Volumetric Analysis of Peri-implant Tissue Change Over Time: Validating an Innovative 3D Method.

PURPOSE: To validate an innovative 3D volumetric method of evaluating tissue changes proposed by Lee et al in 2020 by comparing the results of this method-in which the scanned peri-implant surfaces were transformed, visualized, and analyzed as 3D objects-to the results reported by an existing method based on calculation of the mean distance between measured surfaces. The null hypothesis was that there was no statistically significant difference between the two methods. Additionally, the present study evaluated peri-implant tissue changes 5 years after single implant placement in the esthetic zone. MATERIALS AND METHODS: Both methods were applied to 11 oral implant site casts (6 maxillary central incisor sites, 5 maxillary lateral incisor sites) taken from 11 patients at crown placement and at follow-up examinations 5 years later. The methods are based on digital workflows in which the reference and 5-year casts are scanned and the resulting STL files are superimposed and analyzed for three regions of interest (mesial papilla, central area, and distal papilla). The volumetric changes reported by the Lee et al method and the mean distance method were calculated and compared using the Spearman rank correlation coefficient (P < .01) and the Wilcoxon signed-rank test (P < .05). RESULTS: The correlation between the two sets of measurements was very high (Spearman rank correlation coefficient = 0.885). The new volumetric method indicated a mean volume loss of 2.82 mm3 (SD: 5.06), while the method based on the measurement of mean distance showed a mean volume loss of 2.92 mm3 (SD: 4.43; Wilcoxon signed-rank test result: P = .77). No statistically significant difference was found. The two methods gave equivalent results, and the null hypothesis was accepted. CONCLUSIONS: The new volumetric method was validated and can be considered a trustworthy tool.

Evaluation of tissue engineered models of the oral mucosa to investigate oral candidiasis.

Candida albicans is a commensal organism that can be isolated from the majority of healthy individuals. However, in certain susceptible individuals C. albicans can become pathogenic leading to the mucocutaneous infection; oral candidiasis. Murine models and in vitro monolayer cultures have generated some data on the likely virulence and host factors that contribute to oral candidiasis but these models have limitations. Recently, tissue engineered oral mucosal models have been developed to mimic the normal oral mucosa but little information is available on their true representation. In this study, we assessed the histological features of three different tissue engineered oral mucosal models compared to the normal oral mucosa and analysed both cell damage and cytokine release following infection with C. albicans. Models comprised of normal oral keratinocytes and a fibroblast-containing matrix displayed more similar immunohistological and proliferation characteristics to normal mucosa, compared to models composed of an oral carcinoma cell line. Although all models were invaded and damaged by C. albicans in a similar manner, the cytokine response was much more pronounced in models containing normal keratinocytes. These data suggest that models based on normal keratinocytes atop a fibroblast-containing connective tissue will significantly aid in dissecting the molecular pathogenesis of oral candidiasis.

Pseudohyphal regulation by the transcription factor Rfg1p in Candida albicans.

The opportunistic human fungal pathogen Candida albicans is a major cause of nosocomial infections. One of the fundamental features of C. albicans pathogenesis is the yeast-to-hypha transition. Hypha formation is controlled positively by transcription factors such as Efg1p and Cph1p, which are required for hyphal growth, and negatively by Tup1p, Rfg1p, and Nrg1p. Previous work by our group has shown that modulating NRG1 gene expression, hence altering morphology, is intimately linked to the capacity of C. albicans to cause disease. To further dissect these virulence mechanisms, we employed the same strategy to analyze the role of Rfg1p in filamentation and virulence. Studies using a tet-RFG1 strain revealed that RFG1 overexpression does not inhibit hypha formation in vitro or in the mouse model of hematogenously disseminated candidiasis. Interestingly, RFG1 overexpression drives formation of pseudohyphae under yeast growth conditions-a phenotype similar to that of C. albicans strains with mutations in one of several mitotic regulatory genes. Complementation assays and real-time PCR analysis indicate that, although the morphology of the tet-RFG1 strain resembles that of the mitotic regulator mutants, Rfg1p overexpression does not impact expression of these genes.