Aim: To compare the effectiveness of self-examination, clinical examination and screening methods using 1% toluidine blue and Lugol's iodine in estimating the prevalence of lesions at risk of malignancy and oral malignant disease amongst the male inmates of Yerwada Central Jail, Pune. Material and Methods: Study was carried out on male inmates in two phases. In the first phase self-examination and clinical examination was carried out on 2,257 male inmates. 164 suspicious cases were subjected to phase II of the study out of whom, 82 participants were screened with 1% toluidine blue and 2% Lugol's iodine followed by biopsy procedure. Results: Sensitivity and specificity for self-examination with clinical examination was 92.2% and 96.6% respectively. Sensitivity, specificity, positive (PPV) and negative predictive values (NPV) and positive (+LR) and negative likelihood ratio (-LR) for Toluidine Blue were 88.1%, 66.6% 97.1%, 30%, 2.63 and 0.17 respectively while for Lugol's Iodine they were 94.7%, 83.8%, 98.6%, 55.5%, 5.67 and 0.06 respectively. Conclusions: Prevalence of lesions at risk of malignancy and oral malignant disease by self-examination was 7.8% and by clinical examination was 6.3%. Self-examination is an effective tool in early detection of oral cancer. Use of Lugol's iodine as a screening tool for oral lesions is highly effective in inmate populations.

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The innate immune response is the body's first line of defense against pathogens. The innate immune system recognizes pathogens, including bacteria and viruses by engagement of the germline-encoded pattern recognition receptors (PRRs). There are five families of PRRs which are able to sense vast families of microbial components, referred to as pathogen-associated molecular patterns and damage-associated molecular patterns (DAMPs), they are host cell components produced during inflammation or environmentally derived. Although PRRs are predominately expressed by innate immune cells, many of the PRRs are also found on other cells including epithelial, endothelial, and cells of the adaptive immune system. PRR engagement by its ligand induces downstream signaling cascades that induce multiple effects, including activation of innate immune cells and cytokine/chemokine production for the recruitment of immune cells to the site of infection or tissue damage. There are multiple inflammasomes that are formed, which are named for their sensor PRR that induces its activation. It is still not clear how many sensors are capable of forming inflammasomes, with strong literature support for over 10 different inflammasomes, including NLRP1, NLRP3, NLRP6, NLRP12, pyrin, NAIP/NLRC4, RIG-I AIM2, IFI16, NLRC3, and NLP6 5,7 which are recently reviewed. The study of periodontal disease thus represents an excellent model to study the role of inflammasomes due to the abundance of Microbe Associated Molecular Patterns (MAMP) and DAMPs and the elevated proportion of macrophages in the tissue microenvironment.