Department of Periodontology and Oral Medicine, University of Limpopo, Medunsa Campus, South Africa.
Division of Anatomical Pathology, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Oral Oncol. 2013 Sep;49(9):887-892. doi: 10.1016/j.oraloncology.2013.07.003. Epub 2013 Jul 30.
The link between cancer and inflammation is specific transcription factors that once activated have the capacity to enhance expression of genes that are common to both the regulation and the production of mediators of inflammation, and also to the regulation of the survival and proliferation of cancer cells. Cellular pathways activated by chronic inflammation brought about by chronic infections, by immune-mediated diseases, or by dysregulated wound healing at sites of repetitive tissue injury, constitute risk factors for initial cell transformation and for cancer progression. In established cancers, the cancer cells induce development of an exaggerated inflammatory state in the stroma, which in turn promotes cancer growth, invasion and metastasis. Inflammatory cells of myeloid origin in the tumour-associated stroma, mediate suppression of immune responses against cancer cells, which suppression favours tumour growth. Oral submucous fibrosis, and to a lesser extent oral lichen planus are precancerous conditions in which immuno-inflammatory processes are implicated in their pathogenesis, and in their cancerous transformation, if it occurs. Although there is some evidence for an association between oral squamous cell carcinoma on the one hand and dento-gingival bacterial plaques and chronic periodontitis on the other hand, the role of inflammation as the sole cause of cancerous transformation in such cases is not proven. The purpose of this article is to elaborate on some of the more important relationships between oral cancer and inflammation, and to comment on the role of inflammation in the pathogenesis of oral squamous cell carcinoma.
癌症与炎症之间的联系是特定的转录因子，一旦被激活，就有能力增强共同调节和产生炎症介质的基因的表达，也能调节癌细胞的存活和增殖。由慢性感染、免疫介导的疾病或在重复组织损伤部位失调的伤口愈合引起的慢性炎症激活的细胞途径，构成了初始细胞转化和癌症进展的风险因素。在已建立的癌症中，癌细胞在基质中诱导过度炎症状态的发展，这反过来又促进了癌症的生长、侵袭和转移。肿瘤相关基质中的髓样来源的炎症细胞介导对癌细胞的免疫反应的抑制，这种抑制有利于肿瘤的生长。口腔黏膜下纤维化，在较小程度上还有口腔扁平苔藓，是癌前状态，其发病机制和癌变（如果发生）都涉及免疫炎症过程。虽然有一些证据表明一方面口腔鳞状细胞癌与另一方面牙-牙龈细菌斑块和慢性牙周炎之间存在关联，但炎症作为此类情况下癌变的唯一原因尚没有得到证实。本文的目的是阐述口腔癌与炎症之间一些更重要的关系，并就炎症在口腔鳞状细胞癌发病机制中的作用进行评论。
