8 research outputs found
Peritoneal fine structure of inguinal hernia: a transmission electron microscope study
Fine structure of normal human parietal
peritoneum served as control data for recording
changes in the fine structure of the peritoneum of
hernial sacs. In these sacs, mesothelial cells retracted,
rounded up and some of them eventually separated
altogether to give rise to wide open intercellular spaces
thus creating unhindered passageways (stomata)
between the subserosal connective tissue and the
cavity of the sacs. There was a considerable collagen
build-up in the subserosal fibrous tissue of hernial
sacs. Occurrence of this fibrosis is at variance with an
accepted surgical concept which suggests a defect in
collagen synthesis as the cause of herniation. In some
sacs mesothelial nodules andior peritoneal adhesions
were present. Certain cytological changes in the
mesothelial cells of hernial sacs showed features in
common with cells of malignant tumours in general,
and features mimicing malignant mesotheliomas in
particular. This is in spite of the fact that thorough
gross and light microscopic examination of operative
specimens and cytological evaluation of peritoneal
effusion failed to reveal any evidence of malignancy.
Pathologists should be aware of the consummate
ability of mesothelial cells to mimic carcinomas in
order to avoid possible diagnostic errors. In this report, an electron micrograph of peritoneal adhesion
is being published for the first time in the literature. A
syncytium-like firm bond between adjoining
mesothelial cells constituted the adhesion which is
obviously an irreversible process
Peritonea1 fine structure of inguinal hernia: a scanning electron microscope study
Mesothelial cells of the normal human
peritoneum of the anterior abdominal wall are covered
with numerous surface microvilli. These cells become
partially denuded inside the sacs of direct and indirect
inguinal hernias and so lose the protective property
the microvillar covering may impart on them. These
mesothelial cells of hernial sacs also acquire an extensive
surface coat of fibrin-like material, presumably due
to the loss of that protective property, which may as a
result subject them to adhesions. There is a considerable
collagen build:up in the subserosal fibrous tissue of
sacs of both direct and indirect inguinal hernias. Such a
build-up is at variance with the accepted current surgical
concept which suggests a-defect in collagen synthesis,
rather than a build-up, as the cause of direct hernia