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T C Hart

Publications and source records attributed to T C Hart.

77 records · Page 5Linked to original sources
PubMed1991

Comparison of craniofacial morphology in monozygotic twins with their siblings.

Lateral cephalometric radiographs from 33 families of monozygotic twins and their siblings were digitized. Eight skeletal parameters were measured: FA to SN, SNA, SNB, ANB, angle of convexity, mandibular plane to SN angle, Y axis and pogonion to NB distance. Monozygotic twin pairs and their siblings showed a normal distribution pattern for all the skeletal parameters, except the pogonion to NB distance measurement. There was found to be a statistically significant correlation between age and facial angle and ANB. A familial aggregation effect was found for SNA, ANB and angle of convexity. Some genetic influence was found for FA, mandibular plane angle and Y axis, while the Pg to NB distance showed neither genetic influence, nor a familial aggregation.

Adolescent↗
PubMedDate not supplied

Dental caries and microbial acid production in twins.

OBJECTIVE: To determine the relative contribution of genetic and environmental stimuli on dental caries traits and microbial acid production in a twin model. METHODS: Dental caries examinations and microbial acid production assays were performed on 388 pairs of twins 1.5-8 years old from the city of Montes Claros, Brazil. Genotyping 8 polymorphic DNA markers determined zygosity. Caries exams followed NIDCR criteria modified to distinguish white spot lesions from cavitated lesions. Surface-based caries prevalence rates (SBCPR) were computed and lesion severity was determined by a weighted index (LSI). Biofilm samples were collected from the tongue using a lactic acid indicator swab. Assay scores were categorized based on acid formation as 1 = low, 2 = medium, and 3 = high. Heritability analyses were performed using the SOLAR software package. RESULTS: Heritability estimates for SBCPRs, LSI and for microbial acid production were H = 76.3 (p < 0.001), H = 70.6 (p < 0.001), H = 16.2 (p = 0.0078), respectively. Treating microbial acid production as a covariate in the SBCPR and LSI models did not significantly alter the heritability estimates, i.e. H = 76.5 (p < 0.001) and H = 70.8 (p < 0.001), respectively. CONCLUSIONS: These results suggest that variation in dental caries surface traits has a significant genetic contribution and that microbial acid production is modulated by the environment.

Acids↗
PubMedDate not supplied

Dentin dysplasia, type II linkage to chromosome 4q.

Dentin dysplasia, type II (MIM*125420) is an autosomal dominant disorder of dentin development. Clinically the primary dentition appears opalescent, and radiographically the pulp chambers are obliterated, resembling dentinogenesis imperfecta. However, unlike dentinogenesis imperfecta, the permanent teeth in dentin dysplasia, type II are normal in color and, on radiographs, have a thistle-tube pulp chamber configuration with pulp stones. The similarity of the primary dentition phenotype suggested that the gene for dentin dysplasia, type II is allelic with the gene for dentinogenesis imperfecta, Shields type II (DGII; MIM*125490), which has been localized to chromosome 4q13-q21. Twenty-four members of a three generation family in which ten members are affected with dentin dysplasia, type II were genotyped for microsatellite alleles specific for the area of chromosome 4q linked to DGII. Linkage was assessed by using the LINKAGE computer program, assuming autosomal dominant inheritance, a disease allele frequency of 0.0001, and complete penetrance. The maximum two-point LOD score (Zmax = 4.2 at theta = 0.0) was obtained with SPPI and D4S2691. Multipoint analysis gave a maximum LOD score of 4.33. The candidate region for dentin dysplasia, type II is approximately 14.1 cM, includes SPPI, D4S2691, D4S2690, D4S451, and D4S2456, and overlaps the most likely location of the DGII locus. A candidate gene for DGII should also be considered a candidate gene for dentin dysplasia, type II.

Alleles↗