Hasil Pencarian  ::  Simpan CSV :: Kembali

"Latar Belakang: Kerusakan jaringan periodontal terjadi karena inflamasi terhadap invasi bakteri. Human beta defensin-1 adalah peptida antimikroba dan pertahanan pertama terhadap infeksi.Tujuan Penelitian: Membandingkan kadar ekspresi HBD-1 antara kelompok periodontitis kronis, periodontitis agresif dan normalBahan dan Metode: Kadar HBD-1 dari 94 sampel CKG subjek periodontitis kronis, periodontitis agresif dan normal diukur dengan ELISAHasil: Analisis Mann-Whitney menunjukkan perbedaan kadar HBD-1 antara periodontitis kronis dengan normal (p<0,05) dan tidak terdapat perbedaan signifikan (p>0,05) antara periodontitis agresif dengan normal, dan antara periodontitis kronis dengan periodontitis agresif.Kesimpulan: Kadar HBD-1 pada CKG menurun pada kondisi periodontitis kronis dan periodontitis agresif.

---

Background: Periodontal disease is happened because inflammation reaction ro bacterial invasion. Human beta defensin-1 (HBD-1) is antimicroba peptide which regulate the first defense mechanism.

Objectives: To compare level of HBD-1 between chronic periodontitis, aggressive periodontitis, and normal group.

Material and Methods: Level of HBD-1 from GCF sample of chronic periodontitis, aggressive periodontitis, and normal group were assessed with ELISA.

Results: Mann-Whitney analysis show different level of HBD-1 expression between chronic periodontitis and normal (p<0,05) and there was no significant difference (p>0,05) between aggressive periodontitis and normal, and between chronic periodontitis and aggressive periodontitis.

Conclusion: Level of HBD-1 in GCF decreased in chronic periodontitis and aggressive periodontitis."

"Latar belakang: Periodontitis merupakan interaksi kompleks antara sitokin pro-inflamasi dan sitokin anti-inflamasi. Sitokin anti-inflamasi seperti IL-4 pada cairan krevikular gingiva (CKG) dapat menjadi biomarker penyakit periodontal.Tujuan Penelitian: Menganalisis perbedaan kadar IL-4 dalam CKG penderita periodontitis kronis dan periodontitis agresif.Metode dan Bahan: Sampel CKG dikumpulkan dari pasien normal (n=21), periodontitis kronis (n=38) dan periodontitis agresif (n=35) dan dilakukan analisis kadar IL-4 dengan menggunakan ELISA.Hasil: Terdapat perbedaan kadar IL-4 antara periodontitis kronis dengan normal dan antara periodontitis agresif dengan normal (p=0,000). Tidak ada perbedaan kadar IL-4 (p=0,729) antara periodontitis kronis (14,73±0,32 pg/ml) periodontitis agresif (20,58±23,00 pg/ml).Kesimpulan: Kadar IL-4 menurun pada kondisi inflamasi, baik pada periodontitis kronis ataupun periodontitis agresif.

---

Background: Periodontitis is a complex interaction between pro-inflammatory and anti-inflammatory cytokine. IL-4 is an anti-inflammatory cytokine in GCF that can be used as a periodontal biomarker.

Objectives: To compare level of IL-4 in GCF of chronic periodontitis and aggressive periodontitis.

Material and Methods: GCF sample were collected from normal (n=21), periodontitis chronic (n=38) and aggressive periodontitis (n=35) group and analysis of level IL-4 was performed with ELISA.

Results: There was a difference level of IL-4 between chronic periodontitis with normal and between aggressive periodontitis with normal (p=0,000). There was no difference level of IL-4 (p=0,729) between chronic periodontitis (14,73±0,32 pg/ml) and aggressive periodontitits (20,58±23,00 pg/ml).

Kesimpulan: Level of IL-4 was decreased in inflammation condition, either chronic periodontitis or aggressive periodontitis."

"Latar belakang: Suatu biomarker imunologis diperlukan untuk kasus yang berbatasan antara periodontitis kronis dan periodontitis agresif. Matrix Metalloproteinase-8 (MMP-8) merupakan suatu biomarker penentu risiko dan derajat keparahan penyakit periodonal serta evaluasi hasil perawatan periodontal. Tujuan: Menganalisis kadar MMP-8 pada cairan krevikular gingiva penderita periodontitis kronis dan periodontitis agresif. Metode: Penelitian ini mencakup 12 pasien periodontitis agresif, 17 pasien periodontitis kronis dan 6 subjek sehat. Kadar MMP-8 diukur dengan teknik ELISA. Hasil: Kadar MMP-8 pada periodonitits kronis tidak berbeda bermakna dengan periodontitis agresif (p>0,05). Kesimpulan: MMP-8 tidak dapat digunakan sebagai acuan diagnosis.

---

Background: An immunologic biomarker is needed to distinguish between borderline cases between chronic periodontitis and agressive periodontitis. Matrix Metalloproteinase-8 (MMP-8) can be a risk profile of periodontal disease, disease progression and evaluation of periodontal treatment.

Aim: Analyze MMP-8 levels in gingival crevicular fluid of chronic and aggressive periodontitis patients.

Method: Sampel was collected from 6 healthy subjects, 12 subjects aggressive periodontitis and 17 chronic periodontitis subjects. MMP-8 levels were measured with ELISA.

Result:MMP-8 levels in chronic periodontitis did not show any difference to the MMP-8levels in aggressive periodonitits (p>0,05).

Conclusion: MMP-8 can not serve as a diagnostic parameter."

"Latar Belakang: Periodontitis merupakan faktor risiko terjadinya Penyakit Jantung Koroner (PJK). Interleukin-1β merupakan sitokin pro-inflamasi utama yang dapat ditemukan pada kedua penyakit ini. Tujuan: Menganalisis hubungan kadar interleukin-1β dalam cairan sulkus gingiva (CSG) penderita PJK dan non PJK dengan status periodontal. Metode: Pemeriksaan klinis 40 subjek PJK dan 40 subjek non PJK, pemeriksaan laboratorium kadar Interleukin-1β dengan ELISA. Hasil : Tidak terdapat perbedaan bermakna Interleukin-1β antara penderita PJK dan non PJK (p>0,05); tidak terdapat perbedaan bermakna antara kadar Interleukin-1β dengan status periodontal penderita PJK dan non- PJK (p>0,05). Kesimpulan: Kadar Interleukin-1β penderita PJK tidak memiliki hubungan dengan status periodontal.

---

Background: Periodontitis is a risk factor for coronary heart disease. Interleukin-1β as a pro-inflammatory main cytokine, can be found in this both diseases.

Objective: To analyze the relationship of interleukin-1β levels in CSG CHD and non-CHD patients with periodontal status.

Methods: Clinical Examination for 40 Subject CHD and 40 controls was checked, laboratory test for measured the levels of Interleukin-1β with ELISA.

Results: There were no significant differences between patients Interleukin-1β CHD and non-CHD (p>0.05); there is no significant difference between the levels of Interleukin-1β with periodontal status CHD and control patients (p>0.05).

Conclusions: Levels of Interleukin-1β of CHD patients do not have a relationships with periodontal status."

