The current study may shed some light on the pathogenesis of VED. The venules that drain the sinusoidal spaces and the smooth muscles of the penis coalesce as they approach the CC periphery and form the subtunical venular plexus [
8]. Small veins exit from the plexus through the TA as the emissary veins, and drain into the circumflex veins or directly into the deep dorsal vein. The position of the subtunical venular plexus between the sinusoids and TA allows for their compression and occlusion as the smooth muscle and sinusoids relax and expand against the TA during tumescence [
8‐
11]. This occlusion acts to trap the blood within the penis. The loss of this veno-occlusive function leads to leakage of blood from the penis with a resulting impotence [
8‐
11]. The TA, being composed mainly of collagen fibers, is relatively noncompliant. It occludes the penile venous outflow through compression of the subtunical venular plexus and the perforating emissary veins passing through it. The integrity of the fibroelastic tissue of the TA and CC apparently plays a significant role in the erectile process [
12].
A concept on the pathogenesis of venogenic ED
Venogenic ED is considered to result from an improperly functioning occlusion mechanism [
13,
14]. Investigations lay stress on the role of the TA in the venous occlusion mechanism of the penis during erection [
3,
8,
9,
14]. In the current study, the TA collagen was found degenerated and atrophic and this probably leads to subluxation and
floppiness of the TA as a tube surrounding the penile corporal tissue. It appears that the subluxated TA, during erection, fails to effect compression of both the subtunical venular plexus and the emissary veins passing through it. Failure of occlusion of the penile venous outflow presumably leads to venous leakage during erection and seems to explain the ED in these patients.
Furthermore, under normal physiologic conditions, the TA is responsible for morphologically shaping the penis during erection. The collagenous structure gives the TA a textile nature which firmly supports the penile architecture during penile tumescence. This TA textile nature, with its circularly and longitudinally oriented collagen fibers lends the TA an adaptability to adjust its length and breadth according to the penile status, whether flaccid or erected. Due to their inelasticity, the collagen fibers limit excessive tunical stretch during penile tumescence. This mechanism prevents tunical subluxation and floppiness which may result from repeated penile tumescence which occurs during the sexual life. Meanwhile, an atrophic subluxated TA would not only disrupt the "venous-leak proof" effect of the TA but disturb the solidity of the erected penis during the process of vaginal penetration and thrusting.
It may be argued that the TA changes are the result of venous leakage. However, this does not seem to be the case since the TA rigidity is claimed to act for prevention of venous lelakage during erection [
8,
9,
13,
14]. Therefore, although it appears inappropriate that venous leakage should lead to tunical subluxation and
floppiness, this possibility cannot be excluded.
Investigators reported a significant decrease in elastic fibers in the TA of impotent patients in comparison to a control group [
15]. A reduction of the TA elastic fibers is likely to produce disorders in the arrangement of collagen fibers [
16,
17]. As a matter of fact, electron microscopy revealed severe myopathic, fibrotic changes in the penile tissue [
18].
The possible etiology of the atrophic subluxated TA needs to be discussed. The TA consists of collagen and thus may be involved in the pathology of collagen diseases. However, none of the patients had any of these conditions. Aging may affect the TA integrity, but the studied subjects were middle-aged. The history and investigative results of the patients have shown that they had no relevant pathological conditions nor were under drug regimens that may cause ED. However, a recent study has shown that androgen administered to patients with ED due to VED
has improved erection in some,
but not in all patients [
19]. The investigators suggested that penile tissue remodeling is the mechanism
that is presumably responsible for correction of the VED by androgen treatment. In view of these factual aspects, we hypothesize that collagenous degeneration and atrophy could be a primary pathologic condition affecting the TA.
A limitation of the study is that the cohort of the patients is not homogeneous for their characteristics. It was difficult to convince healthy subjects to have a biopsy taken from their penile TA. Therefore we seized the opportunity to take the TA biopsy from healthy subjects with normal erection during operative interference; this selection did not effect the results.