Periodontal disease (PD) is a chronic, immune-mediated inflammatory condition caused by oral dysbiosis, and it is more frequently linked to systemic diseases. These include chronic kidney disease (CKD), which has been especially emphasized due to shared risk factors and related inflammation and immunometabolic mechanisms. PD has also recently been proposed to potentially relate to renal cell carcinoma (RCC), the most common kidney cancer. Although the connection between PD and CKD has been supported by ongoing epidemiological and mechanistic research, the link with RCC remains less studied but biologically plausible. This scoping review examines the literature on the association between PD, CKD, and RCC. It involves a narrative review of studies sourced from PubMed, Scopus, and Embase (from inception to November 2024) to explore clinical correlations between these conditions. The evidence suggests a bidirectional relationship between PD and CKD, involving cytokines like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), as well as NLRP3 inflammasome activation. Microbial product translocation causes systemic inflammation and renal dysfunction. Preliminary evidence indicates that chronic inflammation and immune dysregulation caused by PD may foster a tumor-promoting microenvironment, particularly in cases of lower glomerular filtration rate (eGFR). In summary, this review outlines a unified inflammatory and microbial pathway linking PD, CKD, and RCC. Understanding this triad offers potential new avenues for prevention, screening, and interdisciplinary care among nephrology, oncology, and oral medicine professionals.

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

From Periodontitis to Renal Disease: A Scoping Review

  • Achille Aveta,
  • Vincenzo Iossa,
  • Giuseppe Minervini,
  • Gianluca Spena,
  • Gianluca Carotenuto,
  • Savio Domenico Pandolfo

摘要

Periodontal disease (PD) is a chronic, immune-mediated inflammatory condition caused by oral dysbiosis, and it is more frequently linked to systemic diseases. These include chronic kidney disease (CKD), which has been especially emphasized due to shared risk factors and related inflammation and immunometabolic mechanisms. PD has also recently been proposed to potentially relate to renal cell carcinoma (RCC), the most common kidney cancer. Although the connection between PD and CKD has been supported by ongoing epidemiological and mechanistic research, the link with RCC remains less studied but biologically plausible. This scoping review examines the literature on the association between PD, CKD, and RCC. It involves a narrative review of studies sourced from PubMed, Scopus, and Embase (from inception to November 2024) to explore clinical correlations between these conditions. The evidence suggests a bidirectional relationship between PD and CKD, involving cytokines like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), as well as NLRP3 inflammasome activation. Microbial product translocation causes systemic inflammation and renal dysfunction. Preliminary evidence indicates that chronic inflammation and immune dysregulation caused by PD may foster a tumor-promoting microenvironment, particularly in cases of lower glomerular filtration rate (eGFR). In summary, this review outlines a unified inflammatory and microbial pathway linking PD, CKD, and RCC. Understanding this triad offers potential new avenues for prevention, screening, and interdisciplinary care among nephrology, oncology, and oral medicine professionals.