Peran Interferon pada Pathogenesis Sindrom Sjogren

Abstract
Sjogren sindrom is a chronic autoimmune exocrinopathy distinguished by dry eyes and mouth. Its commonly affect 0,7% of the European population. Recent studies have reported on the association of interferon in the pathogenesis of Sjogren syndrom. Interferon is lead to salivary gland dysfunction by two mechanism, direct and indirect pathway. In the direct pathway, interferon may alter the structure and function of Tigth junction (TJ), and decrease Transepithelial Resistance (TER) of epithelial salivary gland cell. In the indirect pathway, Interferon could generate autoimmune system by interact with lymphocyte B and T. All these mechanism are lead to salivary gland dysfunction and dry mouth (xerostomia).

Keyword: Interferon, Sjogren syndrom, salivary gland cell, autoimmune, dry mouth.


Referensi
1. Alamanos Y, N Tsifetaki, PV Voulgari, AI Vnetsanopoulou, C Siozos, AA Drosos. Epidemiology of primary Sjogren syndrom in north-west greece, 1982-2003. Rheumatology 2006; 45:187-191.
2. Fox R. I. Sjogren syndrom. Lancet 2005; 366: 321-31.
3. Jonsson R, Vogelsang P, Volchenkov R, Espinosa A, Wahren-Herlenius M, Appel S. The complexity of Sjogren syndrome: novel aspects on pathogenesis. Immunol lett 2011; 141(1):1-9.
4. Cha S, J Brayer, J Gao, V Brown, S Killedar, U Yasunari, et al. A dual role for interferon –γ in the pathogenesis of Sjogren syndrome-like autoimmune exocrinopathy in the nonobese diabetic mouse. Scand J Immunol 2004; 60:552-65. 5. J Rolland. Sjogren’s syndrom. In: Dieppe P, HR Schumacher, FA Wollheim editor. Classic papers in rheumatology. London: Martin Dunitz Ltd. 2005. p.202.
6. Ittah M, C Miceli-Richars, J-E Gotterberg, F Lavie, T Lazure, N Ba. B cell-activating factor of the tumor necrosis factor family (BAFF) is exprssed under stimulation by interferon in salivary gland epithelial cells in promary Sjogren syndrom. Arthritis res Ther 2006; 8:1-9.
7. Brkic Z, NI Maria, CG van Helden-Meeuwsen, JP van de Merwe, PL van Daele, VA Dalm, et al. Prevalence of interferon type I signature in CD14 monocytes of patients with Sjogren’s syndrome and association with disease activity and BAFF gene expression. Ann Rheum Dis 2013; 72:728-35.
8. Bave U, G Nordmark, T Lovgren, J Ronnelid, S Cajander, M-L Eloranta, et al. Activation of the type I interferon system in primary Sjogren syndrom. Arthritis Rheum 2005; 52(4):1185-95.
9. Brkic Z. Interferon type I driven immune activation in generalized autoimmune disease(PhD thesis). Rotterdam, Qld: Erasmus Universiteit Rotterdam; 2011.
10. Manoussakis MN, C Georgopoulou, E Zintzaras, M spyropoulou, A Stavropoulou, FN Skoupouli, et al. Sjogren syndrom associated with systemic lupus erythematosus. Arthritis Rheum 2004; 50(3):882-91.
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A/N:Setelah lama hiatus, akhirnya Dea kembali mengupload salah satu makalah yang kemarin sempat jadi tugas. Semoga bermanfaat ya. Maaf masih belajar, hehe jadi masih jauh dari sempurna makalahnya ^^.
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Peranan IL-17 terhadap Patogenesis Penyakit Periodontal

