Revisiting the association between candidal infection and carcinoma, particularly oral squamous cell carcinoma

To investigate the presence of titanium particles in peri-implant tissues in cases diagnosed with peri-implantitis, and to identify immunological reactions that these particles may elicit. Ten peri-implant tissue biopsies of patients diagnosed clinically and radiographically with peri-implantitis were obtained from the archives of Oral Pathology Centre, University of Otago. The inclusion criteria involves: bleeding on probing, ≥6 mm probing depth and ≥3 mm radiographic bone loss around the dental implant. Peri-implant tissue samples were evaluated using scanning electron microscopy-energy dispersive x-ray spectroscopy (SEM-EDS) to identify of sites with/without titanium particles. Antibodies against human transforming growth factor beta 1 (TGF-β1), receptor activator of nuclear factor kappa-B ligand (RANKL), interleukin 33 (IL-33) and cluster of differentiation 68 (CD68) were used to stain the specimens. ImageJ software was used to standardise the sampling area, compare and characterise the inflammatory infiltrate in tissues with/without titanium particles. Inflammatory cytokines positivity was assessed using the immunoreactive scores (IRSs). Light microscopy and SEM-EDS analysis identified titanium wear particles in 90% of the tissue samples, associated with a mixed chronic inflammatory infiltrate. Quantification analysis of RANKL revealed significantly higher IRS and intensity scores (p < 0.05) in areas containing titanium. High intensity, proportion and IRSs of TGF-β1 and IL-33 were observed in areas with titanium. CD68 had higher IRSs in the absence of titanium particles. Significant overexpression of the cytokine RANKL was observed, with a trend for over-expression of IL-33 and TGF-B1 in areas with titanium. Further studies with large sample size and appropriate control group for quantification analysis is needed to confirm the role of titanium particles in initiating bone loss.

It is becoming increasingly apparent that the tumour microenvironment plays an important role in the progression of cancer. The microenvironment may promote tumour cell survival and proliferation or, alternatively may induce tumour cell apoptosis. Toll-like receptors are transmembrane proteins, expressed on immune cells and epithelial cells, that recognise exogenous and endogenous macromolecules. Once activated they initiate signalling pathways leading to the release of cytokines and chemokines which recruit immune cells inducing further cytokine production, the production of angiogenic mediators and growth factors, all of which may influence tumour progression. This paper examines the actions of toll-like receptors in carcinogenesis with particular emphasis on their role in oral squamous cell carcinoma

Background: Results: Conclusion: