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

Aim: To investigate load‐deformation properties of Thiel‐embalmed human oral mucosa tissues and to compare three different anatomical regions in terms of mechanical, histological and ultrastructural characteristic with focus on the extracellular matrix.Materials and Methods: Thirty specimens from three different regions of the oral cavity: attached gingiva, buccal mucosa and the hard palate were harvested from two Thiel‐embalmed cadavers. Mechanical properties were obtained, combining strain evaluation and digital image correlation in a standardised approach. Elastic modulus, tensile strength, strain at maximum load and strain to failure were computed and analysed statistically. Subsamples were also analysed using scanning electron microscopy (SEM) and histological analysis.Results: The highest elastic modulus of 37.36 ± 17.4 MPa was found in the attached gingiva group, followed by the hard palate and buccal mucosa. The elastic moduli of attached gingiva differed significantly to the buccal mucosa (p = .01) and hard palate (p = .021). However, there was no difference in the elastic moduli between the buccal mucosa and hard palate (p > .22). The tensile strength of the tissue samples ranged from 1.54 ± 0.5MPa to 3.81 ± 0.9 MPa, with a significant difference between gingiva group and buccal mucosa or hard palate (p = .001). No difference was found in the mean tensile strength between the buccal mucosa and hard palate (p = .92). Ultrastructural imaging yielded a morphological basis for the various mechanical properties found intraorally; the attached gingiva showed unidirectional collagen fibre network whereas the buccal mucosa and hard palate showed multi‐directional network, which was more prone to tension failure and less elasticity.Conclusion: This is the first study assessing the various morphological‐mechanical relationships of intraoral soft tissues, utilising Thiel‐embalmed tissues. The findings of this study suggest that the tissues from different intraoral regions showed various morphological‐mechanical behaviour which was also confirmed under the SEM and in the histological analysis.

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

Caries results in the demineralization and destruction of enamel and dentine, and as the disease progresses, irreversible pulpitis can occur. Vital pulp therapy (VPT) is directed towards pulp preservation and the prevention of the progression of inflammation. The outcomes of VPT are not always predictable, and there is often a poor correlation between clinical signs and symptoms, and the events occurring at a molecular level. The inflamed pulp expresses increased levels of cytokines, including tumour necrosis factor (TNF)‐α, interleukin (IL)‐1α, IL‐1β, IL‐4, IL‐6, IL‐8, IL‐17 and IL‐23, which recruit and drive a complex cellular immune response. Chronic inflammation and sustained cytokine release can result in irreversible pulp damage and a decreased capacity for tissue healing. Other chronic inflammatory diseases, such as psoriasis, inflammatory bowel diseases and rheumatoid arthritis, are also characterized by an dysregulated immune response composed of relatively high cytokine levels and increased numbers of immune cells along with microbial and hard–soft tissue destructive pathologies. Whilst anti‐cytokine therapies have been successfully applied in the treatment of these diseases, this approach is yet to be attempted in cases of pulp inflammation. This review therefore focuses on the similarities in the aetiology between chronic inflammatory diseases and pulpitis, and explores how anti‐cytokine therapies could be applied to manage an inflamed pulp and facilitate healing. Further proof‐of‐concept studies and clinical trials are justified to determine the effectiveness of these treatments to enable more predictable outcomes in VPT.