Background and Objectives:Oral cancer constitutes 3% of all neoplasms and is the eighth most frequent cancer in the world. Oral squamous cell carcinoma (OSCC) corresponds to 95% of all oral cancers. It is associated with severe morbidity, recurrence and reduced survival rates. Its prognosis is affected by several clinicopathologic factors, one of which is perineural invasion (PNI). It is the third most common form of tumor spread exhibited by neurotropic malignancies that correlate with aggressive behavior, disease recurrence and increased morbidity and mortality. In this retrospective study, our aim was to assess the presence of PNI in different grades of both primary and recurrent cases of OSCC correlating it with tumor size and lymph node status. The various patterns of PNI we encountered were also noted.Materials and Methods:PNI was assessed in 117 cases of primary and recurrent cases of OSCC. PNI was correlated with tumor thickness, lymph node status and with the different histologic grades. Location of PNI, density of PNI and various patterns of PNI were also assessed.Statistical Analysis:Chi-square test.Results:Our study showed that 47 out of 117 patients (40.5%) showed PNI. Both primary and recurrent tumors showed PNI of 42.50% and 40.50%, respectively. PNI was present in 34 out of 69 cases (49.3%) of clinically positive nodes. Around 79% of the nerves involved by PNI were intratumoral in location, 80% of the cases showed PNI density of 1–3 nerves per section and incomplete and/or “crescent-like” encirclement was the most common pattern of PNI noted in our study.Conclusion:Our study showed that the incidence of PNI was as high as 40% in OSCC. PNI was present in both primary and recurrent tumors, irrespective of its histologic grading. Tumor thickness and lymph node status correlated well with PNI. Therefore, the presence of PNI should be checked in every surgical specimen with OSCC as it gives significant prognostic value, influences treatment decisions, recurrence and distant metastasis. The presence of PNI necessitates more aggressive resection, coincident management of neck lymph nodes and the addition of adjuvant therapy. Also, targeted drug therapy for this type of tumor spread can open up new avenues in the treatment of OSCC.

Introduction:Periodontal diseases, if left untreated, can lead to tooth loss and affect at least one tooth in 80% of adults worldwide, with the main cause being a bacterial plaque. Among subgingival plaque bacterial species, Porphyromonas gingivalis has been implicated as a major etiological agent causing tooth loss. Diabetics and smokers are two patient groups at high risk for periodontal disease. The increase in the number of this organism with the coexistence of other pathogenic microbes leads to rapid destruction of the periodontium, premature loss of teeth and also because of its virulence has implications in systemic pathology. Our aim was to observe the involvement of P. gingivalis in diabetes mellitus (DM) patients associated with periodontitis with and without tobacco-associated habits and to compare them with periodontitis patients having no other systemic pathologies.Materials and Methods:Subgingival plaque samples from a total of seventy subjects were included in the study. DNA was isolated from the collected sample and was quantified using spectrophotometer for standardizing the polymerase chain reaction. The quantity of the isolated DNA was checked in a ultraviolet-visible spectrophotomer.Statistics:One-way ANOVA and Tukey's multiple post hoc procedures were carried out.Results:The maximum score of P. gingivalis was seen in periodontitis patients having DM, whereas the least score was seen in periodontitis patients having DM with tobacco smoking habit compared to the other groups.Conclusion:P. gingivalis count is significantly reduced in periodontitis patients having DM with smoking habit; it is concluded that P. gingivalis might not be a key causative organism responsible for the periodontal destruction in case of smokers despite the DM condition. The decrease in counts may be attributed to change in the local environment like chemical (tobacco nitrosamines) and physical changes preventing the growth of P. gingivalis.