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DAFTAR PUSTAKA

Baehni, P., Tsai, C.C., McArthur, W.P., Hammond, B.F.& Taichman, N.S.

1979. Interaction of inflammatory cells and oral microorganisms.

VIII. Detection of leukotoxic activity of a plaque-derived gram

negative microorganism. Infection and Immunity, Vol. 24, No. 1;

hal.233-243

Baratawidjaja KG. 2004. Imunologi Dasar Edisi Ke 6. Jakarta: Balai Penerbit

Fakultas Kedokteran Universitas Indonesia; hal 153-170

Beck James D, Elter John R, Gerardo Heiss, et al. 2001. Relationship of

Periodontal Disease to Carotid Artery Intima-Media Wall

Thickness: The Atherosclerosis Risk in Communities (ARIC) Study.

Journal of American Heart Association. Arteroiscler Thromb Vasc

Biol; hal 1816-1822

Carranza FA, Newman MG.1990. Clinical Periodontology Edisi Ke 1;

hal.424

Clark RA, Page RC, Wilde G. 1977. Defective Neutrophil Chemotaxis in

Juvenile Periodontitis. Infect Immun; 18;694

Damjanov, Ivan. 2000. Histopatologi. Jakarta: Widya Medika: hal. 23-24.

Derren Ready. 2011. Study offers new insights into link between oral hygiene and

heart health; [Available at http://scopeblog.stanford.edu/files/2011/07/

Actinobacillus_actinomycetemcomitans.jpg]

Darveau R.P. 2010. Periodontitis: a polymicrobial disruption of host homeostasis.

Nature Review Microbiology; hal.481-490.

de Haar SF. Hiemstra, P.S., van Steenbergen, M.T., Everts, V. & Beertsen, W.

2006. Role of polymorphonuclear leukocyte-derived serine proteinases in

defense against Actinobacillus actinomycetemcomitans. Infection and

Immunity; hal 5284-5291

Devijanti. 2012. Characterizationof fimbrial adhesin and OMP from

Actinobacillus actinomycetemcomitans clinical isolate as a material to

manage aggressive periodontitist patient.

ADLN - PERPUSTAKAAN UNIVERSITAS AIRLANGGA

SKRIPSI EFEK INDUKSI PROTEIN ADHESIN ... AHMAD AFIF DZULFIQAR

Doig P, Todd T, Sastry PA, Lee K, Hodges Rs, Paranchych W and Irvin RT.

1988. Role od Pili in Adhesion of Pseudomonas aureginosa to Human

Respiratory Epithelial Cells. Infect Imun

Dumitrescu AL. 2006. Histological comparison of periodontal inflammatory

changes in two models of experimental periodontitis the rat: a pilot study.

TMJ; hal 56 (2) : 211-217

Ebersole, J.L. 2003. Humoral immune responses in gingival crevice fluid: local

and systemic implications. Periodontology 2000, Vol. 31, No. 1; hal135–

166

Fankhauster DB. Histology of circulation system. 2010. Batavia Ohio: University

of Cincinnati Clermont College [internet]. [updated 09 April 2010; cited

2013 Mei]; Available from: http://biology.clc.uc.edu.

Feng Z and Weinberg A, 2006. Role of Bacteria in Health and Disease of

Periodontal Tissues. Periodontology 2000; hal. 40:50-76

Fine, D. H., Kaplan, J. B., Kachlany, S. C. & Schreiner, H. C. (2006). How we got

attached to Actinobacillus actinomycetemcomitans: a model for infectious

diseases. Periodontology 2000; pp.114-157

Guyton AC, Hall JE. 2007. Buku Ajar Fisiologi Kedokteran. Edisi ke-11. Jakarta:

EGC;. hal 150-70

Haber J, Wattles J, Crowley M, et al. 1993. Evidence for cigarette smoking as a

major risk factor for periodontitis. J Periodontol; hal. 64:16.

