2006
DOI: 10.1016/j.juro.2006.07.131
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Detrusor Quantitative Morphometry in Obstructed Males and Controls

Abstract: Morphometric differences in detrusor muscle cell diameter and the connective tissue-to-smooth muscle ratio were observed between controls and patients with obstruction. There is an increase in detrusor muscle cell diameter and fibrosis in bladder outlet obstruction and more intense intrafascicular collagen deposition in patients in acute urinary retention.

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Cited by 36 publications
(46 citation statements)
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“…The most often used method to evaluate the detrusor collagen content in men is the morphometric analysis of the muscle layer and calculation of the C/M. In the present study BPH patients had a C/M of 0.43, while it varied between 0.27 and 0.56 in other series 9, 10, 11, 16. For the controls the C/M was 0.33 in the present study and varied between 0.14 and 0.25 in other series 9, 10, 11, 16.…”
Section: Discussionmentioning
confidence: 45%
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“…The most often used method to evaluate the detrusor collagen content in men is the morphometric analysis of the muscle layer and calculation of the C/M. In the present study BPH patients had a C/M of 0.43, while it varied between 0.27 and 0.56 in other series 9, 10, 11, 16. For the controls the C/M was 0.33 in the present study and varied between 0.14 and 0.25 in other series 9, 10, 11, 16.…”
Section: Discussionmentioning
confidence: 45%
“…Studies have consistently shown increased detrusor collagen content in animal models of obstruction as well as men with BOO/BPH 6, 7, 9, 10, 11, 16. The most often used method to evaluate the detrusor collagen content in men is the morphometric analysis of the muscle layer and calculation of the C/M.…”
Section: Discussionmentioning
confidence: 99%
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“…Optical microscopy studies have demonstrated that a bladder subjected to chronic obstruction that evolves into urinary retention shows significant cellular changes [11], such as an increased detrusor muscle cell diameter and intense intrafascicular collagen deposition. These changes may explain, at least in part, the development of detrusor hypoactivity as a terminal vesical situation [12].…”
Section: Discussionmentioning
confidence: 99%
“…In the early stages of BOO, the bladder wall thickens to compensate for higher outlet resistance. However, over time, the detrusor muscle becomes decompensated and then lower urinary tract symptoms (LUTS) appear, ultimately progressing to urinary retention with overflow incontinence [3,4].. Studies have shown that hypertrophy can be found in both smooth muscle cells and the extracellular matrix (ECM) of the bladder wall in BOO [5], where the ECM hypertrophy is mainly due to collagen accumulation, and the more collagen accumulates, the worse the LUTS are [6,7]. The main reason for collagen accumulation in the bladder wall in BOO is inhibited collagen catabolism rather than increased synthesis; this process is controlled by matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) [8,9].…”
Section: Introductionmentioning
confidence: 99%