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Abstract

Background: Tooth wear (TW) typically requires occlusal reconstruction as an effective treatment. Progression of TW into a pathological state may cause various symptoms, including temporomandibular joint (TMJ) pain, occlusal disorders, and aesthetic concerns. Previous studies mainly focused on oral and facial tissues and electromyographic activity of masticatory muscles rather than the nervous system. This study aims to investigate the effects of bite reconstruction following TW on the peripheral and central nervous systems (CNS).

Methods: The bilateral maxillary molars of 60 Sprague-Dawley rats were examined, and a subgroup of 20 rats was selected to establish an occlusal reconstruction model. Subsequently, four time points were designated for general observation and measurement of pressure pain threshold (PPT). Immunofluorescence was employed to evaluate the expression of substance P (SP), calcitonin gene-related peptide (CGRP), and phosphorylated extracellular signal-regulated kinase (p-ERK) in trigeminal ganglion and medulla oblongata tissues. quantitative real-time polymerase chain reaction (qPCR) was performed to measure expression of tachykinin precursor 1 (Tac1), calcitonin-related polypeptide alpha (CALCA), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and brain-derived neurotrophic factor (BDNF). Additionally, Western blot (WB) was conducted to analyze expression of mitogen-activated protein kinase p38 (p38), phosphorylated p38 (p-p38), extracellular signal-regulated kinase (ERK), and p-ERK proteins.

Results: No bleeding or ulceration was observed in any rat group following each operation. Additionally, no significant tooth loosening or loss occurred, and facial symmetry during chewing and stable body weight were maintained in all groups. In the occlusal reconstruction group, PPT values significantly decreased on the third day post-modeling (p < 0.001) but gradually returned to baseline levels by day 28. SP levels significantly increased over time following occlusal reconstruction (p < 0.001) and returned to normal levels by day 28. The expression of p-ERK increased significantly 3 days after reconstruction (p < 0.001); although the number of positive cells decreased at day 14, it remained significantly higher than the control group (p < 0.01) before returning to baseline levels by day 28. Similarly, the expression of Tac1, CALCA, TNF-α, IL-1β, and BDNF genes exhibited a consistent downward trend on days 3, 7, and 14 post-reconstruction (p < 0.01). WB analysis revealed that expression of p-p38 and p-ERK proteins peaked on day 3 in the occlusal reconstruction group (p < 0.001) and gradually decreased thereafter.

Conclusions: Occlusal reconstruction may alleviate pain perception and nerve injury through activation of the p38 mitogen-activated protein kinase (MAPK)/ERK signaling pathway and regulation of factors such as SP, CGRP, and BDNF.