1. A new osteopetrosis mutant mouse strain (ntl) with odontoma-like proliferations and lack of tooth roots.
- Author
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Lu X, Rios HF, Jiang B, Xing L, Kadlcek R, Greenfield EM, Luo G, and Feng JQ
- Subjects
- Acid Phosphatase analysis, Alleles, Animals, Biomarkers analysis, Bone Resorption genetics, Bone Resorption pathology, Cells, Cultured, Chloride Channels analysis, Chromosomes, Mammalian genetics, Disease Models, Animal, Genes, Recessive genetics, Genetic Linkage genetics, Genotype, Homeostasis genetics, Incisor abnormalities, Isoenzymes analysis, Liver cytology, Mice, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Mutant Strains, Mutation genetics, Odontogenesis genetics, Phenotype, Stem Cells physiology, Tartrate-Resistant Acid Phosphatase, Tooth Eruption genetics, Odontoma genetics, Osteoclasts physiology, Osteopetrosis genetics, Tooth Root abnormalities
- Abstract
A new spontaneous mouse mutant (ntl) with autosomal-recessive osteopetrosis was characterized. These mice formed tartrate-resistant acid phosphate (TRAP)-positive osteoclasts but their osteoclasts had no ruffled border and did not resorb bone. These mice displayed no tooth eruption or tooth root formation. Adult mutant mice developed odontoma-like proliferations near the proximal ends of the incisors. Intraperitoneal injection of progenitor cells from the liver of 16.5 days postcoitum wild-type embryos into newborn mutants rescued the osteopetrosis phenotype, indicating that the defects were intrinsic to the osteoclasts. Our findings not only provide further support for a critical role of osteoclasts in tooth eruption and tooth root development, but also suggest that the perturbation of the homeostasis of the odontogenic precursors of the incisors is primarily responsible for the development of the odontoma-like proliferations in this osteopetrosis mutant. Genetic mapping has narrowed down the location of the mutant allele to a genetic interval of 3.2 cM on mouse chromosome 17.
- Published
- 2009
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