Diagnostic Mock-Up as a Surgical Reduction Guide for Crown Lengthening: Technique Description and Case Report.

Background and Objectives: The report describes a technique using a diagnostic mock-up as a crown-lengthening surgical guide to improve the gingival architecture. Materials and Methods: The patient's primary concern was improving her smile due to her "gummy smile" and short clinical crowns. After clinical evaluation, surgical crown lengthening accompanied by maxillary central full-coverage single-unit prostheses and lateral incisor veneers was recommended. The diagnostic mock-up was placed in the patient's maxillary anterior region and used as a soft tissue reduction guide for the gingivectomy. Once the planned gingival architecture was achieved, a flap was reflected to proceed with ostectomy in order to obtain an appropriate alveolar bone crest level using the overlay. After six months, all-ceramic crowns and porcelain veneers were provided as permanent restorations. Results: A diagnostic mock-up fabricated with a putty guide directly from the diagnostic wax-up can be an adequate surgical guide for crown-lengthening procedures. The diagnostic wax-up was used to fabricate the diagnostic mock-up. These results suggested that it can be used as a crown-lengthening surgical guide to modify the gingival architecture. Several advantages of the overlay used in the aesthetic complex case include: (1) providing a preview of potential restorative outcomes, (2) allowing for the appropriate positioning of gingival margins and the desired alveolar bone crest level for the crown-lengthening procedure, and (3) serving as a provisional restoration after surgery. Conclusions: The use of a diagnostic mock-up, which was based on a diagnostic wax-up, as the surgical guide resulted in successful crown lengthening and provisional restorations. Thus, a diagnostic overlay can be a viable option as a surgical guide for crown lengthening.

Becoming a 'pharmaceutical person': Medication use trajectories from age 26 to 38 in a representative birth cohort from Dunedin, New Zealand.

Despite the abundance of medications available for human consumption, and frequent concerns about increasing medicalization or pharmaceuticalization of everyday life, there is little research investigating medicines-use in young and middle-aged populations and discussing the implications of young people using increasing numbers of medicines and becoming pharmaceutical users over time. We use data from a New Zealand longitudinal study to examine changes in self-reported medication use by a complete birth cohort of young adults. Details of medications taken during the previous two weeks at age 38 are compared to similar data collected at ages 32 and 26, and by gender. Major drug categories are examined. General use profiles and medicine-types are considered in light of our interest in understanding the formation of the young and middle-aging 'pharmaceutical person' - where one's embodied experience is frequently and normally mediated by pharmaceutical interventions having documented benefit/risk outcomes.

The nexus between periodontics and oral pathology.

A wide variety of lesions may arise from the oral mucosa, fibrous connective tissue, bone and cementum of the periodontium. The commonest pathology occurs as a result of bacterial infection and is very well known to dentists and periodontists, but rarer conditions present as gingival pathology. The pathogenesis of these conditions ranges from genetic to traumatic to immunological to neoplastic, and includes benign, malignant and metastatic lesions. This paper outlines some of these conditions and describes how the periodontist and oral pathologist can work together using a framework, and how with careful consideration of the clinical features and the use of appropriate special tests, including obtaining an adequate tissue specimen, a timely and accurate diagnosis can be obtained.

Multiple cells express interleukin 17 in oral squamous cell carcinoma.

BACKGROUND: Interleukin (IL)-17 is a pro-inflammatory cytokine with pro- and antitumour effects. The aim of this study was to investigate the presence and potential sources of IL-17 in oral squamous cell carcinoma (OSCC). METHODS: Immunohistochemistry was used to label and compare IL-17+ cells in the tissue sections of OSCC and inflammatory controls (IC), n = 14 for both. In OSCC, the comparison was made between the number of IL-17+ cells in the tumoral islands (TI), tumour-stroma interface (TS) and more distant stroma (DS). Cells expressing IL-17 were identified using double-labelling immunofluorescence and examined using laser scanning microscopy. The production of IL-17 from tumour cells was determined in the culture supernatants of OSCC cell lines, SCC4, SCC15 and SCC25, using sandwich ELISA. RESULTS: Significantly more IL-17+ cells were observed in OSCC compared with IC (Mann-Whitney, P < 0.0001). In OSCC, the numbers of IL-17+ cells were not significantly different in three compartments, TI, TS and DS (one-way ANOVA, P > 0.05). However, the TI had significantly fewer IL-17+ cells than the combined stroma (both TS and DS together, Mann-Whitney, P < 0.01). Laser scanning microscopy revealed helper T cells, cytotoxic T cells, macrophages and mast cells co-expressed IL-17. ELISA experiments did not detect IL-17 in the supernatants of OSCC cell lines. CONCLUSIONS: Although the tumour cells themselves did not express IL-17, a range of cell types did, suggesting multiple cellular sources for IL-17 in OSCC. The spatial distribution of IL-17+ cells suggests specific interactions with cells within the tumour microenvironment, implying that IL-17+ cells are likely to play a role in the pathogenesis of OSCC.

Downregulation of toll-like receptor-mediated signalling pathways in oral lichen planus.

OBJECTIVE: The objective of this study was to investigate the expression of Toll-like receptors (TLR) and TLR-associated signalling pathway genes in oral lichen planus (OLP). METHODS: Initially, immunohistochemistry was used to determine TLR expression in 12 formalin-fixed archival OLP tissues with 12 non-specifically inflamed oral tissues as controls. RNA was isolated from further fresh samples of OLP and non-specifically inflamed oral tissue controls (n = 6 for both groups) and used in qRT(2)-PCR focused arrays to determine the expression of TLRs and associated signalling pathway genes. Genes with a statistical significance of ±two-fold regulation (FR) and a P-value < 0.05 were considered as significantly regulated. RESULTS: Significantly more TLR4(+) cells were present in the inflammatory infiltrate in OLP compared with the control tissues (P < 0.05). There was no statistically significant difference in the numbers of TLR2(+) and TLR8(+) cells between the groups. TLR3 was significantly downregulated in OLP (P < 0.01). TLR8 was upregulated in OLP, but the difference between the groups was not statistically significant. The TLR-mediated signalling-associated protein genes MyD88 and TIRAP were significantly downregulated (P < 0.01 and P < 0.05), as were IRAK1 (P < 0.05), MAPK8 (P < 0.01), MAP3K1 (P < 0.05), MAP4K4 (P < 0.05), REL (P < 0.01) and RELA (P < 0.01). Stress proteins HMGB1 and the heat shock protein D1 were significantly downregulated in OLP (P < 0.01). CONCLUSION: These findings suggest a downregulation of TLR-mediated signalling pathways in OLP lesions.

Toll-like receptors and cancer, particularly oral squamous cell carcinoma.

It is becoming increasingly apparent that the tumor microenvironment plays an important role in the progression of cancer. The microenvironment may promote tumor cell survival and proliferation or, alternatively may induce tumor cell apoptosis. Toll-like receptors (TLRs) are transmembrane proteins, expressed on immune cells and epithelial cells, that recognize exogenous and endogenous macromolecules. Once activated, they initiate signaling 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 tumor progression. This paper examines the actions of TLRs in carcinogenesis with particular emphasis on their role in oral squamous cell carcinoma.