NOD2 contributes to Parvimonas micra-induced bone resorption in diabetic rats with experimental periodontitis

Ying-Yi Chen; Li Tan; Xiao-Lin Su; Ning-Xin Chen; Qiong Liu; Yun-Zhi Feng; Yue Guo

doi:10.1111/omi.12467

NOD2 contributes to Parvimonas micra-induced bone resorption in diabetic rats with experimental periodontitis

Mol Oral Microbiol. 2024 May 17. doi: 10.1111/omi.12467. Online ahead of print.

Authors

Ying-Yi Chen^{1

2}, Li Tan¹, Xiao-Lin Su¹, Ning-Xin Chen¹, Qiong Liu¹, Yun-Zhi Feng¹, Yue Guo¹

Affiliations

¹ Hunan Provincial Clinical Research Center for Oral Diseases, Hunan Provincial Engineering Research Center of Digital Oral and Maxillofacial Defect Repair, Department of Stomatology, The Second Xiangya Hospital, Central South University, Changsha, China.
² Department of Stomatology, Qingdao Central Hospital, University of Health and Rehabilitation Sciences（Qingdao Central Hospital）, Qingdao, China.

PMID: 38757737
DOI: 10.1111/omi.12467

Abstract

Background: Type 2 diabetes mellitus (T2DM) may affect the oral microbial community, exacerbating periodontal inflammation; however, its pathogenic mechanisms remain unclear. As nucleotide-binding oligomerization domain 2 (NOD2) plays a crucial role in the activation during periodontitis (PD), it is hypothesized that changes in the oral microbial community due to diabetes enhance periodontal inflammation through the activation of NOD2.

Methods: We collected subgingival plaque from 180 subjects who were categorized into two groups based on the presence or absence of T2DM. The composition of oral microbiota was detected by 16S rRNA high-throughput sequencing. In animal models of PD with or without T2DM, we assessed alveolar bone resorption by micro-computerized tomography and used immunohistochemistry to detect NOD2 expression in alveolar bone. Primary osteoblasts were cultured in osteogenic induction medium with high or normal glucose and treated with inactivated bacteria. After 24 h of inactivated bacteria intervention, the osteogenic differentiation ability was detected by alkaline phosphatase (ALP) staining, and the expressions of NOD2 and interleukin-12 (IL-6) were detected by western blot.

Results: The relative abundance of Parvimonas and Filifactor in the T2DM group was increased compared to the group without T2DM. In animal models, alveolar bone mass was decreased in PD, particularly in T2DM with PD (DMPD) group, compared to controls. Immunohistochemistry revealed NOD2 in osteoblasts from the alveolar bone in both the PD group and DMPD group, especially in the DMPD group. In vitro, intervention with inactivated Parvimonas significantly reduced ALP secretion of primary osteoblasts in high glucose medium, accompanied by increased expression of NOD2 and IL-6.

Conclusions: The results suggest that T2DM leading to PD may be associated with the activation of NOD2 by Parvimonas.

Keywords: alveolar bone; nucleotide‐binding oligomerization domain 2; oral microbiome; periodontitis; type 2 diabetes mellitus.

Abstract

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