Background and Aim:Periapical lesions often present differently on the radiograph resulting in a dilemma in the mind of the dentist to arrive at a final diagnosis. Although, histopathologic diagnosis has been used for confirmation of the true nature of periapical lesion, the concept of transformation of periapical granulomas containing epithelium without cystification into cyst remains controversial. The aim of this in vivo study was to evaluate the efficacy of conventional radiography and histopathology in differentiating periapical lesions in adjunct with immunohistochemical analysis.Aim:Periapical lesions often present differently on the radiograph resulting in a dilemma in the mind of the dentist to arrive at a final diagnosis. Although, histopathologic diagnosis has been used for confirmation of the true nature of periapical lesion, the concept of transformation of periapical granulomas containing epithelium without cystification into cyst remains controversial. The aim of this in vivo study was to evaluate the efficacy of conventional radiography and histopathology in differentiating periapical lesions in adjunct with immunohistochemical analysis.Materials and Method:Thirty patients having large periapical radiolucency that do not heal successfully with routine endodontic therapy in relation to either maxillary or mandibular anterior teeth were selected for the study. Intraoral periapical radiographs were obtained and provisional diagnosis of the apical areas were made. Endodontic surgery was performed to enable histopathogical investigation. The histopathological interpretation was done to arrive at a final diagnosis and selected questionable granulomas were subjected for cytokeratin (CK-14) stain.Results:The histopathological profile of lesions consisted of 66.66% periapical granulomas, 10% cysts, 6.67% abscess and 16.67% granulomas with cystic potential. The radiographic and histopathologic correlation was found in only 30% of these cases. Strong CK-14 expression was observed in all five cases of periapical granuloma with cystic potential.Conclusion:The radiographic diagnosis of periapical lesions remains inconclusive. Although histopathologic examination of periapical lesions gives true nature, the precise nature of subsets of periapical granulomas may be achieved with adjunct use of immunohistochemical markers.

Objective:Apart from its well-known deleterious dental and skeletal effects, fluoride excess can have toxic effects on many other tissues. Fluoride, when in excess, is known to interfere with thyroid gland function. Fluoride-induced thyroid disturbances similar to those observed in iodine deficiency state in spite of adequate iodine intake have been documented. Similar thyroid disturbances in individuals with dental fluorosis have not been well studied in populations with endemic fluorosis. This work was undertaken to study the effects of fluoride-induced thyroid disturbances in individuals with dental fluorosis.Methods:The study group included 65 subjects with dental fluorosis from endemic fluorosis populations. An additional control group was comprised of 10 subjects without dental fluorosis. The drinking water fluoride levels of the study populations were analyzed. Serum free FT3, FT4, and TSH levels of both groups were assessed.Results:All subjects with dental fluorosis had serum levels of thyroid hormones (FT3, FT4, and TSH) within the normal range, with the exception of 1 individual, who had elevated levels of TSH. Statistical significance was found when FT3 and TSH values were compared with different Dean’s index groups by a 1-way ANOVA test: FT3 (F = 3.4572; P=.0377) and TSH (F = 3.2649 and P=.0449).Conclusions:Findings of this study did not show any significant alterations in the levels of the thyroid hormones FT3, FT4, and TSH in subjects with dental fluorosis. Our observations suggest that thyroid hormone levels were not altered in subjects with dental fluorosis. Hence, future studies of this kind, along with more detailed investigations are needed.

Epidermoid cysts (ECs) are uncommon, benign cystic lesions derived from the entrapment of surface epithelium or more often from the aberrant healing of infundibular epithelium during an episode of follicular inflammation. ECs occur anywhere on the body, particularly along embryonic fusion lines, most commonly on the face, scalp, neck, chest and upper back. Head and neck ECs constitute only about 7%, whereas only 1.6% of ECs are reported in the oral cavity. They comprise <0.01% of all the oral cysts. Floor of the mouth, tongue, lips, palate, jaws, etc., are some of the reported sites of ECs in the oral cavity. Microscopically, ECs are lined with plain stratified squamous epithelium filled with laminated layers of keratin. Here, we report two rare cases of ECs, one occurring in the gingival aspect and other in the lower third of face. The cases are reported due to rarity of ECs in the head and neck region.

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Context:Diabetes mellitus can have profound effects upon the oral tissues especially in patients with poor glycemic control being prone to severe and/or recurrent infections particularly candidiasis. The main aim was to study the association between Type 1 and Type 2 diabetes mellitus and candidal carriage.Materials and Methods:The study design comprised of previously diagnosed 30 patients each with type 1 diabetes mellitus (Group A) and type 2 diabetes mellitus (Group B) and 30 age-, sex- and dental status-matched healthy non-diabetic individuals as controls (Group C). The saliva samples were collected and inoculated onto Sabouraud dextrose agar (SDA) and chromogenic agar culture medium. Candidal colony forming units per ml (CFU/ml) values were determined.Statistical Analysis:Data were analyzed by χ2 test, Mann-Whitney U-test, Spearman's rank correlation and Karl Pearson's correlation coefficient.Results:Data analysis showed statistically significant higher positive candidal growth in Group A and Group B when compared to Group C. The CFU/ml values were significantly higher in Groups A and B as compared with Group C. Significant positive correlation of CFU/ml with fasting blood sugar level and HbA1c% in both Groups A and B was seen. Oral signs and symptoms observed in diabetics were dry mouth, burning sensation, fissuring and atrophic changes of tongue and erythematous areas, which positively correlated with candidal load.Conclusion:The glycemic control status of the diabetic patients may directly influence candidal colonization. The quantitative and biochemical characterization allows better insight into the study of association of diabetes mellitus and candida.

