Peripheral giant cell granuloma (PGCG) known as “giant cell epulis” is a benign, reactive exophytic gingival lesion that accounts for less than 10% of all gingival lesions. PGCG affects females more than males with middle age predilection. Till now the etiology of PGCG remains unclear but various factors that can cause PGCG include poor oral hygiene, food impaction, following an extraction, dry mouth, hormonal disturbance, and hyperparathyroidism. The reported recurrence rate of the lesion is 5.0%–70.6%. The present case report describes the rare case of PGCG with primary hyperparathyroidism in a male patient with a history of swelling in the mandibular anterior region.
Oral cancer results due to multiple genetic alterations that transform the normal cells in the oral cavity into neoplastic cells. These genetic changes in a particular tumor field lead to a rapid expansion of preneoplastic daughter cells producing malignant phenotype but the malignancy results due to such genetic changes occurr over several years. The morphological changes in these transformed cells help in the diagnosis of malignancy. Thus, the early changes at the gene level are present in the population of daughter cells in the organ, which explains the concept of field cancerization. Cancer stem cells (CSCs) represent a group of cells that have the capacity of self-renewal and have the potential to differentiate into other types of tumor cells. This review explains the cellular and genetic basis of field cancerization and the role of cancer stem cells in field cancerization.
Goldenhar Syndrome or oculoauriculovertebral spectrum is a complex syndrome characterized by an association of maxillomandibular hypoplasia, deformity of the ear, ocular dermoid and vertebral anomalies and the most severe form of hemifacial microsomia. Here, we describe a 26-year-old male patient with unilateral hemifacial microsomia, preauricular ear tags, macrosomia on the right side of the face.
Background:
Salivary pH plays a significant role in the pathogenesis of various oral diseases and conditions. Chewing of areca nut and various tobacco products changes salivary pH.
Aim:
The aim of the study was to measure the effect of habitual chewing of areca nut and various tobacco products on salivary pH.
Materials and Methods:
The present study included 360 individuals (chewers and nonchewers) of age group between 20 and 30 years who visited the Outpatient Department of Hi-Tech Dental College and Hospital. The patient's salivary pH was measured with the help of a digital pH meter before and after chewing areca nut and various tobacco products.
Results:
It was observed that, in all the groups of chewers, pH decreased after chewing except in the gutkha and lime chewing group, where pH increased (pH before chewing was 7.43 ± 0.41 and after chewing was 7.51 ± 0.399), the difference was strongly significant (
P
< 0.001). pH was found to be less in lime and tobacco chewers (6.83 ± 0.33) and more in tobacco, betel nut, and lime chewers (7.50 ± 0.41) in comparison to other groups before chewing; the difference was strongly significant (
P
< 0.001). In the mean ± standard deviation, increase in pH was found among chewers (7.32 ± 0.49) as compared to nonchewers (6.99 ± 0.14), which is the control group, and the data were statically significant (
P
< 0.001).
Conclusion:
pH is altered in areca nut and various tobacco chewers, rendering the oral mucosa vulnerable to the toxic effects of areca nut and various tobacco products.
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