CK13 in craniopharyngioma versus related odontogenic neoplasms and human enamel organ

The monoclonal antibody NCL-CK13 was studied in specimens of craniopharyngioma, ameloblastoma and calcifying odontogenic cyst neoplasms and the mandible and maxillae of normal human fetuses. There was a decrease in NCL-CK13 as the dental lamina developed, with a complete loss in the enamel organ. The neoplastic epithelia of the neoplasms revealed a clear phenotypic and immunohistochemical reactive relationship to the stratified embroyonic mucosa, away from the enamel organ. This suggests that these neoplasms might have their histogenesis from early stage epithelium, the oral part of the dental lamina or its remnants

Microleakage study and pulpal response to light cured and autocured clagg ionomer liners

The microleakage pattern and pupal response to visible light cured ionomer cement liner [Vitrabond] in conjunction with composite resin restoration were evaluated and compared to one auto-cured glass ionomer liner [Ketac bond]. Microleakage were evaluated in class V cavities prepared on 20 teeth which were divided into 2 groups. Cavities in group I were lined with "Vitrabond" Scotch bond 2 dental adhesive were applied over it and the cavities were filled with "Silux plus" light cured composite resin after etching of enamel margins. Cavities in group II were lined with Ketac and filled with Silux plus after acid etching of both cement lining and enamel margin. The specimens were thermocycled for 200 cycles between 5 and 50C for 1 minute. Microleakage was assessed at the cervical margins of the cavities using basic fuchsin dye after teeth sectioning

effect of chronic ethanol consumption on the rat alveolar bone

A total of 21 albino adult male rats were used in this study. 15 rats were classified into 3 study groups, 5 rats each, while the remaining 6 rats were used as a control, 2 for each study group. Group I: 20% ethanol was taken for 3 months. Group II: 20% ethanol was taken for 4 months. Group III: 20% ethanol was taken for 7 months. The results revealed that alcohol was responsible for osteoblastic dysfunction which resulted in osteoporosis. Osteoporosis appeared in the form of thin bone trabeculae with hypocellularity. Also, X-ray films showed that the abuse of alcohol cause diminished bone mineral density. These results were progressively increased from group I, in which rats were taking 20% ethanol for 3 months to group III, in which rats were taken ethanol for 7 months. From this study, it can be concluded that the dentists should be very careful during even minor surgical operation in the jaws of alcoholic patients to avoid the probability of jaw fracture as a result of osteoporosis

Chronic diabetes mellitus: osteotic and mineral changes in human beings and rats

Clinical examination and Laboratory investigations done to IS male type I chronic diabetic patients [insulin dependent more than 5 years] and to an age mached group of 10 normal male volunteers revealed normocalcaemia and normomagnesaemia with significant hyperphosphataemia. Estimation of serum level of parathormone showed significant hypoparathyroidism. An addition, significant hypercalcuria, hyperphosphaturia and hpermagnes uria were also detected. Histopathological examination of trabecular bone biopsies from both groups revealed marked osteoportic changes among the diabetic patients. Biochemical analysis of similar bone samples supported the microscopic findings by demonstrating significant decrease of calcium contents of the bone in the diabetic group. In the chronic rats [7 weeks after streptozotecin induction] significant hypercalcaemia, hyperphosphataemia and normomagnesaemia were found. Their sera showed significant hypoparathyroidism. In addition, significant hypermagnesuria. Histopathological examination of the rat's right tibiae revealed advanced rachitic changes. Biochemical analysis of the left tibias approved the microscopic findings by showing significant decrease in bone calcium contents