Haubek D. 2010. The highly leukotoxic JP2 clone of Aggregatibacter

actinomycetemcomitans: evolutionary aspects, epidemiology and

etiological role in aggressive periodontitis; hal.1–53

Henderson B, Ward JM, Ready D, 2010. Aggregatibacter (Actibacillus)

actinomycetemcomitans : a triple A periodontopathogen Periodontology

2000; hal 54:78-105

Herzberg, M. C., dan Meyer, M. C., 1966. Effects of Oral Flora on Platelets :

Possible Consequences in Cardiovascular Disease, M.I. J. Periodontol, 67

; hal 1138- 1142.

Hoffbrand AV, Petit JE. 2005. Essential Haematology. Edisi 4. Jakarta:

Penerbit Buku Kedokteran EGC; hal 104-9



Jancquira LC, Carneiro J. 2005. Basic Histology Text and Atlas. New York:

McGraw-Hill Companies;. hal 223-36.

Jawetz, Melnick, Adelberg. 2005. Mikrobiologi Kedokteran. Jakarta: Salemba

Medika; hal 169.

Johansson A., Claesson R., Hänström L., Sandström G. & Kalfas S. (2000b).

Polymorphonuclear leukocyte degranulation induced by leukotoxin from

Actinobacillus actinomycetemcomitans. Journal of Periodontal Research, ;

hal 85-92

Johansson A., Sandström, G., Claesson, R., Hänström, L. & Kalfas, S. (2000c).

Anaerobic neutrophil-dependent killing of Actinobacillus

actinomycetemcomitans in relation to the bacterial leukotoxicity.

European Journal Oral Science; hal 136–146

Kachlany, S. C., P. J. Planet, R. DeSalle, D. H. Fine, D. H. Figurski, and J. B.

Kaplan. 2001. flp-1, the first representative of a new pilin gene subfamily,

is required for non-specific adherence of Actinobacillus

actinomycetemcomitans. Mol. Microbiol. hal.542-554

Kantarci A.M., Oyaizu, K. & Van Dyke, T.E. (2003). Neutrophil-mediated tissue

injury in periodontal disease pathogenesis: findings from localized

aggressive periodontitis. Journal of Periodontology, Vol. 74, No. 1,

hal.66-75

Kantarci A. & Van Dyke, T.E. 2005. Resolution of inflammation in periodontitis.

Journal of Periodontology; hal.2168-2174,

Kinane D.F. & Lappin, D.F. 2002. Immune processes in periodontal disease: a

review. Annals of Periodontology; hal.62-71

Kler, Shikha & Rajvir Malik. 2010. An Update on the Virulence Factors ofV

Actinobacillus actinomycetemcomitans - A Systematic Review. A Journal

of DentistryVolume 1, Issue 1, November, 2010; hal 1-10

Korman KS. 2000. Genetics factors in the pathogenesis of periodontitis of

Actinobacillus actinomycetemcomitans. Periodontol; hal. 20:135-167.

Lamont RJ and Yilmaz O. 2002. In or out: the invasiveness of oral bacteria.

Periodontology 2000; hal 30:61-69



Lamster I.B. & Novak, M.J. 1992. Host mediators in gingival crevicular fluid:

implications for the pathogenesis of periodontal disease. Critical Review

in Oral Biology and Medicine; hal.31-60

Lang N , Bartold PM, Cullinan M, et al. 1999. Consensus Report: Aggressive

periodontitis. Ann Periodontol; hal 4:53.

Leino L, Hurttia H. 1999. A potential role of an intracellular signaling defect in

neutrophil functional abnormalities and promotion of tissue damage in

patients with localized juvenile periodontitis. Clin Chem Lab Med; hal.

37:215.

Lemeshow S, Davin WH Jr. 1997. Besar Sampel dalam Penelitian Kesehatan

(terjemahan). Yogyakarta : Gadjahmada University Press.

Lopez NJ. 1992. Clinical, laboratory and immunological studies of a family with

a high prevalence of generalized prepubertal and juvenile periodontitis. J

Periodontol ; hal 63:457.

Manson JD., Eley Bm. 1993. Buku Ajar Periodonti. Ed.2. Outline of Periodontics.