"Latar Belakang: Periodontitis merupakan inflamasi pada jaringan pendukung gigi yang disebabkan oleh mikroorganisme yang menyebabkan destruksi ligamen periodontal dan tulang alveolar, yang ditandai dengan peningkatan kedalaman poket, resesi, ataupun keduanya. Penyakit periodontal diderita oleh sebanyak 20-50% populasi dunia. Penyakit periodontal juga merupakan penyebab terbesar dari kehilangan gigi dan dipertimbangkan menjadi salah satu dari dua ancaman terbesar pada rongga mulut. Salah satu faktor hospes yang berperan penting dalam periodontitis adalah faktor genetik, dan salah satunya yaitu gen MIF-173 G/C (rs755622). Gen MIF berperan dalam menginisiasi ataupun memodulasi respon inflamasi pada jaringan periodontal. Polimorfisme pada gen ini menyebabkan perubahan fungsi dalam regulasi makrofag dan penurunan glukokortikoid. Penelitian ini juga belum pernah dilakukan di Indonesia. Tujuan: Menganalisis gambaran polimorfisme gen MIF-173 G/C (rs755622) pada Penderita Periodontitis di Indonesia. Metode: Analisis polimorfisme gen MIF-173 G/C (rs755622) yang dilakukan dengan metode PCR-RFLP dan divisualisasikan menggunakan Gel Electrophoresis. Hasil: Penelitian ini menggunakan 155 sampel antara lain 76 sampel non-periodontitis dan 79 sampel periodontitis, ditemukan 70 sampel non-periodontitis memiliki genotip GG dan 6 sampel non-periodontitis memiliki genotip GC. Sedangkan kelompok periodontitis memiliki 73 sampel dengan genotip GG dan 6 sampel dengan genotip GC. Tidak ditemukan genotip CC pada sampel non-periodontitis maupun periodontitis. Sementara frekuensi alel yang muncul yaitu 143 alel G dan 12 alel C. Kesimpulan: Tidak terdapat perbedaan bermakna pada distribusi polimorfisme gen MIF-173 G/C antara penderita periodontitis dengan individu sehat (p = 1,0).

---

Background: Periodontitis is an inflammation in periodontal caused by microoganism. It induces periodontal ligament and alveolar bone destruction, which are marked by pocket increased, recession, or both. Periodontal disease were affected by 20-50% of world’s population. Also, periodontal disease is one of the biggest causes of tooth loss and is considered to be one of the two biggest threats to the oral cavity. One of the host factors that play an important role in periodontitis is genetic factors, and one of them is the MIF-173 G / C (rs755622) gene. The MIF gene is involved in initiating or modulating the inflammatory response in periodontal tissues. Polymorphism in this gene causes a change in function of macrophage regulation and glucocorticoids reduction. This research has also not been conducted in Indonesia. Objective: To analyze the polymorphism of MIF-173 G/C (rs755622) gene in periodontitis patients in Indonesia. Methods: Analysis of MIF-173 G/C (rs755622) gene polymorphism carried out by PCR-RFLP method and visualized using Gel Electrophoresis. Results: This study used 155 samples including 76 healthy control samples and 79 periodontitis samples, were found 70 control samples had GG genotypes and 6 control samples had GC genotypes. While the periodontitis group had 73 samples with GG genotype and 6 samples with GC genotypes. CC genotypes were not found in the control sample or periodontitis. While the frequency of alleles that emerged were 143 G alleles and 12 alleles C. Conclusion: There were no significant differences in the distribution of MIF-173 G/C gene polymorphisms between periodontitis patients and the healthy ones (p = 1.0)."

"Latar Belakang: Periodontitis kronis merupakan penyakit multifaktorial yang terjadi akibat interaksi respon host terhadap agregasi bakteri pada poket gingiva. Peran human beta-defensin-1 sebagai peptida antimikroba pada perokok dengan periodontitis kronis masih belum jelas. Tujuan: Menganalisa kadar Human beta defensin-1 pada perokok penderita periodontitis kronis. Bahan dan Metode: Seratus empat subjek berusia 33-78 tahun didiagnosis periodontitis kronis pada Departemen Periodonsia, Rumah Sakit Khusus Gigi Mulut Fakultas Kedokteran Gigi Universitas Indonesia. Penelitian ini merupakan desain penelitian potong lintang dengan pemeriksaan klinis dan laboratoris. Pengumpulan data di dapat secara anamnesis, pemeriksaan klinis (OHIS, kedalaman poket, CAL) serta status merokok. Sampel lalu disimpan di suhu -20°C hingga uji laboratoris dilakukan. Sampel dipilih secara consecutive sampling dan dideteksi dengan uji ELISA. Hasil: Berikut adalah nilai median (minimum-maksimum) dari kadar human beta-defensin-1. Kadar human beta-defensin-1 pada kelompok periodontitis kronis kelompok ringan-sedang adalah 57,61(.87-343.58) pg/ml sedangkan pada kelompok berat adalah 25,04(0.94-198.03) pg/ml dengan nilai kemaknaan p=0,087. Kadar human beta-defensin-1 pada periodontitis kronis bukan perokok adalah 27,82 (0.92-200.58) pg/ml sedangkan pada perokok adalah 25,04 (0.87-343.58) pg/ml dengan nilai kemaknaan p=0,457. Kesimpulan: Tidak terdapat hubungan antara kadar human beta-defensin-1 pada periodontitis kronis terkait keparahan dan status perokok.

