Osteogenesis of the mandibular arch in Ts16 mice.

Males and females homozygous for the Robertsonian translocation specific for chromosomes 16 and 17 Rb(16.17)Bnr and male and females homozygous for the Robertsonian translocation for chromosomes 6 and 16 Rb(6.16)24Lub were bred to produce double heterozygotes [Rb(16.17)Bnr/Rb(6.16)24Lub]. Experimental data were based on 156 features: 70 euploid (control), 86 trisomic. Affected fetuses were identified by decreased size, shortened faces (flattened snouts), oedema, petechiae, open eyelids, and dysplastic ears. Identification of trisomics was substantiated by karyotyping the metaphasic spreads. Five gestational days were studied (14-18). Fetal age was assumed to be accurate as fertilization occurred within half an hour of copulation. Euploid specimens followed normal developmental paths of chondrogenesis, osteogenesis and related tissues. In trisomics, developmental faults increased unequally between gestational days 15 and 17: some tissues were mildly and others acutely affected. Among the trisomic disorders were diminished growth, lagging mitotic activity, and retarded and poorly ordered tissue development, especially of bone. All of these contributed to hypoplasia, hypocellularity, reduced vascular supply and enlarged intercellular spaces. Intensities of the mandibular abnormalities varied among litters and littermates. The severity of the developmental disorders of an individual Ts16 specimen differed among the tissue components studied. Of the trisomic mandibular tissues, bone was most frequently involved and Meckel's cartilage least.