EKSPRESI MATRIKS METALLOPROTEINASE-8 DAN INTERLEUKIN-8 PADA KERUSAKAN JARINGAN PERIAPIKAL AKIBAT INDUKSI BAKTERI ENTEROCOCCUS FAECALIS
Downloads
Background. The main etiology of endodontic treatment failure is caused by bacteries that stay in the root canal. E.faecalis is a bactery that is found as an etiology of endodontic treatment failure. Cell wall of this bacteria is containing Lipoteichoic acid (LTA). LTA can penetrate into the periradicular tissue, act as endotoxin in host and cause periradicular inflammation and destruction. It occurs due to the capability of IL-8 to enhance the inflamation reaction and MMP-8 to stop the collagen formation. The ability of enterococcus faecalis in enhancing inflamation process cause host can not reach the homeostasis phase and performing an even bigger tissue damage. Purpose. The aim of this study is to know about the expression of MMP-8 and IL-8 during the periapical tissue damage due to induction of E.faecalis. Method. This study used laboratory experimental with the post test only control group design. A total of 54 male rats were randomly divided into 2 main groups, which each main group had 3 subgroups. Group A (control) : every tooth was induced only by sterile BHIb. Group A had 3 subgroups (A Control day 3, 10, and 21), group B : every tooth was induced by 10 μl BHI-b E.faecalis ATCC212(106 CFU), it was contained 3 sub groups (B day 3,10, and 21). The animals were sacrificed based on their days scheduled group and prepared for histological examination of tissue damage, then we did the immunohistochemistry followed by calculation on the light microscope. Result. The analysis revealed that the expression of MMP-8 and IL-8 increased significantly in group B when E.faecalis was induced. Conclusion. From this study we know that the expression of MMP-8 and IL-8 are increasing during the periapical tissue damage that induced by E.faecalis.
Siquera JF Jr and Rocas IN. 2004. Polimerase Chain Reaction Based Analysis of Microorganisms Asociated with Failed Endodontic Treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 97 : 85-90.
Hancock HH, Sigurdsson A, Trope M dan Moiseiwitsch J. 2001. Bacteria Isolated After Unsuccessful Endodontic Treatment in A North American Population. Journal Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology Endodontics, 91:579-86.
Baik JE, Han JY and Kum KY. 2008. Lipoteichoic Acid Partially Contributes to The Inflammatory Responses to Enterococcus faecalis. J.Endod. 34(8) : 975-982
S. Liapatas, M. Nakou, and D. Rontogianni, "Inflammatory infiltrate of chronic periradicular lesions: an immunohistochemical study,” International Endodontic Journal, vol. 36, no. 7, pp. 464–471, 2003.
Wahjuningrum, Dian Agustin.2011. Patogenesis Molekuler Resorbsi Tulang Alveolaris pada Periodontitis Apikalis akibat induksi LPS di dalam Saluran Akar Gigi. Disertasi Program Studi Ilmu Kedokteran Jenjang Doktor. Universitas Airlangga
Stashenko et al., 2007. Th1 Immune Response Promotes Severe Bone Resorption Caused by Porphyromonas gingivalis. American Journal of Pathology.170: Pp.203-13
Stuart CH, Schawrtz SA, Beeson TJ and Owatz CB. 2006. Enterococcus faecalis :Its Role in Root Canal Treatment Failure and Current Concepts in Re-Treatment. JOE. 32 (2) : 93-98.
Chaves DPL. 2004. Gram-Positive Organisms in Endodontic Infections. Endodontic Topics. 9 : 79-96.
Yuanita T. 2012. Mekanisme Imunopatobiologi Resorbsi Tulnag Periapikal Gigi Pada Program Studi Ilmu Kedoktteran Jenjang Doktor Universitas Airlangga
Abbas, A.K., Lichtman, A.H., dan Pober, J.S.(2010). Cellular and Molecular Immunology. Edisi ke-6. Philadelphia: WB Saunders Company. Hal 12-16
Rechenberg, Dan-K. Bostanci , Nagihan. Zehnder, Matthias. Belibasakis, Georgios N. Periapical fluid RANKL and IL-8 are differentially regulated in pulpitis and apical periodontitis.
Cecilia Oliveira SILVA, Alesandra. Rubio, FARLA Miriam. FONTES, Alexandra. Sampaio, CAMPOS Marcia. Neves, CAVALCANTI Bruno. 2009. Interleukin -1 Beta and Interlukin in healthy and inflamed dental pulps. J Appl Oral Sci 17 (5) : 527-32.
CDJ by Unair is licensed under a Creative Commons Attribution 4.0 International License.
1. The journal allows the author to hold the copyright of the article without restrictions.
2. The journal allows the author(s) to retain publishing rights without restrictions