A posteroanterior skeletal analysis of Class II subdivision malocclusions

A posteroanterior skeletal analysis of Class II subdivision malocclusions

American Journal of Orthodontics and Dentofacial Orthopedics Voh~me 103, No. 6 Quantification of bone morphogenetic protein-induced bone formation in...

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American Journal of Orthodontics and Dentofacial Orthopedics Voh~me 103, No. 6

Quantification of bone morphogenetic protein-induced bone formation in mast cell-deficient mice. Richard J. Anthony, Los Angeles: University of Southen, California, 1991 Mast cells have been associated with numerous clinical and experimental bone pathophysiologic states and their role in normal bone physiology is not known. The objective of this thesis was to qualitatively and quantitatively access the role of mast cells in the cellular mechanisms that modulate bone formation and remodeling processes. Bone morphogenetic protein-induced bone formation was evaluated in both mast cell-deficient (WBB6FI/J-W/X,W white mutant) and mast cell-normal ( W B B 6 F I / J - + / + black normal) mice by radiographs, histologic sections, and biochemical assays indicative of bone formation. Specifically, the following hypothesis was tested: if mast ceils are involved in the regulatory aspect of bone formation and remodeling, mast cell-deficient mice should have an altered quantity of induced ectopic bone formation compared with mast cell-normal littermates. For mice, BMP induces the differentiation of cartilage within 8 days, cartilage and woven bone within 12 days, and lamellar bone including bone marrow within 21 days. Induced bone formation was evaluated by radiographs at 0, 4, 11, and 19 days; and by histologic sections at 11 and 19 days after BMP implantation. Also, alkaline phosphatase enzyme activity and total calcium mineral content of the ossicles were measured at both 9 and 23 days after implantation. Statistical evaluation of both biochemical assays by two-level ncstcd/ANOVA showed that a large percentage of the variance in BMP-induced ossicle formation occurs within each group; therefore, no significant difference between mast cell-deficient and mast cell-normal mice could be found. Histologically and radiographically, there were no gross qualitative differences in ossicle formation between the groups at the time periods examined. Interestingly, no mast cells were ever observed in proximity or within the ossicles of both the control or experimental groups. It was concluded that mast cells do not play a major role in cctopic bone formation in mice.

The effectiveness of the 308-rim excimer laser for pretreatment of enamel surface: A comparative study of shear bond strength between laser irradiation and acid etching. David Phoon Choe, Los Angeles: Universi~"of Southern California, 1991 The purpose of this study was to determine whether the shear bond strength of samples treated by the 308-nm cxcimer laser is significantly different than that of an acid-treated group, and to evaluate the effects of varying energy density and irradiation time on shear bond strength.

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A summary of findings is as follows: (a) the mean shear bond strength of the laser-treated group is significantly lower than acid-trcatcd group, (b) there is a statistically significant interaction betwcen energy density and irradiation time in effecting the mean shear bond strength, (c) the effect of energy density on mean shear bond strength is greatest at 70 mJ/mm 2, (d) the effcct of irradiation time on mean shear bond strength is seen thegreatest at 75 seconds, (e) the effect of irradiation time is most obvious at energy-density lcvels of 50 and 70 mJ/mm 2 but less apparent at 90 mJ/mm 2, (f) bond breakage among the laser-treated groups occurred mostly at the enamel-composite interface, possibly implying problems with wetting by monomer, reduced undercuts/micropores for retention, and reduced surface area for bonding.

A posteroanterior skeletal analysis of Class II subdivision malocclusions. Stuart J. Hoffman, Los Angeles: Unirersity of Southern California, 1991 Previous research indicates that craniofacial skeletal asymmetries are common occurrences in the general population. Ilowever, a "normal" degree of such skeletal asymmetry has not been determined, nor has an association between occlusal asymmetry and degree of transverse skeletal asymmetry. Therefore the purpose of this investigation was to determine whether there is a greater degree of transverse skeletal asymmetry with a Class II subdivision malocclusion than with a Class I malocclusion. If greater asymmetry does exist within the Class II subdivision malocclusion population, this research would indicate the skeletal location Of the larger-than-normal asymmetry. It was also the purpose of this investigation to quantify the degree of transverse skeletal asymmetry associated with a symmetrical Class I dental malocclusion population. The symmetric sample consisted of 22 individuals with a Class I malocclusion; the asymmetric sample, 22 individuals with a Class II subdivision malocclusion. All individuals were in tile permanent dentition stage of development with no missing permanent teeth. Homologous bilateral linear distances w e r e measured. The population mean difference (right to left) was calculated for each bilateral measurement and uscd to statistically test for variation between the two sample groups. The results indicate that a significantly larger degree of skeletal asymmctry (9 of the 16 measurements) occurs for the asymmetric population than for the symmetric population. The most significant diffcrenccs were as follows: (1) the transverse position of the lateral borders of the maxilla, (2) the condylarramal lengths from the body of the mandible. From the symmetric malocclusion sample data, an index of normal asymmetry was established as a reference for clinical diagnosis of posteroantcrior radiographs.