1.2. Pathophysiology
Strictures result due to ischaemia of the spongy tissue of
the corpus spongiosum (ischaemic spongiofibrosis) resulting with iatrogenic causes, trauma and idiopathic strictures
responsible for most cases in the contemporary world. A
propensity toward recurrence necessitates repeated ure-
thral instrumentation in many patients leading to significant from an insult for example, infective, inflammatory or a
local traumatic process. Macroscopically, the stricture ap-
pears white or grey in contrast to the pink appearance of
healthy vascularized urethral tissue. As a consequence of
this insult, the underlying vascular spongy tissue is lost, and
it heals by fibrosis, resulting in the scar that forms a stric-
ture. In the posterior urethra direct trauma leads to a
disruption of the urethra as seen in the pelvic fracture
urethral injury (PFUI).
Lichen sclerosus (LS), formerly known as balanitis
xerotica obliterans, is responsible for complex strictures
of the anterior urethra. Described by Stu¨hmer in 1928 [3],
it is an inflammatory condition of unknown aetiology
affecting the stratified epithelium of the anterior urethra,
which does not extend proximal to the distal sphincter
mechanism and hence LS does not affect the posterior
urethra. Urethral involvement by LS was first described by
Laymon in 1951 [4]. In LS, excess dermal collagen is pro-
duced resulting in a hyperkeratotic epidermal layer that
leads to its characteristic whitish appearance. LS has a
progressive nature, leading to significant recurrence rates
in urogenital epithelium, particularly if these tissues are
used for urethroplasty [5]. This disease process has his-
torically been regarded as one that progresses from the
distal to proximal anterior urethra, however there is evi-
dence to suggest that LS can be identified in isolated
bulbar strictures without evidence of disease distally [6].
Furthermore, recurrences in this context were noted
distal to the original stricture, contrary to previous
evidence.