SEM-morphology in Dentinogenesis Imperfecta type II: microscopic anatomy and efficacy of a dentine bonding system

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ABSTRACT

Aim

Dentinogenesis Imperfecta is a hereditary defect consisting of opalescent teeth composed of irregularly formed and
undermineralised dentin that obliterates the coronal and root pulpal chambers. The aim of this study was to examine the morphology of
permanent human enamel, dentine and the dentine-enamel junction, in individuals affected by Dentinogenesis Imperfecta type II in
undercalcified sections using scanning electron microscope (SEM) to compare the findings to the normal morphology, and to study the
efficacy of modern bonding system to dentine and enamel DI type II affected.

Methods

Four third molars extracted
from two 19 year-old subjects (one patient affected by Dentinogenesis Imperfecta type II) were included in resin, two divided in slices
with a air-cooled diamond disc, and two used to study the characterisation of the resin-dentin interface. The sections of the teeth were
examined by means of SEM. The slices were finished up with abrasive paper (400, 600, 1000, and 2000), the half surfaces obtained
were etched with 37 phosphoric acid and then joined up to the stubs for SEM analysis. SEM Stereoscan 440 Leica with
magnifications of 20X, 100X, 250X, 1000X, 2000X, 3000X was used. As control group were used four third molars with normal
anatomy.

Results

This study shows that the permanent enamel from patients with DI exhibits few structural changes. No
relationships were found between enamel morphology and the DI type II. Enamel appeared to be regularly mineralised. The major
findings were anomalies in the dentine-enamel junction, locally a lower degree of mineralisation and an undulating morphology. The
dentine showed absence of tubules.

Conclusion

This study confirms that the problem with teeth affected by DI type II is the defect
in dentine and weakness in the way the enamel is attached to the dentine. The adhesive system tested is not able to create a real
hybrid layer in dentine DI type II affected and seems to be less effective than on normal substrates.

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