慢性牙周炎患者血清Semaphorin3A、FGF-23水平与牙周指标、病情严重程度的相关性分析

doi:10.19439/j.sjos.2025.04.011

摘要/Abstract

摘要： 目的：分析慢性牙周炎（CP）患者血清信号素3A（Sema3A）、成纤维细胞生长因子23（FGF-23）水平与牙周指标及病情严重程度的相关性。方法：选择沧州市中心医院2022年6月—2023年6月收治的CP患者115例,根据病情严重程度分为重度组（34例）、中度组（39例）及轻度组（42例）;另选择同期体检牙周健康者115例为对照组。采用酶联免疫吸附法检测所有受试对象血清Sema3A、FGF-23水平,检测CP组血清炎症指标[肿瘤坏死因子α（TNF-α）、白介素6（interleukin 6,IL-6）、IL-17]和牙周指标[牙龈指数（GI）、出血指数（BI）、菌斑指数（PLI）、附着丧失（AL）和探诊深度（PD）]的水平。采用Pearson相关性分析Sema3A、FGF-23水平与牙周指标及炎症指标的相关性;采用多因素logistic回归分析CP患者病情严重程度的影响因素;采用ROC曲线分析CP患者病情严重程度的评估价值。结果：CP组血清Sema3A水平显著低于对照组,FGF-23水平显著高于对照组（P<0.05）。轻、中、重度CP组血清Sema3A水平依次降低,FGF-23水平依次升高（P<0.05）。轻、中、重度CP组GI、AL、BI、PLI、PD、TNF-α、IL-17和IL-6水平依次升高（P<0.05）。血清Sema3A水平与GI、AL、BI、PLI、PD、TNF-α、IL-17、IL-6呈负相关,FGF-23水平与以上指标呈正相关（P<0.05）。Sema3A是CP患者病情加重的保护因素,FGF-23、GI、AL、BI、PLI、PD、TNF-α、IL-17、IL-6是危险因素（P<0.05）。血清Sema3A、FGF-23联合评估CP患者病情严重程度的曲线下面积（AUC）为0.919（95%CI：0.854~0.962）,显著优于单一指标（P<0.05）。结论：CP患者血清Sema3A降低,FGF-23升高,与患者牙周指标及病情严重程度密切相关,两者联合评估CP患者病情严重程度具有较高价值。

关键词: 慢性牙周炎, 信号素3A, 成纤维细胞生长因子23, 牙周指标

Abstract: PURPOSE: To analyze the correlation of serum Semaphorin3A(Sema3A), fibroblast growth factor 23(FGF-23) levels with periodontal indices and disease severity in patients with chronic periodontitis. METHODS: A total of 115 CP patients admitted to Cangzhou Central Hospital from June 2022 to June 2023 were selected and divided into severe group (34 cases), moderate group (39 cases) and mild group (42 cases) according to the severity of the disease; meanwhile, another 115 healthy individuals with periodontitis who underwent physical examination were selected as the control group. Serum Sema3A and FGF-23 levels of all subjects were detected by enzyme-linked immunosorbent assay (ELISA), and serum inflammatory markers [tumor necrosis factor-α(TNF-α) and interleukin 6 (IL-6), IL-17] and the levels of periodontal indices [gingival index(GI), bleeding index (BI), plaque index (PLI), loss of attachment (AL) and probing depth (PD)] in CP group were detected. Pearson correlation analysis was employed to explore the correlations between the levels of Sema3A and FGF-23 and periodontal parameters and inflammatory markers. Multivariate logistic regression was used to analyze the factors affecting the severity of CP patients. ROC curve was used to evaluate the severity of CP patients with SPSS 25.0 software package. RESULTS: The serum Sema3A level in the CP group was significantly lower than that in the control group, while the FGF-23 level was significantly higher than that in the control group (P<0.05). The serum Sema3A level in mild, moderate, and severe CP group decreased sequentially, while FGF-23 level increased sequentially(P<0.05). The levels of GI, AL, BI, PLI, PD, TNF-α, IL-17 and IL-6 in the mild, moderate, and severe CP groups increased sequentially (P<0.05). The serum Sema3A level was negatively correlated with GI, AL, BI, PLI, PD, TNF-α, IL-17, and IL-6, while the FGF-23 level was positively correlated with the above indicators (P<0.05). Sema3A was a protective factor for exacerbation in CP patients, while FGF-23, GI, AL, BI, PLI, PD, TNF-α, IL-17, and IL-6 were risk factors (P<0.05). The AUC of combined evaluation of serum Sema3A and FGF-23 of the severity of CP patients was 0.919 (95%CI: 0.854-0.962), which was obviously better than a single indicator (P<0.05). CONCLUSIONS: Serum Sema3A is decreased and FGF-23 is increased in CP patients, which is closely related to periodontal parameters and disease severity, and combination evaluation has a high value in estimating the severity of CP patients.

Key words: Chronic periodontitis, Semaphorin3A, Fibroblast growth factor 23, Periodontal indicators

中图分类号:

R781.4

肖遵胜, 丁文萃, 王丽晖, 贾惠雯, 靳艳艳, 李新胜. 慢性牙周炎患者血清Semaphorin3A、FGF-23水平与牙周指标、病情严重程度的相关性分析[J]. 上海口腔医学, 2025, 34(4): 403-408.

