Background: Oral squamous cell carcinoma (OSCC), which accounts for over 90% of all oral malignancies, remains a major global health challenge due to its aggressive clinical course and poor prognosis. Periodontitis, a widespread chronic inflammatory condition affecting the supporting structures of the teeth, has increasingly been implicated as a potential risk factor for the development of various cancers. Emerging evidence suggests that microbial dysbiosis within the oral cavity may contribute to the creation of a pro-tumorigenic microenvironment, thereby promoting tumor initiation and progression. Nevertheless, the precise mechanisms linking periodontitis to OSCC, particularly through alterations in the oral microbiota, remain insufficiently understood. This article seeks to comprehensively analyze the association between periodontitis and OSCC and to elucidate the potential role of oral microbiota dysbiosis in mediating this relationship. Methods: In this study, a ligature-induced periodontitis model was established in C57BL/6J mice, and after two weeks, an OSCC model was introduced by the subcutaneous injection of SCC-7 cells to investigate the impact of periodontitis on OSCC progression. The effects of periodontitis on OSCC cell proliferation and invasion were assessed using scratch wound healing assays and CCK-8 proliferation assays. 16S rDNA high-throughput sequencing was conducted to profile the microbial communities present in the oral cavity and OSCC tissues, with particular emphasis on α-diversity indices (including Pielou’s evenness and Chao1 richness) and taxonomic composition at both the phylum and class levels. Furthermore, qPCR was utilized to assess the expression levels of cytokines in both periodontal and OSCC tissues, thereby elucidating the inflammatory milieu, potentially linking periodontitis to OSCC progression. Results: Our findings demonstrated that periodontitis significantly promoted OSCC growth and enhanced the invasive potential of OSCC cells. Microbial profiling revealed marked alterations in both the oral and OSCC microbiota, characterized by significant shifts in community composition and increased microbial diversity. Notably, these microbial changes exhibited consistent patterns between the oral cavity and the OSCC microenvironment, suggesting a potential mechanistic link between periodontitis-associated dysbiosis and OSCC progression. Consistently, qPCR analysis revealed elevated expression levels of IL-1β, IL-10, and IL-18 in both periodontal and OSCC tissues, providing evidence that the microbial alterations were accompanied by intensified inflammatory responses, which may contribute to OSCC progression. Conclusions: This study underscores the intricate interplay between periodontitis-induced microbial dysbiosis and the development of oral squamous cell carcinoma (OSCC). The findings suggest that periodontal inflammation, together with associated shifts in the oral microbiota, acts synergistically to drive OSCC progression. The elevated expression of cytokines further supports the role of a pro-inflammatory tumor microenvironment in mediating this interaction. These results offer important insights into the microbial and inflammatory mechanisms underlying the connection between periodontitis and OSCC, highlighting the critical role of maintaining periodontal health in the prevention and management of OSCC.
背景：口腔鳞状细胞癌（OSCC）占所有口腔恶性肿瘤的90%以上，因其侵袭性临床病程和不良预后，仍是全球主要的健康挑战。牙周炎是一种影响牙齿支持结构的广泛性慢性炎症性疾病，已日益被认为是多种癌症发生的潜在风险因素。新出现的证据表明，口腔内的微生物失调可能有助于形成促肿瘤发生的微环境，从而促进肿瘤的发生和进展。然而，牙周炎与OSCC之间的确切联系机制，特别是通过口腔微生物群的变化，目前仍未得到充分理解。本文旨在全面分析牙周炎与OSCC之间的关联，并阐明口腔微生物群失调在介导这种关系中可能发挥的作用。 方法：本研究在C57BL/6J小鼠中建立了结扎诱导的牙周炎模型，两周后通过皮下注射SCC-7细胞引入OSCC模型，以研究牙周炎对OSCC进展的影响。采用划痕愈合实验和CCK-8增殖实验评估牙周炎对OSCC细胞增殖和侵袭能力的影响。通过16S rDNA高通量测序对口腔和OSCC组织中的微生物群落进行分析，重点关注α-多样性指数（包括Pielou均匀度和Chao1丰富度）以及门和纲水平的分类学组成。此外，利用qPCR评估牙周组织和OSCC组织中细胞因子的表达水平，从而阐明可能将牙周炎与OSCC进展联系起来的炎症微环境。 结果：我们的研究结果表明，牙周炎显著促进了OSCC的生长并增强了OSCC细胞的侵袭潜力。微生物谱分析显示，口腔和OSCC微生物群均发生了显著改变，其特征是群落组成发生显著变化以及微生物多样性增加。值得注意的是，这些微生物变化在口腔和OSCC微环境中表现出一致的模式，表明牙周炎相关的微生物失调与OSCC进展之间可能存在机制性联系。一致地，qPCR分析显示牙周组织和OSCC组织中IL-1β、IL-10和IL-18的表达水平升高，这为微生物改变伴随着加剧的炎症反应提供了证据，而炎症反应可能促进了OSCC的进展。 结论：本研究强调了牙周炎诱导的微生物失调与口腔鳞状细胞癌（OSCC）发展之间复杂的相互作用。研究结果表明，牙周炎症连同相关的口腔微生物群变化，协同作用驱动OSCC的进展。细胞因子表达水平的升高进一步支持了促炎性肿瘤微环境在介导这种相互作用中的作用。这些结果为理解牙周炎与OSCC之间联系的微生物和炎症机制提供了重要见解，突显了维持牙周健康在预防和管理OSCC中的关键作用。
肿瘤(癌症)患者之家