Background:The central giant cell granuloma(CGCG) of bone constitutes about 10% of benign jawbone lesions. It affects females more often than males, mandible than maxilla. Biological behavior of CGCG ranges from a slow growing asymptomatic swelling to an aggressive process. True giant cell tumor (GCT) should be distinguished from CGCG. The histological distinction between these lesions depends on quite subtle differences. Expression of p63 has been demonstrated in GCT of bone conversely, has not been detected in CGCG. Therefore this short study attempts to study the expression of p63 in CGCG in conjunction with clinicopathological profile of the cases reported in the institute.Aims and objectives: To review all the cases of CGCGs of the jaws reported in the institute from 1998 to 2015 and study their clinicopathological profile.To study the immunohistochemical (IHC) expression of p63 in CGCG cases Methods and materials:The retrospective study reviewed records for clinically and histopathologically diagnosed cases of CGCG from the archives of department of Oral pathology. Data was recorded and analyzed. These cases were subjected for IHC analysis for expression of p63, also RANK, RANKL in selected cases to study the nature of giant cells.Results and Conclusion:This paper is an institutional experience of clinicopathological profile of diagnosed cases of CGCG. Clinicopathological findings were in concurrent with previous literature. Total number of cases was ten. Six occurred in females and four in males. Most of them occurred in the second decade, more commonly involving mandible. Three cases showed recurrence. Histologically most showed classical features. Expression of p63 showed negativity in all the cases in accordance with the previous studies. RANK and RANKL showed strong and diffuse immunoexpression in both mononuclear and giant cells. Thus study supports the finding that p63 expression can be used to differentiate between CGCG and GCT. However, more number of studies with larger sample size are required to confirm reliability of using p63 as a distinguishing marker between GCT and CGCG.

Aims: Arecoline, a predominant alkaloid present in arecanut, has been implicated in the pathogenesis of several oral diseases because of its mutagenic and carcinogenic potential. The response of cultured cells to arecoline is highly dependent on its concentration; arecoline stimulates cultured cells above 0.1 μg/ml and is cytotoxic above 10 μg/ ml. Although this alkaloid seems important for areca nut induced oral diseases and carcinogenesis, little is known of the levels achieved before, during and after chewing. Also, it is prudent to understand its effects in arecanut chewers for a comprehensive understanding of its pathogenesis. Accordingly, the present study quantified the salivary arecoline levels in arecanut chewers. Materials and Methods: The study participants were divided into Study Group A & B and Control Group C; unstimulated whole saliva was collected by spitting method for a period of 5 min. Then, participants in Group A and C chewed 0.5 g of areca nut without any other additives while in Group B were asked to chew 0.5 g of inert rubber base impression material. Stimulated whole saliva from all three groups was collected into graduated tubes during chewing at time intervals of 1, 3, 5, 10, 15, 20 and 25 min. Then, all participants were asked to remove nut particles or inert rubber base material from the mouth, and saliva samples were collected further up to 20 min, changing tubes at 5 min interval. Salivary arecoline was quantitated by HPLC-MS. The tabulation and descriptive statistics of the study were carried out. Results: In the present study, baseline levels of arecoline were zero in all three groups, whereas mean salivary arecoline levels during chewing were 76.93 ng/ml, 129.83 ng/ml and 64.83 ng/ml and after chewing were 196.17 ng/ml, 321.12 ng/ml and 43.75 ng/ml in Groups A, B and Control respectively, which were significantly higher than reported threshold levels. Conclusions: The data from this study reveals that a significant amount of arecoline would be trapped in oral cavity, or being re-circulated between blood and saliva might have resulted in surprisingly high levels of arecoline even 10 mins after chewing in both groups after which the levels started declining. The higher levels of salivary arecoline achieved during and after chewing are enough to cause cytotoxic and genotoxic effects on oral tissues over a period of time in chronic chewers. The great differences in salivary arecoline levels achieved during chewing, may contribute to the variable response to areca nut seen in communities where this habit is widespread. Areca nut users have persistent background salivary arecoline levels long after chewing, whereas concentrations achieved are highly variable and consistent with a role in oral pre-malignancy and malignancy..

Our observations in this study affirm that oral submucous fibrosis favors the colonization of Candida. Mucosal alterations due to the underlying disease process or betel quid chewing, coupled with other factors, might lead to candidal colonization, even in the absence of clinically-related mycotic manifestations.