---

Background: Chronic periodontitis is a multifactorial disease that occurs due to the host response to the aggregation of bacteria in the gingival pocket. The role of human beta-defensin-1 as an antimicrobial peptide in a smoker’s periodontitis is still unclear.

Materials and Methods: In total 104, 33-78 years old subjects were diagnosed to have chronic periodontitis in the Department of Periodontology, Oral Disease Special Clinic of The University of Indonesia. This cross-sectional study included clinical and laboratory examination. The data collected included those from anamnesis, clinical examination (OHIS, pocket depth, CAL), and smoking status. The samples were stored in -20oC until testing for human beta-defensin-1 level by ELISA.

Results: The median (min-max) human beta-defensin-1 level in the group of mild to moderate chronic periodontitis was 57.61 (0.87-343.58) pg/ml and in the group of severe periodontitis 15.27 (0.94-198.03) pg/ml (p=0.087). The median (min-max) human beta-defensin-1 level in non-smokers with chronic periodontitis was 27.82 (0.92-200.58) pg/ml, and in smokers 25.04 (0.87-343.58) pg/ml (p=0.457).

Conclusion: There were no significant differences in the human beta-defensin-1 levels in subjects with chronic periodontitis regardless of the smoking status or severity of the disease."

"Generalized aggressive periodontitis is a disease or a disorder of periodontium that occurs in people below 30 years old. These patients usually have several immune response disorders, such as defects in chemotaxis, phagocytic of neturophils and monocytes, and genetic defect. Clinically, there are generalized losses of tissue attachment with extensive, rapid and progressive alveolar bone resorption. In order to repair bone destruction, treatment that produce bone regeneration is needed, i.e. full thickness flap with bone grafting. In these cases, allograft and alloplast bone grafts were used. Allograft is derived from subjects within the same species but different individuals, whereas alloplast is foreign body embedded into the tissue (e.g. hydroxylapatite). In this report, pocket depth, papillae bleeding index (PBI), and clinical attachment were evaluated. Six month after surgery and bone grafting, there were + 4 mm decrease of pocket depths, bleeding on probing index and 3-4 mm increase of clinical attachment. Unstimulated wholes saliva were also collected for DNA isolation. The IL-1beta(+3954) genotypes were performed by Polymerase chain reaction, digested with TagI restriction enzyme and separated by gel electrophoresis. Results showed both patients bearing allele 2 homozygous of IL-1B+3954 genotype. This genotype has been identified as the one of immunogenetic factor that could affect the severity of periodontal disease. Successful treatment depends on the adequacy of oral hygiene. Patients were advised to maintain optimal oral hygiene and to do periodic check every 2-3 months."

"ABSTRAKKondisi stres memiliki efek yang buruk terhadap respon imun, sehingga rentan akan infeksi, termasuk penyakit periodontal. Salah satu biomarker yang dapat mengindikasikan penyakit periodontal adalah interleukin-6 (IL-6). Tiga puluh delapan mahasiswa program profesi FKG UI. Subjek diinstruksikan untuk mengusi kuisioner Dental Environment Stress (DES) dan dilakukan pemeriksaan periodontal dan pengambilan sampel cairan krevikular gingiva serta dianalisis untuk mengetahui kadar IL-6 dengan teknik ELISA. Walaupun uji statistik menunjukkan hubungan yang lemah antara tingkatan stres dengan kondisi periodontal dan kadar IL-6, kondisi klinis menunjukkan kecenderungan perburukan kondisi periodontal seiring peningkatan skor stres.

