossible to prevent IC/BPS. Moreover, there is no therapy available which cures the condition for good. The early diagnosis and the proper treatment can stop the progression of IC/BPS.