Xiao Zunsheng, Ding Wencui, Wang Lihui, Jia Huiwen, Jin Yanyan, Li Xinsheng. Correlation of serum Semaphorin3A, FGF-23 levels with periodontal indices and disease severity in patients with chronic periodontitis[J]. Shanghai Journal of Stomatology, 2025, 34(4): 403-408.

参考文献

[1] Qian SJ, Huang QR, Chen RY, et al.Single-cell RNA sequencing identifies new inflammation-promoting cell subsets in Asian patients with chronic periodontitis[J]. Front Immunol, 2021, 12(1): 711337.
[2] Imai K, Ogata Y.How does Epstein-Barr virus contribute to chronic periodontitis?[J]. Int J Mol Sci, 2020, 21(6): 1-12.
[3] Zheng Y, Jiang F, Wang C, et al.Regulation of Semaphorin3A in the process of cutaneous wound healing[J]. Cell Death Differ, 2022, 29(10): 1941-1954.
[4] 陈荟宇, 白明茹, 叶玲. 信号素3A与口腔常见病关系的研究进展[J]. 国际口腔医学杂志, 2022, 42(5): 593-599.
[5] Sirikul W, Siri-Angkul N, Chattipakorn N, et al.Fibroblast growth factor 23 and osteoporosis: evidence from bench to bedside[J]. Int J Mol Sci, 2022, 23(5): 2500.
[6] Acipinar S, Karsiyaka Hendek M, Olgun E, et al.Evaluation of FGF-23 and 25(OH)D3 levels in peri-implant sulcus fluid in peri-implant health and diseases[J]. Clin Implant Dent Relat Res, 2019, 21(5): 1106-1112.
[7] Caton JG, Armitage G, Berglundh T, et al. A new classification scheme for periodontal and peri-implant diseases and conditions Introduction and key changes from the1999 classification[J]. J Periodontol, 2018, 89(Suppl 1): SI-S8.
[8] Caton JG, Armitage G, Berglundh T, et al.A new classification scheme for periodontal and peri-implant diseases and conditions - introduction and key changes from the 1999 classification[J]. J Periodontol, 2018, 89(Suppl 1): S1-S8.
[9] 张婧, 汪静. 慢性牙周炎患者龈沟液LF, Shh蛋白, TREM-1水平与牙周临床指标和炎性因子的相关性研究[J]. 检验医学与临床, 2023, 20(13):1859-1863.
[10] Kavarthapu A, Gurumoorthy K.Linking chronic periodontitis and oral cancer: a review[J]. Oral Oncol, 2021, 121: 105375.
[11] Hoare A, Soto C, Rojas-Celis V, et al.Chronic inflammation as a link between periodontitis and carcinogenesis[J]. Mediators Inflamm, 2019: 1029857.
[12] Jiang Y, Feng J, Du J, et al.Clinical and biochemical effect of laser as an adjunct to non-surgical treatment of chronic periodontitis[J]. Oral Dis, 2022, 28(4): 1042-1057.
[13] Yun-Jia L, Xi C, Jie-Qiong Z, et al.Semaphorin3A increases M1-like microglia and retinal ganglion cell apoptosis after optic nerve injury[J]. Cell Biosci, 2021, 11(1): 1-16.
[14] Shindo S, Kumagai T, Shirawachi S, et al.Semaphorin3A released from human dental pulp cells inhibits the increase in interleukin-6 and CXC chemokine ligand 10 production induced by tumor necrosis factor-α through suppression of nuclear factor-κB activation[J]. Cell Biol Int, 2021, 45(1): 238-244.
[15] Ceylan M, Erbak Yilmaz H, Narin F, et al.Gingival crevicular fluid lipocalin-2 and semaphorin3A in stage Ⅲ periodontitis: Non-surgical periodontal treatment effects[J]. J Periodontal Res, 2022, 57(4): 724-732.
[16] Lin Y, Xing Q, Qin W, et al.Decreased expression of Semaphorin3A/Neuropilin-1 signaling axis in apical periodontitis[J]. Biomed Res Int, 2017: 8724503.
[17] Satomi K, Nishimura K, Igarashi K.Semaphorin 3A protects against alveolar bone loss during orthodontic tooth movement in mice with periodontitis[J]. J Periodontal Res, 2022, 57(5): 991-1002.
[18] Tian T, Chen L, Wang Z, et al.Sema3A drives alternative macrophage activation in the resolution of periodontitis via PI3K/AKT/mTOR signaling[J]. Inflammation, 2023, 46(3): 876-891.
[19] Clinkenbeard E.Fibroblast growth factor 23 bone regulation and downstream hormonal activity[J]. Calcif Tissue Int, 2023, 113(1): 4-20.
[20] Ratsma DMA, Zillikens MC, van der Eerden BCJ. Upstream regulators of fibroblast growth factor 23[J]. Front Endocrinol (Lausanne), 2021, 12: 588096.
[21] Wang L, Tran AB, Nociti FH Jr, et al.PTH and vitamin D repress DMP1 in cementoblasts[J]. J Dent Res, 2015, 94(10): 1408-1416.
[22] Bakhsh A, Moyes D, Proctor G, et al.The impact of apical periodontitis, non-surgical root canal retreatment and periapical surgery on serum inflammatory biomarkers[J]. Int Endod J, 2022, 55(9): 923-937.