Objective:To evaluate and compare the antimicrobial efficacy of 6% Morinda citrifolia, Azadirachta indica, and 3% sodium hypochlorite (NaOCl) as root canal irrigants.Materials and Methods:Thirty nonvital maxillary anteriors were randomly assigned to one of the three groups corresponding to the irrigant to be tested; 6% Morinda citrifolia juice (MCJ) (n = 10), A. indica (n = 10) and 3% NaOCl (n = 10). After the root canal access opening a root canal culture sample was taken with two paper points and cultured under aerobic and anaerobic conditions. Cleaning and shaping were completed with irrigation by 10 mL of respective irrigants and 5 mL of final rinse. The patients were recalled after 3 days and canals were rinsed again with 5 mL of the test irrigants. This was followed by obtaining a posttreatment root canal culture sample and culturing and analyzed by counting the colony forming units (CFUs).Results:Six percentage MCJ, A. indica, and 3% NaOCl showed a significant reduction (P < 0.05) in the mean CFU counts for aerobic and anaerobic bacteria between baseline and 3 days.Conclusion:There was no difference in the antimicrobial efficacy of 6% M. citrifolia, A. indica, and 3% NaOCl as root canal irrigants.
The incidence of oral cancer remains high in both Asian and Western countries. Several risk factors associated with development of oral cancer are now well-known, including tobacco chewing, smoking, and alcohol consumption. Cancerous risk factors may cause many genetic events through chromosomal alteration or mutations in genetic material and lead to progression and development of oral cancer through histological progress, carcinogenesis. Oral squamous carcinogenesis is a multistep process in which multiple genetic events occur that alter the normal functions of proto-oncogenes/oncogenes and tumor suppressor genes. Furthermore, these gene alterations can deregulate the normal activity such as increase in the production of growth factors (transforming growth factor-α [TGF-α], TGF-β, platelet-derived growth factor, etc.) or numbers of cell surface receptors (epidermal growth factor receptor, G-protein-coupled receptor, etc.), enhanced intracellular messenger signaling and mutated production of transcription factors (ras gene family, c-myc gene) which results disturb to tightly regulated signaling pathways of normal cell. Several oncogenes and tumor suppressor genes have been implicated in oral cancer especially cyclin family, ras, PRAD-1, cyclin-dependent kinase inhibitors, p53 and RB1. Viral infections, particularly with oncogenic human papilloma virus subtype (16 and 18) and Epstein-Barr virus have tumorigenic effect on oral epithelia. Worldwide, this is an urgent need to initiate oral cancer research programs at molecular and genetic level which investigates the causes of genetic and molecular defect, responsible for malignancy. This approach may lead to development of target dependent tumor-specific drugs and appropriate gene therapy.
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