---

ABSTRACTStress conditions have a bad effect on the immune response, leading to an imbalance between the host and the parasite so susceptible to infections, including periodontal disease. One biomarker that can indicate periodontal disease is interleukin-6 (IL-6). Thirty eight samples were instructed to filled the Dental Environment Stress (DES) questionnaire, periodontal examination and gingival crevicular fluid were collected. Although statistical tests showed a weak relationship between stress levels and the periodontal condition levels of IL-6, showed a trend of worsening clinical condition of periodontal conditions with increases in stress scores."

"Latar belakang: Kondisi penyakit periodontal dapat diidentifikasi dengan pemeriksaan klinis dan radiografi.Pada teknik radiografi digitaldapat dilakukan image enhancement untuk memperbaiki kualitas gambar dengan mengoptimalkan brightness dan contrast. Tujuan :Mengetahui batasan valueyang dapat ditoleransi pada pengaturan brightnessdan contrast pada kasus periodontitis mild - moderate.Metode :Dilakukan image enhancementdengan mengubah brightnessdan contrastpada 100 radiograf dengan kasus periodontitis mild-moderatedengan interval poin -20,-10, +10 dan +20 pada setiap sampel pada masing-masing kelompok menggunakan program software Digora for Windows. Hasil :Valueyang dapat ditoleransi pada pengaturan brightness pada kasus periodontitis mild-moderateberkisarpada valuedibawah +10 dan yang dapat ditoleransi dalam pengaturan contrastberkisardari valuediatas -20.Kesimpulan :Pengaturan brightnessdan contrastdilakukan pada valuetersebut tidak akan mempengaruhi ataupun mengubah interpretasi radiografik periodontitis mild - moderatejika dilakukan pada value toleransinya.

---

Background :Periodontal disease condition can be checked by clinical and radiograph examination. In digital radiography techniques, image enhancement can be done to improve image quality by optimizing brightness and contrast. Objective :To determine the limit of values that can be tolerated in brightness and contrast setting in mild-moderate periodontitis cases. Methods :Adjust the image enhancement setting by changing the brightness and contrast of 100 radiographs with mild-moderate periodontitis with points intervals of -20, -10, +10 and +20 each sample in each group using the Digora for Windows. Result :Values that can be tolerated in brightness setting in interpretation of mild-moderate periodontitis rangeat values below +10 and values that can be tolerated in contrast setting rangefrom values above -20. Conclusion :Brightness and contrast adjustment made at these values will not affect the radiographic interpretation of mild-moderate periodontitis if carried out at their tolerance values."

