Publication: Bone marrow angiogenesis: methods of quantification and changes evolving
in chronic myeloproliferative disorders
Authors
Kvasnicka, H.M. ; Thiele, J.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Until now little information is available
about bone marrow (BM) angiogenesis in chronic
myeloproliferative disorders (CMPDs). Amongst the
various immunohistochemical markers for endothelial
cells CD34 and CD105 have proven to be most reliable
since they exhibit no relevant co-staining. Determination
of vascularity has to include pathophysiological aspects
of perfusion. Therefore, quantification of the
microvascular density (MVD) by the so-called hot spot
method has to be improved by parameters that
characterize blood flow more properly like microvessel
area (luminal distension), shape (form factor), tortuosity,
and branching (maximal vessel length). In comparison to
the normal BM chronic myeloid leukemia (CML)
revealed a significant increase in MVD which was
functionally associated with elevated levels of
angiogenic cytokines. Structure of vessels was
significantly altered by showing an enhanced irregularity
of shape and tortuosity and increase in fibers was
conspicuously accompanied by a higher degree of MVD.
Contrasting the group of patients with Imatinib (STI571)
therapy interferon failed to reduce the number of vessels.
Following bone marrow transplantation a significant
enhancement of the MVD was found in the early posttransplant
period, but after about 6 months normalization
occurred. Anomalies of microvascular architecture were
easily demonstrable by three-dimensional reconstruction
and consisted of a complex branching network of
irregular shaped sinuses. Chronic idiopathic
myelofibrosis displayed a significant increase in the
MVD only in the advanced fibrosclerotic stages. This
feature was accompanied by an enhanced luminal
distension and tortuosity, thus contrasting the prefibrotic
and early fibrotic phases of this disorder. Similar to
CML a relationship between evolving myelofibrosis and
change in vascular architecture was encountered. This
feature may present a possible target for future antiangiogenic antiangiogenic
therapy. In essential thrombocythemia there
is only a mild increase in MVD detectable while in
polycythemia vera besides an enlarged number, a
luminal dilation due to the densely packed erythrocytes
is recognizable.
In conclusion, contrasting the usually applied
quantification technique more elaborate morphometrical
methods are warranted to obtain a better insight into the
vascular architecture of the BM. In CMPDs angiogenesis
is significantly associated with the evolution of
myelofibrosis and may be altered by therapeutic
regimens probably due to changes in cytokine release.
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