One of the primary tasks of systematic biology is the development of our biological nomenclature and classifications. The key purpose for the development of a standard nomenclature for a disease is the need for a common language for the statement of diagnostic terms and for a means or system whereby diagnosis could be suitably recorded without chaos. Odontogenic tumor nomenclature and classification have confused physicians over the years. Ameloblastoma is one such entity among odontogenic tumors, which has continuously changed to be an evolution of the terms and taxonomy used in literature. In this review, we aim to provide a fundamental basis for the understanding of how the etymology and the position of ameloblastoma in odontogenic tumor classification have evolved over the years.
Background. Chronic inflammation is estimated to contribute to approximately 25% of human cancers. Inflammation can be induced by chronic mechanical irritation which can lead to oral pre-cancer and oral cancer. Though many studies have been conducted to identify the genetic damage in oral cancer or dysplastic stages, no study has been completed so far on early detection of genetic damage in healthy individuals presenting with sharp teeth in contact with the lateral border of the tongue.
Objective. The study is aimed at analyzing the genetic damage (micronuclei) in healthy individuals with sharp teeth in contact with the lateral border of the tongue causing chronic mechanical irritation.
Methods. The study group comprised of 75 clinically healthy individuals with sharp teeth in contact with the lateral border of the tongue and 25 clinically healthy individuals with normal teeth in contact with the lateral border of the tongue as a control group. Brush samples of epithelial cells were collected, then spread over clean glass slide and fixed in 100% alcohol, stained with rapid PAP and analyzed under the light microscope. The exfoliated cells were examined to detect micronuclei.
Results. Micronuclei frequency was found to be increased in the study group where sharp teeth were in contact with the lateral border of the tongue of healthy individuals without deleterious habits such as usage of tobacco in smoking/smokeless form, areca nut chewing or alcohol consumption.
Conclusions. Cytogenetic analysis is a simple and scantly invasive technique allowing clinicians the early detection of DNA damage in patients with sharp teeth and subsequently preventing carcinogenesis by proper treatment and follow-up.
Objective. The aim of this study was to evaluate gingival and periodontal status in obese and non-obese type II Diabetic Patients.
Methods. The study population comprised of 75 subjects visiting the outpatient department of our institution, divided into three different groups, group 1 (obese diabetic), group 2 (non-obese diabetic), and group 3 (obese, non-diabetic). Diabetic status was assessed with HbA1c values and obesity status was assessed by body mass index (BMI) score greater than or equal to 30 kg/m2. Gingival and periodontal status were assessed using the Gingival Index (GI) and Community Periodontal Index (CPI) respectively.
Results. The mean gingival index score in group 1, group 2, and group 3 were 1.58, 1.54, and 1.25, respectively. Gingival status was poor among obese and non-obese diabetic subjects [Groups 1 & 2] when compared with obese non-diabetic patients [Group – 3]. The periodontal status showed that periodontal pockets were increased in diabetic obese group (15.4%), followed by diabetic non obese (4.66%), and non-diabetic obese (2%) group respectively and loss of attachment was severe in diabetic obese group (60.7%), followed by diabetic non obese (45.9%) and non-diabetic obese (15.3%) respectively.
Conclusion. Gingival and periodontal status was poor in the obese diabetic group compared to non-obese diabetic and obese non diabetic group. Hence, the risk of gingivitis and periodontitis in obese diabetic patients should be addressed earlier to prevent further complications and achieve a good oral health status.
A
BSTRACT
Background:
Ameloblastoma is the second most common odontogenic tumor that holds a unique position among benign tumors due to its locally destructive and invasive nature. The differed tumor biology behind follicular and plexiform ameloblastoma is always an enigma. Nerve growth factor (NGF), a neurotrophin that plays a major role during odontogenesis, could also possibly play a role in the pathogenesis of odontogenic tumors such as ameloblastoma. With this background, the study was aimed to investigate the expression of NGF in follicular and plexiform ameloblastoma.
Objectives:
The objectives of this study were to analyze the immunohistochemical expression pattern of NGF in ameloblastoma and to compare the immunohistochemical expression pattern of NGF among the follicular and plexiform histological types of ameloblastoma.
Materials and Methods:
Forty histological sections of ameloblastomas (20 follicular and 20 plexiform) were stained immunohistochemically with anti-human NGF mouse IgG monoclonal antibody and the staining was analyzed statistically.
Results:
Almost all the 40 ameloblastoma samples (20 follicular and 20 plexiform) showed positive immunoreactivity to NGF. Both peripheral pre-ameloblast-like tall columnar cells and central stellate-reticulum-like cells showed positive reactivity. The pattern of staining was membranous in the immunoreactive cells. The χ
2
value for the immunoexpression between follicular and plexiform ameloblastoma was statistically significant with a
P
value <0.002. A possible mechanism has been proposed after studying the results with the downstream pathways obtained from literature.
Conclusion:
The pattern of expression of NGF is seen in both follicular and plexiform ameloblastoma. But the intensity is more in plexiform than that of follicular ameloblastoma.
Aim: To evaluate and correlate the epidermal growth factor receptor (EGFR) expression in oral squamous cell carcinomas (OSCC) patients with metastasis and without metastasis.
Materials and methods:The study comprised of 40 samples, 20 cases of metastatic and 20 nonmetastatic OSCC. All the cases were immunostained for EGFR antibody. Epidermal growth factor receptor stained sections were evaluated for staining intensity and distribution. The differences between the groups were statistically analyzed using Chi-square test. Results: Immunoexpression of EGFR in OSCC was 100% among the study groups, where metastatic group showed an increased positive expression comparing to nonmetastatic OSCC that show statistically significance among the study groups. Conclusion: Expression of EGFR can be used as reliable biomarker for prognosis which can be employed in the prediction of the survival of the patient with OSCC. Clinical significance: Since we are in the theragnostic era, evaluating and quantifying the expression of EGFR in OSCC patient will definitely pave a way in targeted drug therapy and personalized medicine for the diseased.
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