Editor Susianti Kentjana. Jakarta : Hipokrates

Manson JD, Lehner T. 1974. Clinical features of juvenile periodontitis

(periodontosis). J.Periodontol ; hal. 45:636.

Marazita ML, Burmeister JA, Gunsolley JC, et al. 1994. Evidence for autosomal

dominant inheritance and race-specific heterogeneity in early-onset

periodontitis. J Periodontol; hal. 65:623.

Meyer DH, Lippman JE, Fives-Taylor PM. 1996. Invasion of epithelial cells by

Actinobacillus actinomycetemcomitans: a dynamic multistep process.

Infect Immun; hal. 64: 2988– 2997.

Meyer DH, Rose JE, Lippman JE, Fives-Taylor PM. 1999. Microtubules are

associated with intracellular movement and spread of the

periodontopathogen Actinobacillus actinomycetemcomitans. Infect

Immun; hal 67: 6518– 6525.

Newman MG, Takei N, Klokkevold P,2006. Carranza’s Clinical Periodontology.

10th ed. WB Saunders Co. Philadelphia, New York, London,

hal.168- 181, 409-414, 675-668



Oelschlaeger TA, Hacker J. 2000. Bacterial invasion into eukaryotic cells. New

York, Kluwer Academic.

Per Klemm, Mark A. Schembri. 2000. Bacterial adhesins: function and structure.

International Journal of Medical Microbiology; hal 290 (1): 27–35.

Pihlstrom, B.C., Michalowicz, B.S. & Johnson, D.W. 2005. Periodontal diseases.

Lancet, Vol. 366, No. 9499; hal 1809-1820

Prince SA and Wilson LM. 2006. Patofisiologi Konsep Klinis Proses-Proses

Penyakit Volume I Edisi 6. Editor Bahasa Indonesia: Huriawati Hartant

dkk. Jakarta: Penerbit Buku Kedokteran EGC; hal 247-55.

Pütsep K., Carlsson, G., Boman, H.G. & Andersson, M. 2002. Deficiency of

antibacterial peptides in patients with morbus Kostmann: an observation

study; hal.1144-1149

Riskesdas. 2007. Laporan Hasil Riset Kesehatan Dasar (Riskesdas) Nasional.

Hal.130-2

Robbins & Kumar. 1995. Buku Ajar Patologi 1 edisi 4. Jakarta: EGC:

hal.23,28,29,33

Roitt, Ivan. Immunology essential Edisi 8..Editor Bahasa Indonesia: Alida

Harahap et al. 2003. Jakarta: Widya Medika;. hal 4-5.

Schenkein JA, Gunsolley JC, Koertge TE, et al. 1995. Smoking and its effects on

early-onset periodontitis. J Am Dent Assoc; hal 126:1107.

Soini Y., Paako P. and LehtoV-P.1997. Histopathological Evaluation of Apoptosis

in Cancer. American Journal of Pathology; hal 153(4): 1041-1048.

Taichman, N.S., Dean, R.T. & Sanderson, C.J. 1980. Biochemical and

morphological characterization of the killing of human monocytes by a

leukotoxin derived from Actinobacillus actinomycetemcomitans. Infection

and Immunity, Vol. 28, No. 1; hal 258-268

Todar Kenneth. 2008. Colonization and Invasion by Bacterial Pathogens.

Wisconsin :Todar’s Online Text Books of Bacteriology; hal 4 ; Available

from http://www.textbookofbacteriology.net



http://www.textbookofbacteriology.net/

Tsai, C.C., McArthur, W.P., Baehni, P.C., Hammond, B.F. & Taichman, N.S.

1979. Extraction and partial characterization of a leukotoxin from a

plaque-derived Gram-negative microorganism. Infection and Immunity,

Vol. 25, No. 1; hal 427-439

Tonetti MS, Mombelli A. 1999. Early-onset periodontitis. Ann Periodontol;

hal.4:39.

Velden V, Abbas F, Armand S, Loos BG, Timmerman MF, Weijden V, 2006.

Java project on periodontal disease. The Natural Development Of

Periodontitis : risk factor, risk predictor and risk determinants. J Clin.

