Aims:
Evaluation of total serum creatine phosphokinase and serum lactate dehydrogenase levels as a biochemical parameter in the diagnosis of oral cancer, oral leukoplakia by the case-control method.
Settings and Design:
A hospital-based, case-control study was conducted at the Department of Oral Medicine, Diagnosis, and Radiology.
Materials and Methods:
The study included clinically and histopathologically diagnosed oral leukoplakia and oral cancers with 20 patients in each group. The control group consisted of 20 healthy patients without lesions or tobacco-related habits or any systemic diseases. The blood samples were collected from the study and control groups, centrifuged, and serum was analyzed for serum creatine phosphokinase and serum lactate dehydrogenase (CK and LDH) levels using an autoanalyzer.
Statistical Analysis:
Comparison of three groups with respect to each biochemical parameter was done by one-way ANOVA. Comparison between the groups was done by Tukey's multiple post hoc test.
Results:
It was found that total serum CK levels were statistically significantly decreased in both oral leukoplakia and oral cancer when compared with that of the control group. Total serum LDH levels were statistically significantly increased in both oral leukoplakia and oral cancer when compared with that of the control group.
Conclusion:
Although the results of the present study showed increased levels of LDH in both oral leukoplakia and oral cancer, and CK levels statistically decreased but they were within normal limits. Further. studies with a greater number of samples, different grades of epithelial dysplasias, and assessment of individual isoenzymes has to be carried out to evaluate the exact role of CK and LDH in the etiopathogenesis of oral cancer.
status tends to change, thus leading to an increase in inflammation in the periodontal tissues.Dental health is an important component of somatic human health. Various aggressive environmental and nutritional factors affect adversely the oral cavity homeostasis, serve as a prerequisite for emergence of inflammatory-destructive diseases of the dentofacial system. Development of general periodontitis (GP) is accompanied by a complex of pathological changes with a predominance of inflammatory and dystrophic phenomena. 1 These changes vary much, depending on the intensity of the periodontal tissue affection, and reflect the processes of local inflammation and activation of the immune defense mechanisms. All this requires adequate measures to control dental health of the population. 2 Diseases of periodontal tissues remain one of the urgent problems in the modern dentistry. 3 In recent decades, a large number of studies have been devoted to the relationship between the intensity of the periodontal complex affection and a number of somatic diseases, which are currently classified as socially significant ones. These are, first of all, cardiovascular diseases (CVD), diabetes mellitus, oncopathology, osteoporosis, osteoarthrosis, etc. 2,[4][5][6][7] In the industrialized countries the prevalence of metabolic syndrome among the population of 30years and older is 10-20%, significantly increasing with age.
Goal of the studyidentifying the correlation of the cytokine status, arterial stiffness and oral health status in patients with the metabolic syndrome.
Ameloblastoma are benign tumors whose importance lies in its potential to grow into enormous size with resulting bone deformity. They are typically classified as unicystic, multicystic, peripheral, and malignant subtypes. Unicystic ameloblastoma (UA) refers to those cystic lesions that show clinical, radiographic, or gross features of an odontogenic cyst but on histological examination show a typical ameloblastomatous epithelium lining, with or without luminal and/or mural tumor growth. We present a very rare case of unicystic ameloblastoma in a girl child with an age of 10 years; clinical and radiographic features of UCA, its differential diagnosis, histopathology, and current concepts of management have also been discussed in the present paper.
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