Ling Qiao, Wang Ai-Jing, Wang Xiao-Yan
Department of Cariology and Endodontology, Peking University School and Hospital of Stomatology, Beijing, China.
National Center for Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices & Beijing Key Laboratory of Digital Stomatology & NHC Key Laboratory of Digital Stomatology & NMPA Key Laboratory for Dental Materials, Beijing, China.
J Dent Sci. 2025 Jan;20(1):402-409. doi: 10.1016/j.jds.2024.06.005. Epub 2024 Jun 14.
BACKGROUND/PURPOSE: Macrophages are considered to play an important role in the development of chronic apical periodontitis (CAP). However the function of tissue resident macrophages in CAP is unclear. This study aims to investigate the potential role of macrophages of different origins in CAP.
Chemokine receptor-2 deficiency (CCR2) mice and C57BL/6N mice (control group, WT mice) were used to induce apical periodontitis. The pulp of mandibular first molars of both sides were exposed to the oral environment. After 0, 7, 21, 28 days of pulp explosion, animals were sacrificed, the mandibular bones were collected and scanned with micro-CT, further processed for HE & IHC Staining to analyze the development of CAP, as well as the expression of surface markers of macrophages.
Both CCR2 and WT mice exhibited CCR2 negative macrophages in normal periapical area, which indicated the presence of tissue resident macrophages. CCR2 deficiency decreased the number of macrophages in periapical lesions, the M1 type macrophages' number as well as osteoclasts around the edge of the lesion decreased compared to wild type. Meanwhile CCR2 deficiency decreased the volume of periapical lesion significantly compared to wild type, but did not inhibite and disappeare the lesion thoroughly.
Monocyte-macrophage system derived macrophages promote the progression of periapical lesions, while tissue resident macrophages in periodontal ligament might also be involved in the progression of periapical lesion.
背景/目的：巨噬细胞被认为在慢性根尖周炎（CAP）的发展中起重要作用。然而，组织驻留巨噬细胞在CAP中的功能尚不清楚。本研究旨在探讨不同来源的巨噬细胞在CAP中的潜在作用。
使用趋化因子受体2缺陷（CCR2）小鼠和C57BL/6N小鼠（对照组，野生型小鼠）诱导根尖周炎。将两侧下颌第一磨牙的牙髓暴露于口腔环境。在牙髓暴露0、7、21、28天后，处死动物，收集下颌骨并用微型CT扫描，进一步进行苏木精-伊红（HE）和免疫组化（IHC）染色，以分析CAP的发展情况以及巨噬细胞表面标志物的表达。
CCR2小鼠和野生型小鼠在正常根尖周区域均表现出CCR2阴性巨噬细胞，这表明存在组织驻留巨噬细胞。与野生型相比，CCR2缺陷减少了根尖周病变中巨噬细胞的数量，病变边缘的M1型巨噬细胞数量以及破骨细胞数量均减少。同时，与野生型相比，CCR2缺陷显著降低了根尖周病变的体积，但并未完全抑制和消除病变。
单核细胞-巨噬细胞系统衍生的巨噬细胞促进根尖周病变的进展，而牙周膜中的组织驻留巨噬细胞可能也参与根尖周病变的进展。