Periodontal.33 hal :540 – 49

Wilson M, McNab R, Henderson B. . 2002. Bacterial disease mechanisms: an

introduction to cellular microbiology. Cambridge, Cambridge University

Press

Wolf HF, Rateitschak, and Hassel TM, 2004. Colour Atlas of Dental Medicine.

Periodontology.

Zambon, J.J., Slots, J. & Genco, R.J. 1983. Serology of oral Actinobacillus

actinomycetemcomitans and serotype distribution in human periodontal

disease. Infection and Immunity; hal.19-27,

Zhou Q, Desta T, Fentom M, Graves DT, Amar s, 2005. LPS cytokines profiling

of macrophage exposed to Porphyromonas gingivalis, its

lipopolysacharide, or its FimA protein, Infect Immun; hal 73(2): 935-942



Lampiran A Keterangan Laik Etik ADLN - PERPUSTAKAAN UNIVERSITAS AIRLANGGA


Lampiran B Prosedur Penelitian yang Telah Dilakukan Sebelumnya

1. Persiapan Bakteri

Bakteri A. actinomycetemcomitans diambil dengan cara swab pada

jaringan gingival penderita periodontitis agresif di klinik periodonsia FKG

Universitas Airlangga. Bakteri A. actinomycetemcomitans di kultur pada

media AAGM. Identifikasi A.actinomycetemcomitans dari pederita

periodontitis agresif dilakukan dengan pemeriksaan mikroskopis,

menggunakan uji fermentasi dan dengan pemeriksaan PCR.

2. Persiapan Protein Adhesin A. actinomycetemcomitans

Protein adhesin A.actinomycetemcomitans yang digunakan adalah

protein adhesin dengan berat molekul 24 kDa sebanyak 4000 µL. Setiap

perlakuan menggunakan adhesin sebanyak 200µL dengan kadar protein

sebesar 200 µL

3. Persiapan Hewan Coba

Penelitian ini menggunakan tikus Wistar karena tikus ini memiliki

genom yang hampir mirip atau homolog dengan manusia, serta merupakan

hewan model untuk penyakit periodontal (Dumitrescu, 2006). Adaptasi tikus

dilakukan selama 7x24 jam .Tikus Wistar dibagi dalam 4 kelompok yang

nantinya tiap kelompok akan diberi perlakuan yang berbeda, masing –

masing kelompok terdiri dari 10 ekor tikus.



4. Pemeriksaan Ketiadaan Bakteri A.actinomycetemcomitans pada

Rongga Mulut Tikus

Sebelum tikus dilakukan perlakuan, dilakukan pemeriksaan ada

tidaknya bakteri A.actinomycetemcomitans di dalam rongga mulut tikus.

Identifikasi A.actinomycetemcomitans dilakukan dengan melakukan swab di

pada jaringan gingival di dalam rongga mulut tikus tikus, kemudian dikultur

dan dilakukan identifikasi ada tidaknya bakteri A.actinomycetemcomitans.

Identifikasi A.actinomycetemcomitans ini dimaksudkan bahwa perlakuan

yang diberikan pada tikus tersebut benar berasal dari

A.actinomycetemcomitans yang diinduksi dari luar rongga mulut tikus.

Namun secara teori hal ini bisa tidak dilakukan karena bakteri

A.actinomycetemcomitans bukan merupakan flora normal pada rongga mulut

tikus.

5. Induksi Protein Adhesin pada Tikus Wistar

Tikus dibagi dalam 4 kelompok perlakuan sesuai dengan prosedur

penelitian yaitu tikus di kelompok pertama merupakan kontrol negatif

dilakukan induksi dengan NaCl 0,9%, tikus di kelompok kedua diinduksi

dengan kombinasi bahan antara protein adhesin 24 kDa dan whole cell

A.actinomycetemcomitans masing masing sebanyak 200 µL dengan kadar

protein sebesar 200 µg/mL, sedangkan kepadatan A.actinomycetemcomitans

adalah sebesar 108 diberikan minimal 7 hari untuk mendapatkan gejala

periodontitis agresif yang nyata (Zhou et al., 2005). Gejala klinis yang



menandakan bahwa hewan coba dalam kondisi periodontitis adalah kondisi

poket yang menjadi lebih dalam, ligament periodontal rusak dan tulang

alveolar akan lebih tersorbsi (Manson and Eley, 1993). Induksi dilakukan

dibagian poket periodontal gigi molar pertama (M1) kanan atas tikus wistar

yang dilakukan sesuai dengan metode (Dumitrescu, 2006). Setelah itu

dilakukan pemeriksaan untuk mengetahui jumlah sel radang akut PMN

dengan pengecatan HE.