"Inflamasi periodontal merupakan kelainan periodontal dengan prevalensi tinggi di masyarakat. Periodontitis kronis dipengaruhi oleh akumulasi plak dan kalkulus sebagai faktor local, ditambah faktor sistemis misalnya diabetes mellitus (DM) dan infeksi HIV. Sitokin terutama IL-1β sebagai mediator inflamasi utama penyakit periodontal, menstimulasi ekspresi iNOS (inducible nitric oxide synthase) dan produksi NO (nitric oxide) oleh sel β, menyebabkan disfungsi sel β. Leukotoksin dan protease yang dihasilkan patogen periodontal menyebabkan jejas kemotaktik dan fagositotik, dan menurunkan fungsi fagositosis PMN. Hiperglikemia pada penyandang DM menyebabkan peningkatan kadar kalsium sitosol (Ca2+), yang menyebabkan disfungsi PMN dan menurunkan fungsi fagositosis. Advanced glycosilation endproduct pada DM tipe 2 berikatan dengan monosit menyebabkan peningkatan sitokin proinflamasi (IL-1, TNFα) dan menyebabkan aktivasi makrofag dan osteoklas. Hiperglikemia menyebabkan aktivasi diasil gliserol (DAG)-protein kinase C (PKC), yang menyebabkan peningkatan PGE2 dan ekspresi sitokin yang mempengaruhi proses inflamasi dan destruksi. Penelitian tentang pengaruh scaling (pembersihan karang gigi sebagai tindakan non-bedah pada terapi periodontal) pada penyandang DM terhadap kadar gula darah dan respons imun selular belum pernah dilakukan di Indonesia. Penelitian ini bertujuan menganalisis pengaruh pembersihan karang gigi terhadap kadar IL-1β, fungsi fagositosis PMN dan kadar glukosa darah penyandang DM tipe 2. Subyek penelitian adalah penyandang DM tipe 2, 60 penyandang DM Terkendali dan 60 penyandang DM Tidak Terkendali di Poliklinik Metabolik-Endokrin RSUPN Ciptomangunkusumo, umur 40-60 tahun. Subyek dibagi menjadi kelompok perlakuan dan kelonpok tanpa perlakuan, untuk menilai respons imun selular dan status DM, sebelum dan 6 minggu sesudah perlakuan. Analisis statistik (t test) dengan komputer menggunakan perangkat Stata 7,0 dilakukan untuk membandingkan parameter sebelum dan sesudah scaling pada kedua kelompok. Hasil penelitian menunjukkan bahwa scaling dapat menurunkan kadar IL-1β dan meningkatkan fungsi fagositosis secara bermakna (P<0,05), menurunkan kadar glukosa puasa, glukosa 2 jam PP dan kadar HbA1c, tetapi penurunannya secara statistik tidak bermakna (P>0,05), kecuali penurunan kadar HbA1c pada DM Tidak Terkendali (P=0,00).

---

Abstract

Periodontal inflammation is a periodontal disorder of high prevalence in the population. Chronic periodontitis is associated with the accumulation of plaque and calculus as local factors, and systemic factors such an diabetes mellitus (DM) and HIV infection. Cytokine, especially IL-1β as inflammatory mediator for periodontal disease, may directly stimulated iNOS (inducible nitric oxide synthase) expression and NO (nitric oxide) production by β-cells, resulting in NO-mediated β-cell damage. The leucotoxin and proteases produced by periodontal pathogens will induce chemotactic and phagocytotic defect; therefore causing decreased PMN phagocytotic function. Hyperglicemia which occurs in diabetic patients increases calcium influx to the cell, resulting in the increased cytosol?s calcium ([Ca 2+]i) level and; therefore, resulting in dysfunction of PMN and impaired PMN phagocytotic function. Advanced glycosilation endproduct in NIDDM binds to monocytes resulting in the increase of pro-inflammatory cytokines (IL-1, TNFβ) and produces activation of macrophages and osteoclasts. Hyperglicemia activates diacyl glycerol (DAG)-protein kinase C (PKC), thus increasing PGE2 and cytokine expression that induce inflammation and periodontal tissue destruction processes. Studies on the effect of scaling to remove calculus disposition on blood glucose control and cellular immune response in DM patient has never been carried out. The aim of the study was to analyze the effect of scaling as non-surgical periodontal therapy on immune response (IL-1β level and PMN phagocytotic function) and blood glucose level of type 2 diabetic patients. Subjects were diabetic patients, 60 controlled-DM (CDM) and 60 uncontrolled-DM (UCDM), in Metabolic-Endocrinology Clinic of Ciptomangunkusumo Hospital, aged 40-60 years. The subjects were divided into treatment (scaling) and control group, and cellular immune response and diabetic status, before and 6 weeks after treatment were evaluated. Statistical analysis (t test) were done using Stata 7.0 software, to compare the parameters before and after scaling in CDM and UCMD subjects. The results showed that scaling decreased IL-1β level and increased phagocytotic function significantly (P<0.05). Scaling decreased fasting and 2 hours post-prandial blood glucose levels and HbA1c level, but the decrease were not significant statistically (P>0.05), except for the decrease in HbA1c level in uncontrolled DM (P=0.00)."