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Your search keyword '"Pirih, F.Q."' showing total 7 results
Start Over Author "Pirih, F.Q." Language english
7 results on '"Pirih, F.Q."'

3. The receptor AT1 appears to be important for the maintenance of bone mass and AT2 receptor function in periodontal bone loss appears to be regulated by AT1 receptor

Author

Lima, M.L.S., Martins, A.A., Medeiros, C.A.C.X., Guerra, G.C.B., Santos, R., Bader, M., Pirih, F.Q., Araújo Júnior, R.F., Brito, G.A.C., Leitão, R.F.C., Silva, R.A., Barbosa, S.J.A., Melo, R.C.O., and Araújo, A.A.

Subjects
endocrine system, Cardiovascular and Metabolic Diseases, cardiovascular system, hormones, hormone substitutes, and hormone antagonists, circulatory and respiratory physiology
Abstract

A large number of experimental studies has demonstrated that angiotensin II (Ang II) is involved in key events of the inflammatory process. This study aimed to evaluate the role of Ang II type 1 (AT1) and Ang II type 2 (AT2) receptors on periodontitis. Methods: Experimental periodontitis was induced by placing a 5.0 nylon thread ligature around the second upper left molar of AT1 mice, no-ligature or ligature (AT1-NL and AT1-L), AT2 (AT2-NL or AT2-L) and wild type (WT-NL or L). Alveolar bone loss was scanned using Micro-CT. Cytokines, peptides and enzymes were analyzed from gingival tissues by Elisa and RT-PCR. Results: The blockade of AT1 receptor resulted in bone loss, even in healthy animals. Ang II receptor blockades did not prevent linear bone loss. Ang II and Ang 1-7 levels were significantly increased in the AT2-L (p < 0.01) group compared to AT2-NL and AT1-L. The genic expression of the Mas receptor was significantly increased in WT-L and AT2-L compared to (WT-NL and AT2-NL, respectively) and in AT1-L. Conclusions: Our data suggest that the receptor AT1 appears to be important for the maintenance of bone mass. AT2 receptor molecular function in periodontitis appears to be regulated by AT1.

Published
2021

4. Antiresorptive-Type and Discontinuation-Timing Affect ONJ Burden.

Author

Hadaya, D., Soundia, A., Gkouveris, I., Bezouglaia, O., Dry, S.M., Pirih, F.Q., Aghaloo, T.L., and Tetradis, S.

Subjects
OSTEONECROSIS, JAW diseases, DENTAL extraction, BONE resorption inhibitors, LABORATORY rats
Abstract

Osteonecrosis of the jaws (ONJ), a severe side effect of antiresorptive medications, is characterized by exposed, nonhealing bone in the oral cavity. Treatment options for ONJ range from management of symptomology to surgical resection of the affected area. Antiresorptive discontinuation, often termed a "drug holiday," has been used for managing ONJ patients. Antiresorptives can be discontinued prior to oral surgical procedures, such as tooth extraction, to prevent ONJ development or in patients with established ONJ to accelerate healing. Here, our objective was to test these clinical scenarios using the potent bisphosphonate, zoledronic acid (ZA), and the denosumab surrogate for rodents, OPG-Fc, in a rat model of ONJ. Animals were pretreated with antiresorptives or saline, after which we induced ONJ using periapical disease and tooth extraction. In our first experimental design, antiresorptives were discontinued 1 wk prior to tooth extraction, and animals were evaluated 4 wk later for clinical, radiographic, and histologic features of ONJ. In the second experiment, ONJ was established and antiresorptives were discontinued for 4 wk. Discontinuation of OPG-Fc, but not ZA, prior to tooth extraction ameliorated subsequent ONJ development. In contrast, discontinuation of either ZA or OPG-Fc in rats with established ONJ did not lead to ONJ resolution. In conclusion, our findings suggest that antiresorptive discontinuation is dependent on both the type of antiresorptive and the timing of discontinuation. [ABSTRACT FROM AUTHOR]

Published
2021
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7. Contributors

Author

Abt, E., Aguirre, A., Allen, E.P., Ammons, W.F., Jr, Anderson, M.H., Aoki, A., Azzi, R.R., Bauer, J.G., Bloom, M.J., Bulkacz, J., Butler, B., Camargo, P.M., Carranza, F.A., Chambrone, L., Chang, T.-L., Cho, S.-C., Chou, C.-H., Chung, E., Ciancio, S.G., Cochran, D.L., Cooney, J.P., Crall, J.J., Cross, J.D., Dadamio, J., De Geest, S., Derycke, R.R., Diehl, S.R., Do, J., Dommisch, H., Duperon, D.F., Etienne, D.H., Fazio, R.C., Finkelman, R.D., Fiorellini, J.P., Forrest, J.L., Froum, S.H., Froum, S.J., Galindo, G., Godts, C., Gu, Y., Haake, S.K., Han, T.J., Harrington, G.W., Haytac, M.C., Hinrichs, J.E., Hogan, E.L., Huang, C.-Y., Hujoel, P.P., Ishikawa, I., Jahn, C.A., Jakubovics, N., Jepsen, S., Jolkovsky, D.L., Kamel, B.P., Kang, M.K., Kao, D.W.K., Kao, R.T., Kebschull, M., Kim, D.M., Kim, G.U., Kirkwood, K.L., Klokkevold, P.R., Kokich, V.G., Korczeniewska, O.A., Kotsakis, G., Kuo, F., Laleman, I., Law, C.S., Lieberman, M.B., Mallya, S.M., Mariotti, A., McDevitt, M.J., McGregor, A., Mealey, B.L., Melnick, P.R., Merin, R.L., Miller, G.W., Miller, S.A., Miyasaki, K.T., Needleman, I., Newman, M.G., Nevins, M.L., Nisengard, R.J., Novak, K.F., Novak, M.J., Otomo-Corgel, J., Ozcelik, O., Park, K.-B., Pattison, A.M., Pattison, G.L., Pelsmaekers, B., Perry, D.A., Pirih, F.Q., Polson, A.M., Preshaw, P.M., Quirynen, M., Rees, T.D., Reynolds, M.A., Rossa, C., Jr, Ryan, M.E., Sanz, M., Scheyer, E.T., Schleyer, T., Serhal, C.B., Shanelec, D.A., Shin, K., Shklar, G., Silva, D.R., Sims, T.N., Spackman, S.S., Spear, F.M., Spolsky, V.W., Stathopoulou, P.G., Stein, C., Takei, H.H., Tarnow, D.P., Taylor, J.J., Tetradis, S., Teughels, W., Math, V.T., Thyvalikakath, T., Tibbetts, L.S., Trabert, K.C., Urban, I.A., Uzel, N.B., Van den Velde, S., Vandekerckhove, B., Vasquez, J.L.T., Vercellotti, T., Wada, K., Zacher, A., Zackin, S.J., Ambalavanan, N., Dwarakanath, C.D., Jain, A., Naik, D.G., and Uppoor, A.

Published
2016
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