Lampiran C. Data Penelitian Hasil Penghitungan Jumlah Sel Radang Akut

PMN

Laboratorium Patologi Veteriner

Fakultas Kedokteran Hewan

Universitas Airlangga

Kampus C Mulyorejo Surabaya 60115 Telp. (031) 5992785, Fax (031) 5993015; email : [email protected]

HASIL PEMERIKSAAN HISTOPATOLOGI

Nama Pemilik : Sdr. Afif, Instansi : FKG UNAIR Alamat : Telepon : Sediaan : Ginggiva Pewarnaan : HE Waku Pemeriksaan : 20 September 2013 Pemeriksa : Djoko Legowo, MKes., drh Perubahan yang diamati dan Metode Pemeriksaan

Pemeriksaan ini dimaksudkan untuk mengetahui jumlah sel-sel radang, meliputi sel

Makrofag, Limfosit, Plasma, Neutrofil, Eosinofil dan Basofil serta sel fibroblast pada

ginggiva pasca perlakuan. Pemeriksaan dilakukan pada 5 lapangan pandang (LP) yang

berbeda terutama dilakukan pada pusat penyembuhan (healing center), serta area

disekitarnya. Seluruh pemeriksaan ini menggunakan mikroskop cahaya biasa merk Nikon

H600L yang dilengkapi dengan digital camera DS Fi2 300 megapixel dan soft ware

pengolah gambar Nikkon Image System pada pembesaran 1000x .



