Efek eugenol terhadap jumlah sel inflamasi pada pulpa gigi molar tikus Sprague Dawley

https://doi.org/10.22146/majkedgiind.8730

Raras Ajeng Enggardipta(1*), Tetiana Haniastuti(2), Juni Handajani(3)

(1) Universitas Gadjah Mada
(2) Departemen Biologi Mulut, Fakultas Kedokteran Gigi, Universitas Gadjah Mada, Yogyakarta, Indonesia
(3) Departemen Biologi Mulut, Fakultas Kedokteran Gigi, Universitas Gadjah Mada, Yogyakarta, Indonesia
(*) Corresponding Author

Abstract


Inflammatory cells infiltration after eugenol administration in Sprague Dawley rat’s molars. The purpose of this study was to determine effect of eugenol on inflammatory cells infiltration (neutrophils, macrophages and lymphocytes) in the inflamed dental pulp. Thirty male Sprague Dawley rats aged 3-4 months and weighed 300-350 g were randomly divided into 2 groups: treated and control groups. Rats were injected with ketamine HCl i.m. (0.1 ml/100 grams BW) before cavity preparation at occlusal surface of the upper molars. Cavity preparation was made using a round bur No.010 to pulp perforation. At the cavity base of treated group, 15 rats were given eugenol and of control group 15 rats were given aquadest, before filled with temporary filling. Three rats from each group were sacrificed at 1, 3, 5, 7 and 14 days after the cavity preparation. Rats were injected with ketamine HCl im (0.1 ml / 100 g BW) on the thigh then tissues were collected for histological process and stained using haematoxylin eosin. The number of inflammatory cells (neutrophils, macrophages and lymphocytes) was analysed by Two-Way Anova. The result of the study showed number of inflammatory cells infiltration of treated group was lower than control and showed significant differences between groups (p <0.05). The conclusion from this study is eugenol administration in Sprague Dawley rats’s inflamed dental pulp can reduce the number of inflammatory cells (neutrophils, macrophages and lymphocytes).


ABSTRAK

Penelitian ini bertujuan untuk mengetahui pengaruh eugenol terhadap jumlah sel inflamasi (netrofil, makrofag dan limfosit) pada pulpa gigi terinflamasi. Tiga puluh ekor tikus Sprague Dawley jantan berumur  3-4 bulan dengan berat badan 300-350 g dibagi secara acak dalam 2 kelompok yaitu perlakuan dan kontrol. Tikus diinjeksi ketamine HCl i.m. (0,1 ml/100 gram BB) sebelum dilakukan preparasi kavitas pada permukaan oklusal gigi molar satu rahang atas. Preparasi kavitas dibuat dengan menggunakan bur bulat No.010 hingga kedalaman pulpa. Pada dasar kavitas kelompok perlakuan (15 ekor) diberi eugenol dan kelompok kontrol (15 ekor) diberi akuades, kemudian kavitas ditumpat sementara. Tiga ekor tikus dari masing-masing kelompok dikorbankan pada 1, 3, 5, 7 dan 14 hari pasca preparasi kavitas. Tikus diinjeksi ketamine HCl i.m. (0,1 ml/100 gram BB) pada paha kemudian jaringan diambil, diproses secara histologis dan dicat dengan hematoxylin eosin. Data jumlah sel inflamasi (netrofil, makrofag dan limfosit) dianalisis dengan Two Way Anova. Hasil penelitian menunjukkan rerata jumlah infiltrasi sel inflamasi kelompok perlakuan lebih rendah dibandingkan kontrol dan berbeda bermakna (p<0,05). Kesimpulan dari penelitian ini adalah pemberian eugenol pada pulpa gigi tikus Sprague Dawley yang mengalami inflamasi dapat menurunkan jumlah sel inflamasi (netrofil, makrofag dan limfosit).



Keywords


eugenol; pulpitis; inflammatory cells

Full Text:

PDF


References

Walton RE, Torabinejad M. Prinsip dan praktik ilmu endodonsia terj. Edisi 3. Penerbit Buku Jakarta: Kedokteran EGC; 2008.

Mj r IA. Pulp-dentin biology in restorative dentistry. Chicago: Quintessence Publishing Co.Inc.; 2002.

Dondy. Standard Operating Procedure Poli Gigi di Puskesmas [Internet]. 2009 [diakses 8 September 2014]. http://www.scribd.com/ doc/16732277/SOP-poli-gigi-puskesmas.

Chen G, Sung Po-Ta. Gingival and localized alveolar bone necrosis related to the use of arsenic trioxide paste- two case reports. J Form Med Assoc. 2014; 113(3): 187 – 190.

Garip H, Salih IM, Sener BC, Gӧker K, Garip Y. Management of arsenic trioxide necrosis in the maxilla. JOE. 2004; 30(10): 732 – 736.

