Effects of Rheumatoid Arthritis on the Progression of Pulpitis and Apical Periodontitis in SKG Mice

Shiori Yamazaki; Reona Hayashi; Noriko Mutoh; Hayato Ohshima; Nobuyuki Tani-Ishii

doi:10.1016/j.joen.2023.08.003

Effects of Rheumatoid Arthritis on the Progression of Pulpitis and Apical Periodontitis in SKG Mice

J Endod. 2023 Aug 17:S0099-2399(23)00497-1. doi: 10.1016/j.joen.2023.08.003. Online ahead of print.

Authors

Shiori Yamazaki¹, Reona Hayashi¹, Noriko Mutoh¹, Hayato Ohshima², Nobuyuki Tani-Ishii³

Affiliations

¹ Department of Pulp Biology and Endodontics, Graduate School of Dentistry, Kanagawa Dental University, Kanagawa, Japan.
² Division of Anatomy and Cell Biology of the Hard Tissue, Department of Tissue Regeneration and Reconstruction, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
³ Department of Pulp Biology and Endodontics, Graduate School of Dentistry, Kanagawa Dental University, Kanagawa, Japan. Electronic address: n.ishii@kdu.ac.jp.

PMID: 37595682
DOI: 10.1016/j.joen.2023.08.003

Abstract

Introduction: Rheumatoid arthritis (RA) is an autoimmune disease that involves joint inflammation. Although periodontal disease reportedly contributes to RA onset, the associations of RA with pulpitis and apical periodontitis have not been described. The purpose of this study was to examine the effects of immune response disruption of RA for pulpitis and apical periodontitis with SKG mice.

Methods: SKG and BALB/c (control) mice were used to establish models of pulp infection. Histologic studies of pulp and apical periodontal tissue were performed at 3, 5, 7, 14, and 28 days; odontoblast dynamics were analyzed by antinestin staining, and apoptotic cells were examined by TdT-mediated digoxygenin (biotin)-dUTP nick end labeling staining.

Results: Inflammatory cell infiltration into the exposed pulp was observed at 3 days in the SKG and control group groups; the infiltration extended to the apical pulp area at 14 days after surgery. Inflammatory cell infiltration and bone resorption in the apical pulp area were observed from 14-28 days in the SKG and control groups; there were significant increases in inflammatory cell infiltration and bone resorption in the control group at 28 days. The numbers of apoptotic cells in pulp and apical periodontal tissue were higher in the SKG group than in the control group at 14 and 28 days. The number of odontoblasts decreased in the SKG and control groups until 14 days and then disappeared in the SKG and control groups at 28 days.

Conclusions: This study suggested that immune response disruption in RA is involved in prolonging the inflammatory state of pulpitis and apical periodontitis.

Keywords: Apical periodontitis; apoptosis; odontoblasts; pulpitis; rheumatoid arthritis.