KODE PREPARAT

JUMLAH SEL/5 LAPANGAN PANDANG KETERANGAN

FIBRO LIMFO MAKRO PLASM NEUTR EOSIN BASOF

K1 4 - 6 - - - -

K2 41 6 11 - 14 - -

K3 5 - 3 - 1 - -

K4 13 2 15 - 3 - -

K5 5 3 12 - 5 - -

K6 12 4 22 - 7 - -

K7 43 29 31 6 4 - -

K8 7 19 16 3 9 - -

K9 4 7 5 - 1 - -

K10 - 7 3 - 2 - -

RERATA

II.1 13 2 3 - 26 - -

II.2 11 5 15 - 24 - -

II.3 148 17 32 4 122 - -

II.4 155 18 29 2 137 -- -

II.5 9 2 8 - - - -

II.6 48 1 2 - 30 - -

II.7 52 8 17 - 51 - -

II.8 29 6 3 2 24 - -

II.9 62 10 41 - 51 - -

II.10 36 1 17 - 9 - -

RERATA



KODE PREPARAT

JUMLAH SEL/10 LAPANGAN PANDANG KETERANGAN

FIBRO LIMFO MAKRO PLASM NEUTR EOSIN BASOF

III.1 16 - 3 - - - -

III.2 35 2 9 - 2 - -

III.3 31 9 6 - 12 - -

III.4 29 2 6 - 11 - -

III.5 9 - 5 - 8 -

III.6 41 18 4 - 10 - -

III.7 7 11 2 - 3 - -

III.8 5 6 13 - 7 - -

III.9 51 3 8 - 10 - -

III.10 14 2 6 - 5 - -

RERATA

IV.1 16 7 5 - 3 - -

IV.2 28 2 4 - 22 - -

IV.3 31 - -- -- - - -

IV.4 - - 5 - 5 - -

IV.5 6 3 3 - - - -

IV.6 4 - - - 2 - -

IV.7 41 - - - - - -

IV.8 16 5 3 - - - -

IV.9 31 2 7 - 12 - -

IV.10 39 1 5 - 2 - -

RERATA



Lampiran D. Analisis Data Penelitian

B.1 Rerata Jumlah Sel radang akut PMN Pada Berbagai Perlakuan

Statistics

kontrol perlakuan 1 perlakuan 2 perlakuan 3

N Valid 10 10 10 10

Missing 0 0 0 0

Mean 4.6000 47.4000 6.8000 4.6000

Std. Deviation 4.35125 46.18369 4.13118 7.13676

B.2 Uji Normalitas Kolmogorov-Smirnov

One-Sample Kolmogorov-Smirnov Test

kontrol perlakuan 1 perlakuan 2 perlakuan 3

N 10 10 10 10

Normal Parametersa,,b Mean 4.6000 47.4000 6.8000 4.6000

Std. Deviation 4.35125 46.18369 4.13118 7.13676

Most Extreme Differences Absolute .163 .269 .181 .289

Positive .163 .269 .121 .289

Negative -.145 -.152 -.181 -.260

Kolmogorov-Smirnov Z .517 .850 .571 .913

Asymp. Sig. (2-tailed) .952 .465 .900 .375

a. Test distribution is Normal.

b. Calculated from data.

B.3 Analisis One Way ANOVA

Oneway

Descriptives

jumlah neutrofil

N Mean Std. Deviation Std. Error

95% Confidence Interval for Mean

Minimum Maximum Lower Bound Upper Bound

1.00 10 4.6000 4.35125 1.37598 1.4873 7.7127 .00 14.00

2.00 10 47.4000 46.18369 14.60457 14.3622 80.4378 .00 137.00

3.00 10 6.8000 4.13118 1.30639 3.8447 9.7553 .00 12.00



4.00 10 4.6000 7.13676 2.25684 -.5053 9.7053 .00 22.00

Total 40 15.8500 29.21323 4.61902 6.5072 25.1928 .00 137.00

ANOVA

jumlah neutrofil

Sum of Squares Df Mean Square F Sig.

Between Groups 13304.300 3 4434.767 7.991 .000

Within Groups 19978.800 36 554.967

Total 33283.100 39

B.4 Post Hoc Test

Multiple Comparisons

jumlah neutrofil

Tukey HSD

(I)

kelompo

k

perlakua

n

(J)

kelompo

k

perlakua

n

Mean Difference

(I-J) Std. Error Sig.

95% Confidence Interval

Lower Bound Upper Bound

1.00 2.00 -42.80000* 10.53534 .001 -71.1741 -14.4259

3.00 -2.20000 10.53534 .997 -30.5741 26.1741

4.00 .00000 10.53534 1.000 -28.3741 28.3741

2.00 1.00 42.80000* 10.53534 .001 14.4259 71.1741

3.00 40.60000* 10.53534 .002 12.2259 68.9741

4.00 42.80000* 10.53534 .001 14.4259 71.1741

3.00 1.00 2.20000 10.53534 .997 -26.1741 30.5741

2.00 -40.60000* 10.53534 .002 -68.9741 -12.2259

4.00 2.20000 10.53534 .997 -26.1741 30.5741

4.00 1.00 .00000 10.53534 1.000 -28.3741 28.3741

2.00 -42.80000* 10.53534 .001 -71.1741 -14.4259

3.00 -2.20000 10.53534 .997 -30.5741 26.1741

*. The mean difference is significant at the 0.05 level.



Homogeneous Subsets

jumlah neutrofil

Tukey HSDa

kelompok

perlakuan N

Subset for alpha = 0.05

1 2

1.00 10 4.6000

4.00 10 4.6000

3.00 10 6.8000

2.00 10 47.4000

Sig. .997 1.000

Means for groups in

homogeneous subsets

are displayed.

a. Uses Harmonic Mean

Sample Size = 10.000.



Lampiran E. Foto Alat Penelitian

jj

Gambar C.1 Mikrotom (Sakura Accu-Cut SRM)

Gambar C.2 Hot Plate

Gambar C.3 Sediaan jaringan dalam parafin blok yang siap dipotong dengan mikrotom



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