The detection and prevalence of reactive and physiologic sclerotic dentin, reparative dentin and dead tracts beneath various types of dental lesions according to tooth surface and age

Abstract

The pulpo-dentinal complex responds to external injuries with dentin sclerosis (DS), dead tracts (DT), or reparative dentin (RD). This investigation correlates the prevalence of these responses with age, sex, type and surface location of tooth lesions (caries, restorations, attrition, abrasion and erosion) utilizing ground sections, microradiographs and decalcified paraffin-embedded tooth sections treated with the Pollak trichome stains (270 teeth from 113 patients). The main response to caries, restorations and erosion was DS, followed by RD and DT. DS, RD and DT occurred equally in any tooth, on any tooth surface and even beneath the same lesion. DS did not necessarily prevent RD. Root and furcation DS and RD in the floor of the pulp chamber and root canals were unrelated to particular lesions but did relate to increasing age. Root DS extended from apical to cervical area with increasing age. Beneath caries and restorations DS and RD were more prevalent in males, but DT was more prevalent in females. Pollak staining of decalcified paraffin sections for DS was approximately 80% as accurate as ground sections and microradiography. In pulp studies, where the result is contrary to previous experience, the Pollak stains reveal whether DS has decreased dentin permeability.

Effect of Substrate Age and Adhesive Composition on Dentin Bonding

“…2 This increased calcification is part of physiological aging (or physiological sclerosis), as well as a response to external stimuli such as attrition and caries. 2,3 Adhesion studies have not shown a direct correlation between dentin age and dentin bonding. A study compared the secondgeneration adhesive Scotchbond DC with the thirdgeneration adhesive Scotchbond 2, both of which were applied in teeth with a mean age of 22.5 vs 65.6 years.…”

“…1 Physiological changes resulting from dentin aging or changes in response to caries and other aggressive stimuli increase the degree of mineralization of dentin, with a consequent increase in dentin thickness and reduction of dentin permeability. [2][3][4] Since dentin permeability is an important factor in the adhesion process, reduction of permeability with age may have a direct effect on dentin bond strengths. 1,5 In spite of increased dentin calcification with age, adhesion studies [6][7][8][9] have not shown an obvious correlation between dentin age and bonding ability of dentin adhesives.…”

Effect of tooth age on bond strength to dentin

“…Close to the pulp in newly erupted teeth, the dentin matrices are less mineralized and represent a small fraction of dentin area, whereas the tubules occupy a large area 6,14 . The main age-related change in older teeth includes a gradual enlargement of the peritubular dentin and intratubular mineral deposits, which often result in narrowed or completely occluded tubules 20,25 . Dentin sclerosis increases in teeth that have been subjected to attrition, to oral exposure of the dentin, to caries or dental restorative procedures 12,15,16,17 .…”

“…Studies show hybridization of the tubules' walls in the funnel-shaped portion, produced by acid etching 28,29 . The dentinal structure undergoes histological and physiological alterations with aging or maturation in vital teeth 4,12,17,20,25,26 . Thus, permanent teeth of elderly patients may have different morphology and composition, which may affect the results of acid etching or infiltration of resin monomer.…”

The role of transforming growth factor beta in tertiary dentinogenesis

“…3 The formation of the tertiary dentin on the pulpal aspect of stimulated dentinal tubules occurs in human deciduous teeth 4 as well as in permanent teeth. 5 It starts during the active stage of the carious process and continues after lesion arrest. 6 The rate of carious attack seems to be an influencing factor since more dentin is formed in response to a slowly progressing chronic caries than to a rapidly advancing acute caries.…”