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The Journal of Heredity 1985:76(3):171-176
© 1985 The American Genetic Association 76:171-176

research-article

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

Sandy C. Marks, Jr., Mark F. Seifert, and Priscilla W. Lane

The authors are associated with the Department of Anatomy, University of Massachusetts Medical School, 55 Lake Avenue, Worcester, MA 01605 (SCM and MFS) and the Jackson Laboratory, Bar Harbor, ME 04609 (PWL). They thank C. MacKay, A. Lucia, B. Harris, and C. Spencer for excellent technical assistance. Supported by grant no. 1-869 from the March of Dimes/Birth Defects Foundation (SCM), Postdoctoral Fellowship no. DE 05361 (MFS), grants DEB 79-26708 from the National Science Foundation, and 1 P30 CA 34196 from the National Cancer Institute (PWL). Animals used in this study were maintained and used in accordance with recommendations in the Guide for the Care and Use of Laboratory Animals, prepared by the ILAR, NRC (DHEW Publication No., NIH 78-23, 1978) and guidelines of the Animal Care Advisory Committee of the University of Massachusetts Medical School. The Jackson Laboratory is fully accredited by the American Association for Laboratory Animal Care.

Abstract

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.


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