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M F Seifert

Publications and source records attributed to M F Seifert.

42 records · Page 3Linked to original sources
PubMed1984

Congenitally osteopetrotic (oplop) mice are not cured by transplants of spleen or bone marrow cells from normal littermates.

Congenital mammalian osteopetrosis is characterized by a generalized skeletal sclerosis due to reduced bone resorption by osteoclasts. This condition can be cured in several mutant strains of mice and rats by transplantation of spleen or bone marrow cells from normal littermates. The ability of this regimen to cure osteopetrosis in oplop mice was examined in 23 mice treated with spleen or bone marrow cells from normal littermates and followed for up to 80 days. In no instance was there radiographic or histologic evidence of removal of the excessive skeletal mass characteristic of the disease. These data show that spleen or bone marrow cells do not cure osteopetrosis in this mutation. Recent demonstrations that not all children with congenital osteopetrosis are cured by bone marrow transplants from HLA-matched donors suggest that the oplop mouse mutation may be a useful model system in which to develop alternate treatments.

Animals↗
PubMed1984

Osteoclast populations in congenital osteopetrosis: additional evidence of heterogeneity.

Osteopetrosis is a metabolic bone disease characterized by excessive accumulation of skeletal mass due to a reduction in bone resorption. The pathogenesis of osteopetrosis is reduced osteoclast function. Reports of osteoclast numbers in several mammalian mutations exhibiting osteopetrosis have shown them to be increased, decreased, or normal in numbers. The present investigation quantitated the osteoclast populations and examined the cytology of osteoclasts by light microscopy in calvarial and tibial sites in one rabbit and two mouse mutations and compared them with their normal littermates. Our observations show that osteoclast numbers are, depending on the particular mutation, increased, decreased, or comparable to those found in normal littermates. In each mutation, however, osteoclasts fail to exhibit the cytoplasmic vacuolization next to bone surfaces seen in normal osteoclasts. These data provide additional evidence of heterogeneity in the congenital mammalian osteopetrosis and suggest that these mutations may be significant sources of new information about the biology of osteoclasts.

Animals↗
PubMedDate not supplied

Bioactive fatty acids: role in bone biology and bone cell function.

Bone is a unique tissue providing support, movement, and mineral balance for the body. Bone growth is achieved in the young by a process called modeling, and maintained during adulthood by a process termed remodeling. Three types of cells are responsible for the formation of cartilage and bone; the chondrocyte, osteoblast, and osteoclast. These cells are under the influence of a plethora of regulatory molecules, which govern their action to provide an individual optimal bone mass. Interruption of this homeostatic machinery, especially in the elderly, often results in a loss of bone mass (osteoporosis) or cartilage damage (rheumatoid arthritis). Many pharmacological agents have been made available in an effort to prevent or alleviate these pathologies, however, one vector often overlooked is the diet. This review focuses on the relationship between dietary polyunsaturated fatty acids and bone biology, both in vivo and in vitro.

Adult↗
PubMedDate not supplied

Osteosclerosis, a recessive skeletal mutation on chromosome 19 in the mouse.

Osteosclerosis (oc) is an osteopetrotic mutation in the mouse inherited as an autosomal recessive on chromosome 19. Affected animals (oc/oc) exhibit the characteristic radiologic and histologic hallmarks of osteopetrosis including a generalized increase in skeletal density and absence of marrow cavities. Most die within three weeks after birth. Osteoclasts are cytologically abnormal by light microscopy in that they do not have cytoplasmic vacuoles. Presumptive evidence of rickets in this mutation includes thick cartilagenous growth plates and excessive osteoid. Extensive extramedullary hemopoiesis occurs in the liver and spleen of mutants. This unique constellation of features suggests that the oc mutation is a valuable model in which to investigate the pathogenesis of osteopetrosis.

Animals↗
PubMedDate not supplied

The biology of macrophages in osteopetrosis. Structure and function.

Osteoclasts from ia rats are present in excessive numbers, contain an excessive amount of the lysosomal enzyme acid phosphatase, and show reduced-bone-resorptive function due to lack of ruffled borders. Given the current theory of a mononuclear phagocytic cell origin for osteoclasts, it was anticipated that the presence or absence of similarities between macrophages of both phenotypes might address the relatedness of these two cells. Thus, peritoneal macrophages from littermate normal and incisors-absent (ia) osteopetrotic rats were examined for differences in structure, acid phosphatase content, and phagocytic activity. The results of this investigation did not reveal any significant differences in these parameters in mutants compared with normal littermates. From these data it is suggested that macrophages are distinct, differentiated cells with functions separate from those of osteoclasts but that they may be related through a common stem cell early in development. Use of more immature cells or monocyte subpopulations may represent better choices for future studies of defects within the mononuclear phagocyte system in the ia mutation.

Acid Phosphatase↗