ISSN:
1432-2307
Schlagwort(e):
Cyclic hematopoiesis
;
Bone marrow
;
Ultrastructure
;
Nuclearcytoplasmic asynchrony
;
Döhle-like bodies
Quelle:
Springer Online Journal Archives 1860-2000
Thema:
Medizin
Notizen:
Summary The pathogenesis of cyclic hematopoiesis (CH) in the grey collie dog is still unknown. It has been proposed that periodic bursts of necrosis of the bone marrow neutrophils would induce cyclic arrests of the stem cell differentiation. In the present study, the sequential changes undergone by the erythroid and neutrophil series of the bone marrow of CH dogs were evaluated by electron microscopy. Erythroid cells presented quantitative periodic oscillations but the morphologic features of both immature and mature cells were normal. On the contrary, nonspecific necrotic changes were observed to occur in the myeloid series. Those abnormalities, which were more marked between days 9 and 11 of the cycle, mainly involved the immature cells and, to a lesser extent, the mature neutrophils. The number of necrotic cells was variable in different cycles, but always represented a small portion of the myeloid cells. In addition, few bone marrow macrophages displayed signs of phagocytic activity containing cell debris. The ultrastructural changes of the myeloid series were accompanied by an abnormal decrease of peroxidase activity and the permanence of large acid phosphatase-positive Golgi complexes in mature neutrophils, as defined by morphologic criteria. Döhle-like arrays of rough endoplasmic reticulum were present in many cells. Our findings suggest that an asynchronic development of myelocytes occurs as a result of regulatory abnormalities related to the congenital defect of the bone marrow which interferes with the differentiation and maturation of the stem cells. Necrosis in some myeloid cells would be a secondary phenomenon rather than a causal factor for the cyclic arrest of cell maturation as has been previously submitted. Furthermore, the small size of the necrotic cell population could not justify the production of “inhibitors” in sufficient amounts as to block the normal evolution of the bone marrow stem cell pool.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1007/BF00443900
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