Aim of the work-Methotrexate (MTX), a structural analogue of folic acid, is an antineoplastic and antirheumatic agent which is used in a variety of clinical schedules and combination therapy regimens in man. Material and methods-Sixty mice of nearly the same age were randomly categorized into four groups (one control and three treated groups with different doses of methotrexate). Mice of the treated groups 1, 2 and 3 were intraperitoneally injected with a single dose of methotrexate (2.5, 5 or 10 mg/kg b. wt. respectively) at the first day of the experiment. All the control and the treated animals were sacrificed after 24, 48 or 72 hour by cervical dislocation post treatment. Results-Methotrexate treatment induced structural and numerical chromosomal aberrations in male mice bone marrow cells which were significantly increased (P< 0.001) by dose and time. Structural aberrations were chromosomal gap, fragment, break, centromeric attenuation, deletion, centric fusion, ring formation, end to end association and beaded chromosomes. Numerical aberration was polyploidy. Also, methotrexate treatment decreased the mitotic index in bone marrow cells of all the treated mice in comparison with the control group by increasing dose and time of treatment. Comet assay results indicated that treatment with methotrexate significantly increased (P< 0.001) DNA damage in the blood leukocytes in dose and time dependent manner. Conclusion-It can be concluded that methotrexate induced genetic damage on the chromosomes and DNA content of male albino mice even after single treatment with low doses .

Background: Methotrexate is an antineoplastic, antipsoriatic and antirheumatic agent belongs to the group of antimetabolites and inhibits folic acid metabolism. Materials and methods: To investigate its possible effect, sixty male mice were randomly assigned to one of four groups (one control and three treated groups with different doses of methotrexate). Mice of groups 1, 2 and 3 were intraperitoneally injected with 2.5, 5 and 10 mg /kg b.wt. methotrexate respectively. All the control and treated animals were sacrificed at 24, 48 and 72 hour by cervical dislocation post treatment. Results: Micronucleus assay results showed that methotrexate treatment induced genotoxicity in bone marrow cells, the number of micronucleated polychromatic erythrocytes (MNPCEs) and the ratio of polychromatic erythrocytes / normochromatic erythrocytes was gradually increased significantly (P < 0.001) by increasing dose and time of treatment in methotrexate treated groups in comparison with the control group. An analysis of randomly amplified polymorphism DNA-polymerase chain reaction (RAPD-PCR) showed different ranges of DNA modifications in the treated groups after 24, 48 and 72 hour of treatment in comparison with the control group. Results of this study indicate that methotrexate treatment induced cytotoxic and genotoxic effect on bone marrow cells and DNA content of male albino mice even after a low dose and single treatment. Conclusion: Therefore, the therapeutic uses of methotrexate should be restricted to a very narrow range border.

The administration of glucocorticoids is proven to cause serious adverse events. Objectives: This study was conducted to compare the possible hazards of the short-and long-term administration of glucocorticoids on the periodontium in rats, using histological examination and scanning electron microscopy. Methods: Fifteen adult male albino rats were included in the study and divided into the 3 groups. Group I served as a control, group II received 7 mg/kg dexamethasone intramuscularly once a week for 5 wk, and group III received 7 mg/kg dexamethasone intramuscularly once a week for 10 wk. The mandibles were dissected and examined histologically as well as with scanning electron microscopy and energy dispersive radiography. Results: Histologically, group I showed normal an alveolar process. In group II, bone trabeculae demonstrated obvious Howship's lacunae of osteoclasts. In group III, bone trabeculae exhibited multiple degenerated osteocytes with apparent vacuolization. Scanning electron microscopy revealed smooth alveolar bone architecture in group I. Groups II and III demonstrated irregular bone architecture with widening of the neurovascular canals. EDX analysis demonstrated the highest calcium-phosphorous concentration in the control group and the lowest in group III. Conclusions: Dexamethasone has a devastating impact on the alveolar bone via the acceleration of bone resorption and decreased activity of osteoblasts. This effect was more pronounced with prolonged drug administration.How to cite this article: Hagag TAEK, Fathy E, Mahmoud MF, Salem Z. Hazards of short-and long-term administration of glucocorticoids on the periodontium in rats: a histological and electron microscopic study. J Dent Indones. 2019;26(3):145-152.

Background Tamiflu (Oseltamivir) and Adamine (Amantadine HCl) are antiviral drugs which are used for prevention and treatment for influenza. The present study was carried out to evaluate the effect of Tamiflu and Adamine on the liver of adult male albino mice from the histological and ultrastructural points of views. Results Histological examination of liver sections treated with Tamiflu and Adamine included enlargement and congestion of central and hepatic veins in addition to erosion of their endothelial lining cells, cytoplasmic vacuolation of hepatocytes, pyknosis of their nuclei, and dilatation of hepatic sinusoid. The electron microscopic investigation illustrated mitochondrial swelling, fragmented rough endoplasmic reticulum, cytoplasmic vacuolation, the nuclei with irregular envelope and condensed heterochromatin, dilated microvilli in sinusoid, in addition to active Kupffer cells have many lysosomes and filopodia in its membrane. Conclusion The study suggested that both drugs induced histopathological and ultrastructural alterations in hepatic tissue. In conclusion, Tamiflu and Adamine have pathological effects on liver of albino mice (Mus musculus).