Poster abstracts
Poster number 7 submitted by Gabriela Wandling
SEMA7A Deletion Impairs Reparative Dentin Bridge Formation After Direct Pulp Capping
Gabriela M. Wandling (Neuroscience Graduate Program), Aashi Sharma (Division of Biosciences, College of Dentistry, Ohio State University), Siya Chhibber (Division of Biosciences, College of Dentistry, Ohio State University), Fatma Fenesha, Sarah B. Peters (Division of Biosciences, College of Dentistry, Ohio State University)
Abstract:
Background: Primary sensory afferents from the trigeminal ganglion are crucial for tooth maintenance and repair. After direct insult, dental pulp sensory nerves sprout to modulate inflammation and promote migration of dental pulp stem cells that differentiate into odontoblast-like cells, surround the damaged area, and secrete a new, reparative tertiary dentin layer1,2. Vital pulp therapy, or direct pulp capping, aims to preserve tooth vitality during endodontic procedures by reactivating developmental signaling pathways that promote pulpal healing3. Axon guidance protein SEMA7A is known to promote neuronal outgrowth and is expressed in odontoblasts during development and adulthood4. Here, we investigated whether global deletion of SEMA7A would lead to impaired dentin bridge formation in a direct pulp capping mouse model.
Methods: 8-week-old WT and Sema7a-/- mice were anesthetized, and first maxillary molars were treated with a deep dentin pulpal injury. Exposed pulps were capped with EndoSequence RRM Putty and sealed with a glass ionomer cement. Injured first molars were harvested at 21 days post injury for analysis of tertiary dentin density and volume with Micro-Computed Tomography (MicroCT). Fixed tissues were then decalcified, sectioned, and stained for histological evaluation with hematoxylin and eosin (H&E).
Results: We observed that Sema7a-/- mice had significantly lower tertiary dentin density and volume three weeks post injury compared to WT mice. Furthermore, in lieu of reparative dentin, H&E examination of the Sema7a-/- injured molars revealed an abundance of inflammatory cells surrounding the injury site.
Conclusion: SEMA7A protein expression could play an important role in directing pulpal healing response after injury. Due to the importance of sensory innervation in pulpal repair and the potential for SEMA7A expression to promote axon outgrowth, we are conducting experiments to elucidate whether the impaired healing response observed in Sema7a-/- mice is caused by altered odontoblast-sensory nerve signaling after injury.
References:
1.) Wang C, Liu X, Zhou J, Zhang X, Zhou Z, Zhang Q. Sensory nerves drive migration of dental pulp stem cells via the CGRP-Ramp1 axis in pulp repair. Cellular and Molecular Life Sciences: CMLS. 2024 Aug 28;81(1). doi: 10.1007/s00018-024-05400-2.
2.)Taylor PE, Byers MR, Redd PE. Sprouting of CGRP nerve fibers in response to dentin injury in rat molars. Brain Research. 1988/10/04;461(2). doi: 10.1016/0006-8993(88)90270-3.
3.) Bjørndal L, Simon S, Tomson PL, Duncan HF. Management of deep caries and the exposed pulp. International Endodontic Journal. 2019/07/01;52(7). doi: 10.1111/iej.13128.
4.)Jeroen Pasterkamp R, Peschon JJ, Spriggs MK, Kolodkin AL, Jeroen Pasterkamp R, Peschon JJ, Spriggs MK, Kolodkin AL. Semaphorin 7A promotes axon outgrowth through integrins and MAPKs. Nature 2003 424:6947. 2003/07;424(6947). doi: 10.1038/nature01790.
Keywords: Axon guidance, Semaphorins, Mineralization