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.
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.
Background: Oral submucous fibrosis (OSMF) is a chronic, potentially malignant condition of the oral mucosa, predominantly seen in people of Asian descent. The reported malignant transformation rate of OSMF is 7%–13%. In the context of the understanding progression of OSMF, the study of prime molecular expressions is essential. Various markers have received more attention, one of them is E-cadherin. Various factors which promote epithelial–mesenchymal transition (EMT) and inhibit E-Cadherin include Snail1, Snail2, Twist and EF1/ZEB1. The intended study was undertaken to evaluate the possible role of E-cadherin and its regulatory markers Twist1 and Snail1 in OSMF. Aims and Objectives: To evaluate the expression of E-cadherin, Twist1 and Snail1 in OSMF To evaluate their possible association with malignant transformation of OSMF. Materials and Methods: Histologically proven 20 cases of each OSMF with and without dysplasia were taken as the study group, 20 normal mucosa as control group and were subjected for immunohistochemical (IHC) expression with E-cadherin, Twist1 and snail1. Results: Immunohistochemical expression of all the three markers showed statistically significant expression of all the three markers. Intensity and percentage of staining between the groups were statistically significant for E-cadherin between normal oral mucosa (NOM) and OSMF with dysplasia (OSMFD), no significance was found between NOM and OSMF, whereas Snail1 and Twsit1 were statistically significant between NOM and OSMF and also between NOM and OSMFD. However, no significance was found for all the three markers when compared between the groups OSMF and OSMFD. Conclusion: The increased expression of Snail1 and Twist1 with concomitant loss of E -cadherin in OSMF suggests the role of the EMT.
Oligodontia, a form of hypodontia commonly seen in permanent than in deciduous dentition. It is defined as the congenital absence of six or more teeth, excluding third molars. It is relatively a rare condition that can occur either as an isolated finding or as part of a syndrome. A case of nonsyndromic oligodontia in a 12-year-old boy with congenital absence of all permanent teeth except the premolars (excluding third molars) and over-retained deciduous dentition with conical shaped anteriors is reported. The prevalence, possible etiological factors and treatment options of the condition is reviewed.
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