EFEK PEMBERIAN DEKSAMETASON DAN PREDNISON DOSIS RENDAH TERHADAP PENURUNAN JUMLAH OSTEOBLAS FEMUR TIKUS WISTAR (RATTUS NORVEGICUS)
DOI:
https://doi.org/10.31004/jkt.v5i1.24194Keywords:
Dexamethasone, osteoblasts, osteoporosis, prednisoneAbstract
Osteoporosis merupakan penyakit skeletal sistemik yang dikarakteristikan oleh adanya penurunan kepadatan tulang dan kerusakan mikroarsitektur jaringan tulang sehingga sifat tulang menjadi rapuh. Osteoporosis dibagi menjadi 2 yaitu osteoporosis primer dan sekunder. Osteoporosis primer meliputi osteoporosis pascameopause (tipe 1) dan osteoporosis senile (tipe 2). Sedangkan osteoporosis sekunder diakibatkan oleh malabsorpsi, obat- obatan seperti glukokortikoid, dan beberapa penyakit seperti hiperparatiroidisme. Glucocorticoid-induced osteoporosis (GIOP) merupakan penyebab paling sering terjadinya osteoporosis sekunder. Tujuan penelitian ini untuk mengetahui efek pemberian obat prednison dan deksametason terhadap peningkatan jumlah apoptosis osteoblas femur tikus wistar (Rattus norvegicus). Penelitian ini menganut true experimental post test only control group design. Hasil perhitungan jumlah osteoblas pada setiap kelompok didapatkan rata-ratanya sebagai berikut, kelompok normal hari ke-14 berjumlah 25, kelompok prednison hari ke-14 berjumlah 16,8, dan kelompok deksametason hari ke-14 berjumlah 15. Sedangkan pada kelompok normal hari ke-28 memiliki rata- rata berjumlah 36,4, kelompok prednison hari ke-28 berjumlah 18,2, dan kelompok deksametason hari ke-28 berjumlah 16,6. Dari hasil tersebut dapat disimpulkan bahwa pemberian obat deksametason dan prednison dalam dosis rendah dapat menurunkan jumlah osteoblas yang diakibatkan karena terjadinya peningkatan apoptosis osteoblas dan kondisi tersebut dapat mengakibatkan terjadinya osteoporosis sekunder, serta dari hasil tersebut kita dapat mengetahui bahwa obat deksametason memiliki efek dalam menurunkan jumlah osteoblas yang lebih besar daripada obat prednison.References
Aditama, A. P., Muslikh, F. A., Shirvi, I. N., Islamiyah, F. R., Putra, K. H., Inayatilah, F. R., Et Al. (2021). Efek Induksi Proliferasi Sel Osteoblas Tulang Trabekular Mencit Jantan Oleh Ekstrak Etanol 96% Daun Semanggi (Marsilea Crenata Presl.) . Jurnal Sains Dan Kesehatan .
Akkawi, I., & Zmerly, H. (2018). Osteoporosis: Current Concepts. Thieme , 122.
Arias-Pinilla, G. A., & Brown, J. (2022). Bone Sarcomes And Bone Metastases - From Bench To Bedside (Third Edition). Amsterdam: Elsevier.
Bradley, E., Westendorf, J. J., Wijnen, A. J., & Dudakovic, A. (2018). Osteoblasts: Function, Development, And Regulation. Wiley .
Cao, X. (2018). RANKL-RANK Signaling Regulates Osteoblast Differentiation And Bone Formation.
Bone Research .
Chaichit, S., Sato, T., Yu, H., Tanaka, Y.-K., Ogra, Y., Mizoguchi, T., Et Al. (2021). Evaluation Of Dexamethasone-Induced Osteoporosis In Vivo Using Zebrafish Scales. Pharmaceuticals .
Chotiyarnwong, P., & Mccloskey, E. V. (2020). Pathogenesis Of Glucocorticoid-Induced Osteoporosis And Options For Treatment. Nature Reviews Endocrinology .
Duan, P., & Bonewald, L. (2016). The Role Of The Wnt/?-Catenin Signaling Pathway In Formation And Maintenance Of Bone And Teeth. The International Journal Of Biochemistry & Cell Biology .
Esclassan, E. N., Valera, M. C., Tremollieres, F., Arnal, J. F., Lenfant, F., Fontaine, C., Et Al. (2021). Critical Role Of Estrogens On Bone Homeostasis In Both Male And Female: From Physiology To Medical Implications. International Journal Of Molecular Sciences .
Gado, M., Baschant, U., Hofbauer, L. C., & Henneicke, H. (2022). Bad To The Bone: The Effects Of Therapeutic Glucocorticoids On Osteoblasts And Osteocytes. Frontiers In Endocrinology .
Honma, M. (2023). Potential Of RANKL Reverse Signal As A New Pharmacological Target. Japanese Pharmacology Journal .
Hu, K., & Olsen, B. R. (2017). Vascular Endothelial Growth Factor Control Mechanisms In Skeletal Growth And Repair. Developmental Dynamics : An Official Publication Of The American Association Of Anatomists .
Huang, J., Ye, Y., Xiao, Y., Ren, Q., Zhou, Q., Mingliang, Z., Et Al. (2022). Geniposide Ameliorates Glucocorticoid-Induced Osteoblast Apoptosis By Activating Autophagy. Biomedicine & Pharmacotherapy .
Johnson, D. B., Lopez, M. J., & Kelley, B. (2022). Dexamethasone. Statpearls .
Lane, N. E. (2019). Glucocorticoid Induced Osteoporosis: New Insights Into The Pathophysiology And Treatments. Current Osteoporosis Reports .
Maynard, R. L., & Downes, N. (2019). Anatomy And Histology Of The Laboratory Rat In Toxicology And Biomedical Research. Birmingham: Academic Press.
Mendoza, S. V., Genetos, D. C., & Yellowley, C. E. (2023). Hypoxia-Inducible Factor-2? Signaling In The Skeletal System. JBMR Plus .
Mollazadeh, S., Bazzaz, B. S., & Kerachian, M. A. (2015). Role Of Apoptosis In Pathogenesis And Treatment Of Bone-Related Diseases. Journal Of Orthopaedic Surgery And Research
Sengupta, P. (2013). The Laboratory Rat: Relating Its Age With Human's . International Journal Of Preventive Medicine .
Sromova, V., Sobola, D., & Kaspar, P. (2023). A Brief Review Of Bone Cell Function And Importance. Cells .
Suryana, B. P. (2021). Diagnosis Dan Pengelolaan Osteoporosis Akibat Glukokortikoid. Jakarta: Perhimpunan Reumatologi Indonesia.
Vimalraj, S. (2020). Alkaline Phosphatase: Structure, Expression And Its Function In Bone Mineralization.
Weinstein, R. S., Hogan, E. A., Borrelli, M. J., Liachenko, S., O'Brien, C. A., & Manolagas, S. C. (2017). The Pathophysiological Sequence Of Glucocorticoid-Induced Osteonecrosis Of The Femoral Head In Male Mice. Endocrinology .
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