A/N: Yeah, untuk kesekian kalinya, saya kembali mengulas mengenai keterlibatan Interleukin-17 dalam progresifitas penyakit yang ada di rongga mulut. Saat ini, saya membahasnya pada penyakit periodontal.
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Abstrak
Interleukin 17 (IL-17) is product of TH17 that induced by TGFβ and IL-6. IL-17 play role in inflammatory respone as one of cytokine proinflamatory. Directly, its stimulates LIX and CXC1 (reseptor of lipopolysacharide) in neutrofil. LIX and CXC1 is used for recruiting neutrofil to the infected area. Furthermore, IL-17 co-operate with TLR 2 and TLR 5 induces human epithelial gingiva cells to produce cytokine proinflamatory, such as IL-1β and TNF-α. However, IL-17 initiates bone destruction by activates RANKL. These effect is lead to periodontal disease.

Keyword: IL-17, Periodontal disease, cytokine proinflamatory, neutrofil



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PATOGENESIS TERJADINYA PENYAKIT PERIAPIKAL MELIPUTI RESPON INFLAMASI DAN IMUN

Inflamasi adalah respon fisiologis tubuh terhadap suatu peradangan dan gangguan oleh faktor eksternal. Inflamasi terbagi menjadi dua yaitu inflamasi akut dan inflamasi kronis. Inflamasi akut adalah proses peradangan yang berlansung relatif singkat, dari beberapa menit sampai beberapa hari, dan ditandai dengan perubahan vaskular, eksudasi cairan dan protein plasma serta akumulasi neutrofil yang menonjol. Inflamasi akut dapat berkembang menjadi suatu inflamasi kronis jika agen penyebab peradangan masih tetap ada. Inflamasi kronis adalah respon proliferatif dimana terjadi proliferasi fibroblas, endotelium vaskuler, dan infiltrasi sel mononuklear (limfosit, sel plasma dan makrofag). Respon peradangan meliputi suatu perangkat kompleks yang mempengaruhi perubahan vaskular dan selular.

Bakteri dapat masuk ke dalam pulpa dengan tiga cara: Pertama, invasi langsung melalui dentin, seperti karies, fraktur mahkota atau akar, terbukanya pulpa pada waktu preparasi kavitas, atrisi, abrasi, erosi atau retak pada mahkota. Kedua, invasi melalui pembuluh darah atau limfatik terbuka yang ada hubungannya dengan penyakit periodontal, suatu kanal aksesori pada daerah furkasi, infeksi gusi, atau scaling gigi-gigi. Ketiga, invasi melalui darah, misalnya selama penyakit infeksius atau bakteremia transient. Bakteri dapat menembus dentin pada waktu preparasi kavitas karena kontaminasi lapisan smear karena bakteri pada tubuli dentin terbuka disebabkan oleh proses karies dan masuknya bakteri karena tindakan operatif yang tidak bersih. Oleh sebab itu, tubuh menanggulangi dengan adanya sistem pertahanan diri yang mampu mengeliminir dan menetralkan antigen serta zat-zat yang dihasilkannya.

Imunologis adalah cabang ilmu biomedis yang berkaitan dengan respon organisme terhadap penolakan antigen, pengenalan diri sendiri (self) dan bukan dirinya (nonself) , serta semua efek biologis, serologis, dan kimia fisika fenomena imun. Pada penyakit periapikal, respon imun spesifik yang berperan adalah humoral dan seluler, sementara respon imun nonspesifik pada sistem imun humoral adalah reaksi antigen dan antibodi yang membentuk komplemen.



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Penggunaan Raman Spectroscopy sebagai Pendeteksi Karies Dini

Abstrak
Commonly, caries occurs in 43,3% of population in Indonesia. Detecting earliest stage of caries could be the best ways to control the dental caries. Therefore, author aim to discuss the using of raman spectroscopy as a method for detecting early caries. This study concluded that the using of raman spectroscopy is useful for the dentist to detect earliest caries on their patients, so they could give dental fluoride treatment to avoid from the severe caries.
Keyword: early caries, raman spectroscopy, demineralization, raman spectra

