Cellular and Molecular Mechanisms Involved in the Physiological Root Resorption of Primary Teeth

Abstract

Introduction: The physiological resorption of primary teeth is a complex physiological phenomenon that is not completely known and is a subject of great interest. The cellular and molecular mechanisms involved in the phenomenon of physiological root resorption seem to be similar to those involved in bone resorption mediated by osteoclasts. The main cells responsible for the active resorption of the dental tissues are the odontoclasts, which are also known as clasts or osteoclasts; multinucleated giant cells originated from hematopoietic precursors of monocytes or macrophages. Recent advances published in the literature have shown that the differentiation and activity of osteoclasts, a phenomenon that is also known as osteoclastgenesis, are initiated and regulated by different stimuli and molecular signalizing agents such as cytokines, chemokines, products of degradation released by the affected root surface, adhesion molecules, metalloproteinases, and the RANK/RANKL/OPG system. Moreover, the physical contact between the osteoclasts and osteoblast precursors or stromal cells also seems to be necessary for the activation of osteoclastgenesis. However, the specific role of the factors involved in the initiation and modulation of root resorption of the primary teeth remains unknown. Objective: To perform a review of the literature about the cellular and molecular mechanisms involved in the process of physiological resorption of the primary teeth, emphasizing their clinical implications. Conclusion: A complex integration among osteoclasts, osteoblasts, macrophages, cytokines, chemokines, metalloproteinases, adhesion molecules and the RANK/RANKL/OPG system seems to contribute to the physiological resorption of teeth. Knowing the cellular and molecular mechanisms involved in the process of physiological root resorption of primary teeth may contribute to the investigation of the immunepathogenesis of dental resorptions, and allow for the clinical application of molecular mediators to delay or even inhibit this process.