Role of Dental Profession in Oral Cancer Prevention and Diagnosis.

The incidence of oral cancer is increasing worldwide. Malignant neoplasms of the mouth and pharynx have been rated as the 10th most common cancer in men and 7th in women, though geographical variations exist.1Generally, in a society, oral cancer is not properly understood. The sign and symptoms are frequently overlooked in the initial stages when it is responsive to treat.

Assessing the Risk of Oral Cancer associated with Gutka and Other Smokeless Tobacco Products: A Case-control Study.

INTRODUCTION: Tobacco and tobacco-related products have been attributed to be causative factors for oral cancer. Newer, chewable, and commercially available smokeless tobacco (ST) products, such as gutka pose further threat in this direction. The aim of the study was to evaluate the risk of oral cancer associated with gutka and other ST products. MATERIALS AND METHODS: A case-control study of 134 cases and 134 controls, over a period of 6 months (July-December 2014), was carried out at the Baqai University, Karachi, Pakistan. An interview-based questionnaire was used to collect data on sociodemographic characteristics, oral hygiene practices and type, duration, and frequency of use of tobacco-related products. Data were analyzed using the Pearson's chi-square (χ2) test with the level of significance set as p < 0.05. RESULTS: Gutka showed the highest odds ratio toward developing oral cancer ratio among all the tobacco-related products [odds ratio (OR) 5.54; 95% CI 2.83-10.83; p < 0.001)]. Participants who consumed other ST products also showed 2 to 4 times higher odds ratio of developing oral cancer than compared to those who did not consume these products. CONCLUSION: The study provided strong evidence that gutka and other ST products are independent risk factors for oral cancer. CLINICAL SIGNIFICANCE: This study highlights the strong association of different types of ST and oral cancer. This results in identification of high-risk groups for targeted screening for potential oral cancer lesions.

Detection of adrenomedullin and nitric oxide in different forms of periodontal disease.

BACKGROUND AND OBJECTIVE: The multifunctional molecules adrenomedullin (AM) and nitric oxide (NO) are both involved in the host response to microbial challenge during periodontal disease. Whether they coexist in periodontal inflammation and if equally produced in the different forms of periodontal disease has not previously been investigated. The aims of this study were to describe the locations of AM and NO in healthy and inflamed gingival tissues and to determine and compare their levels in the gingival crevicular fluid and saliva of patients with gingivitis, chronic periodontitis and aggressive periodontitis. MATERIAL AND METHODS: AM and inducible nitric oxide synthase (iNOS) were immunolocalized in clinically healthy and inflamed gingival tissue sections. The cells expressing AM and iNOS were characterized using immunocytochemistry with different markers for macrophages [cluster differentiation (CD)68 and CD14)], dendritic cells (CD83), neutrophils [neutrophil gelatinase-associated lipocalin (nGAL)] and natural killer cells (CD56). In an initial study, the levels of AM and NO were also measured in samples of gingival crevicular fluid and saliva obtained from patients with a diagnosis of gingivitis (n = 9), chronic periodontitis (n = 9) and aggressive periodontitis (n = 9) using an ELISA and the nitrate/nitrite (NO metabolites) Griess assay, respectively. RESULTS: Low levels of AM- and iNOS-expressing cells were detected in healthy gingival tissues in comparison with three-fold higher levels of these cells in inflamed tissues. These cells were localized mainly in the epithelial layer but were also present in deeper connective tissue. AM and iNOS were co-localized in particular cells within inflamed tissues, namely CD68(+) (52%) and CD14(+) (36%) macrophages, but also in nGAL(+) neutrophils (16%) and CD83(+) dendritic cells (14%). Interestingly, AM and NO levels in saliva were both found to be higher (p < 0.01) in patients with aggressive periodontitis than in patients with chronic periodontitis or gingivitis. In contrast, in gingival crevicular fluid, the levels of NO showed marked differences among patients with chronic periodontitis, aggressive periodontitis and gingivitis (p < 0.01), and the levels of AM were higher (p < 0.01) in both chronic and aggressive periodontitis compared with gingivitis alone. CONCLUSION: The data presented demonstrate a functional linkage between AM and NO in periodontal disease, with salivary and gingival crevicular fluid levels possibly associated with different forms and severities of periodontal disease. Exacerbated production of both AM and NO in saliva suggests their potential use as salivary markers of aggressive periodontitis.

Regulation of adrenomedullin and nitric oxide production by periodontal bacteria.

OBJECTIVES: In periodontitis the host response to bacterial challenge includes activity of the multifunctional molecules adrenomedullin (AM) and nitric oxide (NO). The aim of this study was to investigate the role of periodontal bacteria in regulating the production of these molecules from cultured cells. MATERIAL AND METHODS: Regulation of AM and NO production from oral keratinocytes when challenged with culture supernatants from Aggregatibacter actinomycetemcomitans, Campylobacter rectus, Fusobacterium nucleatum, Porphyromonas gingivalis, Prevotella intermedia, Veillonella atypica, Streptococcus salivarius and Candida albicans was examined. AM and NO were measured in cell culture supernatants using an enzyme-linked immunosorbent assay and the nitrate/nitrite (NO metabolites) Griess assay respectively. Cellular production of AM and inducible NO synthase was also analysed in target cells by immunofluorescence and Western blot analysis. The inter-relationship of AM and NO production were further investigated with macrophages. RESULTS: A. actinomycetemcomitans and C. rectus induced maximal levels of both AM and NO after 6 and 48 h respectively from oral keratinocytes. AM production in macrophages was upregulated in response to the NO donor S-nitrosoglutathione and partially blocked by the inducible NO synthase inhibitor, N(ω) -Nitro-l-arginine methyl ester hydrochloride. Likewise, NO production was increased upon exposure to AM, while the AM receptor antagonist AM 22-52 reduced the release of NO. CONCLUSIONS: Pathogens associated with aggressive periodontitis, A. actinomycetemcomitans and C. rectus, were more effective than those associated with chronic periodontitis, P. gingivalis and Prev. intermedia, and commensals, S. salivarius and V. atypica, as regards the upregulation of AM and NO production from oral keratinocytes. Interaction between these molecules was also demonstrated with macrophages. Understanding the coordinated regulation of AM and NO production in response to periodontal bacteria may identify ways to promote their protective effects and minimize destructive potential.