Referensi
1. Kidd, E. A. M., Joyston-Bechal S. Dasar-dasar karies. Jakarta: EGC; 2012
2. Depkes. Laporan Riset Kesehatan Dasar 2007; 2008
3. Ko, A. C.-t, Hewko. M., Sowa. M. G., Dong C. C. S., Cleghorn B., Choo-Smith L.-P. Early dental caries detection using a fibre-optic coupled polarization-resolved Raman spectroscopic system. Optical express. 2008 April; 16(9): 6274-84
4. Smith, E., Dent G. Modern raman spectroscopy: a practical approach. England: John Wiley & Sons; 2005
5. Ko, A. C.-t, Hewko. M., Sowa. M. G., Dong C. C. S., Cleghorn B., Choo-Smith L.-P. Detection of early dental caries sing polarized Raman spectroscopy. Optics Express, 9 Januari 2006, Vol. 14, no.1; 1-13
6. Ionita. Diagnosis of tooth decay using plarized miro-raman confocal spectroscopy. Romanian Reports in Physics, Vol. 61, No. 3, 2009; 567-74
7. Ko, A. C.-t, Hewko. M., Sowa. M. G., Dong C. C. S., Cleghorn B., Choo-Smith L.-P. Ex vivo detection and characterization of early dental caries by optical coherence tomography and raman spectroscopy. Journal of Biomedical optics, Vol. 10(03), May/June 2005;1-16
8. Fejerskov, O., Kidd, E. Dental caries: the disease and its clinical management. Singapore: Blackwell Munksgaard; 2008



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Pengaruh FGF10 terhadap Terjadinya Celah Palatum

Abstrak
Palatogenesis is the process of palate formation that develop via epithelium-mesenchymal interaction. The failure of this process causes cleft palate. Cleft palate commonly occurs in 1/15000 birth of worldwide. It is caused by genetic, environment, and also teratogenic component, which genetic is the most factor that causes cleft palate. Therefore, author aim to discuss about the effect of Fgf10 to the cleft palate. This study concluded that mutation in Fgf10 causes cleft palate as the result of epithelium-mesenchymal interaction error. It is because Fgf10 plays critical role to epithelium-mesenchymal interaction.
Keyword : Fgf10, cleft palate, epithelium-mesenchymal interaction, mutation

Referensi
1. Underwood, J.C.E., alih bahasa: Sarjadi. 1999. Patologi Umum dan Sistematik, vol.1 edisi 2. Jakarta: EGC.
2. Lynn Betz Cecily dan Linda A. Sowden. 2009. Buku Saku Keperawatan Pediarti Edisi 5. Jakarta : EGC
3. Stainer, Philip and Moore, G. E. “Genetics of Cleft Lip and Palate: Syndromic Genes Contribute to The Incidence of Non-Syndromic Clefts”. Human Molecular Genetic vol. 13, Januari 2004, hal 73-81.
4. Rice R., Spencer-Dene B., Connor E. C., Gritli-Linde A., McMahon A.P., Dickson C., et all. “Disruption of Fgf10/Fgfr2b coordinated epithelial-mesenchymal interactions causes cleft palate”. Journal of Clinic Investigation, vol. 113, Juni 2004, hal. 1692-700.
5. Sadler, T. W., alih bahasa: Pendit, B. U. 2012. Embriologi Kedokteran Langman, Ed. 10. Jakarta: EGC.
6. Alappat, S. R.,, Zhang Z., Suzuki K., Zhang X., Liu H., Jiang R., et all. “The Cellular and Molecular Etiology of The Cleft Secondary Palate in FGF10 Mutant Mice”. Developmental Biology, vol. 277, 2005, hal. 102-13.
7. Riley, B. M., Mansilla M. A., Ma J., Daack-Hirsch S., Maher B. S., Raffensperger L. M., et all. “Impaired FGF Signaling Contributes to Cleft Lip and Palate”. PNAS, vol. 104, Maret 2007, hal. 4512-7.



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