A narrative review of cracks in teeth: Aetiology, microstructure and diagnostic challenges.

OBJECTIVES: To summarize the available evidence of crack formation in teeth and to discuss the limitations of the current clinical diagnostic modalities for crack detection in teeth. BACKGROUND: Cracks are a common clinical finding in teeth and yet clinicians still struggle to identify the full extent and orientation of cracks for their appropriate timely management. The biomechanics of crack development can be due to multiple factors and can differ from an unrestored tooth to a restored or endodontically treated tooth. DATA & SOURCES: This narrative review has been designed following the guidelines published by Green et al. 2006 [1] Published literature in the English language that addresses the objectives of this review up to July 2022 was sourced from online databases and reference lists. The relevance of the papers was assessed and discussed by two reviewers. A total of 101 publications were included in this narrative review. CONCLUSIONS: The initiation and development of cracks in teeth are likely linked to an interplay between the masticatory forces and fracture resistance of the remaining tooth structure. From the identified literature, the quality and quantity of remaining tooth structure in a restored or endodontically-treated tooth affects the biomechanics of crack development compared to an unrestored tooth. The extent, orientation, and size of the cracks do affect a clinician's ability to detect cracks in teeth. There is still a need to develop reliable diagnostic tools that will accurately identify cracks in teeth beneath restorations to enable effective monitoring of their propagation and provide appropriate interventions. CLINICAL SIGNIFICANCE: The development and propagation of cracks in an unrestored tooth differ greatly from a restored and endodontically treated tooth; mainly linked to the quantity and quality of the remaining tooth structure and the forces acting on them. Identifying the extent of cracks in teeth remains challenging for early clinical intervention.

A novel cyclic dinuclear gold(I) complex induces anticancer activity via an oxidative stress-mediated intrinsic apoptotic pathway in MDA-MB-231 cancer cells.

A new dinuclear cyclic gold(I) complex [Au2(DCyPA)2](PF6)2, 1, based on bis[2-(dicyclohexylphosphano)ethyl]amine (DCyPA) has been synthesized and characterized by elemental analysis, IR and NMR spectroscopy, and X-ray crystallography. In the dinuclear complex cation [Au2(DCyPA)2]2+, the two gold(I) ions are bridged by the ligand bis[2-(dicyclohexylphosphano)ethyl]amine (DCyPA) giving rise to a 16-membered ring centrosymmetric metallacycle. The cytotoxicity of the complex was evaluated against the triple-negative human breast cancer cells MDA-MB-231. In order to understand the mechanism of the cytotoxic behavior, a variety of assays, including Annexin V-FITC/Propidium iodide double staining, ROS production, and mitochondrial membrane potential and migration assays were carried out. The results indicated that complex 1 induced cytotoxicity via an oxidative stress-mediated intrinsic apoptotic pathway in MDA-MB-231 cancer cells.