Striations Resulting from Fatigue Crack Growth in Dentin

Abstract

The primary objective of this study was to evaluate the striation spacing resulting from fatigue crack growth in dentin of human teeth. Compact tension (CT) specimens obtained from coronal dentin of patients of two age groups (young 50 years) were subjected to cyclic Mode I loads. Fracture surfaces of the CT specimens were examined using a scanning electron microscope (SEM) and contact profilometer. A power spectrum analysis of the surface profiles showed that the striation spacing ranged from 50 to 170 μm. In old dentin (125 ± 23 μm) the spacing was significantly larger than that in young dentin (93 ± 27 μm), suggesting that the mechanisms contributing to crack tip blunting were potentially suppressed by changes in structure of this tissue with age. Fatigue crack growth striations were also identified and examined on cracks that underwent extension in vivo. The striation spacing for in vivo cracks was within the range resulting from the in vitro evaluation. Results of this study suggest that fatigue crack growth contributes to restored tooth failures and the in vitro approach provides a viable model for evaluating the mechanics and mechanisms of cyclic crack extension in dentin. INTRODUCTION The human tooth is comprised of three distinct tissues, namely enamel, dentin and pulp. Dentin forms the bulk of the tooth by both weight and volume. While serving many functions, dentin provides an elastic foundation for the outermost brittle enamel. It also serves as a protective enclosure for the more sensitive pulp and as a conduit for transferring external stimuli to the nerves. Most importantly, dentin acts as an integral foundation for restorative materials which are placed to restore form and function to damaged or diseased tooth structure. Recent advances in restorative dentistry have led to improvements in the overall oral health of patients. New materials and methods have not only improved the aesthetics of restorations but also their performance. Despite these advances, the failure of restored teeth and tooth fracture is relatively common [1,2]. While it is plausible that fracture in the restored tooth results from a single catastrophic load, it is generally believed that such failures are the result of subcritical cracking induced by repetitive stresses, i.e., fatigue [3]. Damage induced by restorative processes can grow with time due to cyclic stresses resulting from mastication and can enable complete fracture of the tooth [4-7]. A number of in vitro studies on cyclic crack growth in bovine [8-10], elephant [11,12] and human dentin [13-15] have been conducted in the recent past. These studies have been successful in quantifying the fatigue properties of dentin. According to an evaluation of the mechanisms of fatigue crack growth in dentin, cyclic extension is comprised of crack-tip blunting and resharpening [12]. Fatigue failures in metals are often evaluated in terms of striations on the fractured surfaces. Yet, no study has identified fatigue striations resulting from cyclic crack extension in