Özmeriç N. Localized alveolar bone necrosis following the use of an arsenical paste: a case report. Int Endod J. 2002; 35(3): 295 – 299.

Dumlu A, Yalcinkaya S, Olgac V, Güvercin M. Osteomyelitis due to arsenic trioxide use for tooth devitalization. Int Endod J. 2007; 40(4): 317 – 322.

Departemen Kesehatan RI. Pedoman pengobatan dasar di Puskesmas 2007, Jakarta: Direktorat Jenderal Bina Kefarmasian Departemen Kesehatan RI; 2008.

Tronstad L. Clinical endodontology: a textbook 2nd ed. Stuttgart :Thieme; 2003.

Javdani M, Nikousefat Z. Research opinion in animal and veterinary science. Res Op Anim Vet Sci. 2012; 2(2): 141 – 144.

Chung G, Oh SB. Eugenol as local anesthetic, dalam natural products, Editor: Ramawat KB, Mérillon JM. Berlin: Springer Berlin Heidelberg; 2013.

Magalhães CB, Riva DR, DePaula LJ, Brando-Lima A, Koatz VL, Leal-Cardoso JH, Zin WA, Faffe DS. In vivo anti-inflammatory action of eugenol on lipopolysaccharide- induced lung injury. J App Phys. 2010; 108(4): 845 – 851.

Grespan R, Paludo M, Lemos P, Barbosa CP, Bersani-Amado, Dalalio MM, Cuman RK. Anti- arthritic effect of eugenol on collagen-induced arthritis experimental model. Biol Pharm Bulletin. 2012; 35(10): 1818 – 1820.

Ingle JI, Bakland LK. Endodontics 5th ed. USA: PMPH; 2002.

Kumar V, Abbas AK, Fausto N, Mitchell R. Robbins basic pathology 8th ed. China: Saunders Elsevier; 2010.

Hargreaves KM, Berman LH. Cohen’s pathways of the pulp 11th ed. Missouri: Elsevier; 2011.

Feng Mei Yu, Yamaza T, Atsuta I, Danjo A, Yamashita Y, Kido MA, Goto M, Akamine A, Tanaka T. Sequential expression of endothelial nitric oxide synthase, inducible nitric oxide synthase, and nitrotyrosine in odontoblasts and pulp cells during dentin repair after tooth preparation in rat molars.Cell Tissue Res. 2007; 328: 117 – 127.

Roitt IM. Essential immunology 8th Ed. Jakarta: Widya Medika; 2002.Kolaczkowska E, Kubes P. Neutrophil recruitment and function in health and inammation. Nature Reviews Immun. 2013; 13(3): 159 – 175.

Kumar V, Abbas A, Fausto N. Robbins and Cotran, Pathologic basis of disease 8th Ed. Philadelphia: Saunders: 2006.

Levin LG, Rudd A, Bletsa A, Reisner H. Expression of IL-8 by cells of the odontoblast layer in vitro. Eur J Oral Sci.1999; 107(2): 131

– 137.

Gensel JC, Zhang B. Macrophage activation and its role in repair and pathology after spinal cord injury. Brain Res. 2015; 1619: 1 – 11.

Gehrig SJ, Wilmann DE. Foundation of periodontics for the dental hygienist. Illinois: Wolter Kluwer; 2008.

Luo HR, Loison F. Constitutive neutrophil apoptosis: mechanism and regulation. American J Hem. 2008; 83(4): 288 – 295.

Velnar T, Bailey T, Smrkolj V. The wound healing process: an overview of the cellular and molecular mechanisms. J Int Med Res. 2009; 37: 1528 – 1542.

Roy S, Bagchi D, Raychaudhuri SP. Chronic inflammation: molecular pathophysiology, nutritional and therapeutic interventions. New York: CRC Press; 2013.

Fitridge R, Thompson M. Mechanism of vascular disease: a reference book for vascular specialists. Adelaide: The Barr Smith Press; 2011.

Burzyn D, Benoist C, Mathis D. Regulatory T cells in nonlymphoid tissues. Nature Immun. 2013; 14; 1007 – 1013.

Regan MC, Barbul A. The cellular biology of wound healing [Internet]. 2015 [diakses 12 November 2015]. www.neuro.ki.se/neuro/ KK2/Jimmy_GoogleCACHE1.html.

Raja MRC, Srinivasan V, Selvaraj S, Mahapatra SK. Versatile and synergetic potential of eugenol: a review. Pharmaceutica Analytica Acta.2015; 6: 367.

Larjava H. Oral wound healing: cell biology and clinical management. United Kingdom: John Wiley and Sons Inc; 2012.



DOI: https://doi.org/10.22146/majkedgiind.8730

Article Metrics

Abstract views : 6080 | views : 14505

Refbacks

  • There are currently no refbacks.




Copyright (c) 2017 Majalah Kedokteran Gigi Indonesia

Creative Commons License
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.


 

 View My Stats


real
time web analytics