Pathophysiological Mechanisms Involved in Overactive Bladder/Detrusor Overactivity

Abstract

Abstract Purpose of Review To examine the latest published findings on the pathophysiological mechanisms involved in the development of overactive bladder (OAB) and detrusor overactivity (DO), and to identify common pathways linked to the risk factors associated with these conditions. Recent Findings Evidence is accumulating, both clinical and experimental, that many of the factors linked to the development of OAB/DO, including ageing, bladder outlet obstruction, psychological stress, and obesity are associated with reduced bladder blood flow. This induces local tissue inflammation with cytokine release and enhanced oxidative stress, ultimately resulting in altered detrusor sensitivity, detrusor hypertrophy and fibrosis, together with afferent hypersensitivity. These mechanisms would explain the symptoms of urgency and frequency observed in OAB patients. Although not a characteristic of OAB, undetected low level bacterial infections of the bladder have been proposed to explain the OAB symptoms in patients resistant to standard treatments. In this condition, inflammatory responses without reductions in perfusion activate the inflammatory pathways. Summary Evidence is mounting that poor bladder perfusion and local inflammatory responses are central mechanisms involved in the development of OAB/DO. As our understanding of these pathophysiological mechanisms advances, new avenues for drug development will be identified and ultimately treatment may become more individualized depending on the particular pathway involved and the drugs available.