Odontoblasts are dentin-secreting cells that survive for the whole life of a healthy tooth. Once teeth are completely erupted, odontoblasts transform into a mature stage that allows for their functional conservation for decades, while maintaining the capacity for secondary and reactionary dentin secretion. Odontoblasts are also critically involved in the transmission of sensory stimuli from the dentin-pulp complex and in the cellular defense against pathogens. Their longevity is sustained by an elaborate autophagic-lysosomal system that ensures organelle and protein renewal. However, progressive dysfunction of this system, in part caused by lipofuscin accumulation, reduces the fitness of odontoblasts and eventually impairs their dentin maintenance capacity. Here we review the functional activities assumed by mature odontoblasts throughout life. Understanding the biological basis of age-related changes in human odontoblasts is crucial to improving tooth preservation in the elderly.

Reactionary dentin formation is an adaptive secretory response mediated by odontoblasts to moderate dentin injury. The implications of this process for neuroimmune interactions operating to contain pathogens have not been fully appreciated. The purpose of the present study was to describe the relationship between reactionary dentinogenesis, the neurogenic changes of dental pulp innervation, and dendritic cell recruitment to caries progression, using a comparative immunohistochemical approach in human teeth from young adult individuals. Reactionary dentin formation during dentin caries progression is associated with changes in the integrity of junctional complexes within the odontoblast layer. Diminished coexpression of Cx43 and zonula occludens 1 implies a reduced level of intercellular connectivity between odontoblasts. Dentin caries also causes overexpression of growth-associated protein 43, a modulator of neural plasticity that promotes extensive sprouting of nerve endings into the reactionary dentin matrix. At the same time, an elevated number of HLA-DR-positive dendritic cells infiltrate the odontoblast layer and subsequently invade reactionary dentin formed underneath the early caries-affected regions. Simultaneous odontoblast layer remodeling, nerve fiber sprouting, and activation of dendritic cells during caries progression suggest a coordinated neuroimmune response to fight caries pathogen invasion and to promote dentin-pulp healing. We propose that reactionary dentin formation hinders pathogen invasion and supports defensive neuroimmune interactions against infection. The eventual understanding of this complex scenario may contribute to the development of novel approaches to dental caries treatment.

About half of all extant vertebrates are teleost fishes. Although our knowledge about anatomy and function of their olfactory systems still lags behind that of mammals, recent advances in cellular and molecular biology have provided us with a wealth of novel information about the sense of smell in this important animal group. Its paired olfactory organs contain up to five types of olfactory receptor neurons expressing OR, TAAR, VR1- and VR2-class odorant receptors associated with individual transduction machineries. The different types of receptor neurons are preferentially tuned towards particular classes of odorants, that are associated with specific behaviors, such as feeding, mating or migration. We discuss the connections of the receptor neurons in the olfactory bulb, the differences in bulbar circuitry compared to mammals, and the characteristics of second order projections to telencephalic olfactory areas, considering the everted ontogeny of the teleost telencephalon. The review concludes with a brief overview of current theories about odor coding and the prominent neural oscillations observed in the teleost olfactory system.

Odontoblasts are long-lived post-mitotic cells in the dental pulp, whose function is to form and maintain dentin. The survival mechanisms that preserve the viability of terminally differentiated odontoblasts during the life of a healthy tooth have not been described. In the present study, we characterized the autophagic-lysosomal system of human odontoblasts with transmission electron microscopy and immunocytochemistry, to analyze the mechanisms that maintain the functional viability of these dentinogenic cells. Odontoblasts were found to develop an autophagic-lysosomal system organized mainly by large autophagic vacuoles that are acid-phosphatase-positive to various degrees. These vacuoles expressed the autophagosomal and lysosomal markers LC3 and LAMP2, respectively, in an age-related pattern indicating the organization of a dynamic autophagic machinery. Progressive accumulation of lipofuscin within lysosomes indicates reduced lysosomal activity as a function of odontoblast aging. Our results suggest that autophagic activity in odontoblasts is a fundamental mechanism to ensure turnover and degradation of subcellular components. A reduction in the efficacy of this system might compromise cell viability and dentinogenic secretory capacity. In adult teeth, this condition is described as an ‘old odontoblast’ stage.