<ul><li><p>VOLUME 40 NUMBER 4 APRIL 2009 271</p><p>QUINTESSENCE INTERNATIONAL</p><p>The case of a female with aggressive peri-</p><p>odontitis over 14 years is presented. From</p><p>1993 to 2000, no therapy was performed,</p><p>and disease progression could be recon-</p><p>structed upon radiographic findings. The</p><p>radiographs of 1993 (Fig 1a) when the</p><p>patient was 16 years of age, showed local-</p><p>ized bone loss at the maxillary premolars of</p><p>about 50% and localized intrabony bone</p><p>defects at the mandibular right and left first</p><p>molars of 30% of the root length. These</p><p>defects increased in 1996 to 70% for the</p><p>maxillary premolars and 50% for the</p><p>mandibular molars (Fig 1b), and up to 90%</p><p>for the maxillary premolars and 75% for the</p><p>mandibular molars with furcation involve-</p><p>ment in 1999 (Fig 1c). This indicated a rapid</p><p>disease progression with yearly bone loss of</p><p>about 2 mm.</p><p>At the first visit to our dental clinic in</p><p>2000, when the patient was 23 years of age</p><p>(Figs 2a to 2d), preservation of the maxillary</p><p>premolars was uncertain because of the</p><p>advanced periodontal destruction. Clinical</p><p>and radiographic findings indicated severe</p><p>aggressive periodontitis.1 A microbiologic</p><p>test based upon a polymerase chain reaction</p><p>(Hain Diagnostika) for periodontal pathogens</p><p>found high levels of Aggregatibacter (former-</p><p>ly Actinobacillus) actinomycetemcomitans,</p><p>Tanerella forsythensis, Treponema denticola,</p><p>and Fusobacterium nucleatum, and we</p><p>therefore started treatment with a full-mouth</p><p>disinfection in combination with a systemic</p><p>antibiotic regime according to van Winkelhoff</p><p>et al.2 After 3 months, the patient was re-</p><p>evaluated, and localized surgical procedures</p><p>were performed at the mandibular first</p><p>molars using enamel matrix proteins for</p><p>regeneration of the extended intrabony</p><p>3-wall bone defects.3 For the maxillary pre-</p><p>molars, no surgical treatment was planned</p><p>because an improvement of the periodontal</p><p>situation could not be predicted.</p><p>Since then, supportive periodontal thera-</p><p>py has been performed every 3 months. In</p><p>2007, when the patient was 31 years of age,</p><p>radiographs showed, for the mandibular first</p><p>molars, a nearly complete regeneration of</p><p>the former defects up to the surrounding</p><p>bone level (Figs 3a to 3c). The maxillary pre-</p><p>molars were preserved, and slight bone</p><p>regeneration was present.</p><p>Localized severe aggressive periodontitis.Disease progression and tooth preservation:A short case report over 14 yearsMatthias Pelka, Priv-Doz Dr Med Dent1/Anselm Petschelt, Prof Dr Med Dent1</p><p>A case of a 31-year-old female with aggressive periodontitis over 14 years is presented.</p><p>From 1993 to 2000, no periodontal therapy occurred; disease development and</p><p>progression could be reconstructed upon radiographic findings. In 2000, full-mouth</p><p>disinfection therapy and antibiotic therapy was performed, as well as regenerative surgical</p><p>treatments. Seven years after surgical treatment, stable periodontal conditions and clear</p><p>bone regeneration in the surgical areas was evident. (Quintessence Int 2009;40:271273)</p><p>Key words: aggressive periodontitis, disease progression, full-mouth disinfection therapy,</p><p>long-term outcome, regeneration, supportive therapy</p><p>1Dental Clinic 1, Operative Dentistry and Periodontology,</p><p>University of Erlangen-Nuremberg, Erlangen, Germany.</p><p>Correspondence: PD Dr Matthias Pelka, Dental Clinic 1</p><p>Operative Dentistry and Periodontology, University Erlangen</p><p>Nuremberg, Glckstrasse 11, D-91054 Erlangen, Germany. Fax:</p><p>499131 8533603. Email: [email protected]</p><p>Presented as a poster at the meeting of the German Society of</p><p>Peridontology (DGP), October 2005, in Berlin.</p><p>2009 Quintessence Publishing Co, Inc.All Rights Reserved</p></li><li><p>272 VOLUME 40 NUMBER 4 APRIL 2009</p><p>QUINTESSENCE INTERNATIONAL</p><p>Pelka/Petschel t</p><p>Figs 2a to 2d Detailed radiographic statusand clinical situation in 2000 before system-atic nonsurgical and surgical periodontaltreatment.</p><p>Figs 1a to 1c Radiographs from (a) 1993, (b) 1996, and (c) 1999 showing progression of disease.</p><p>a</p><p>a</p><p>cb</p><p>b</p><p>d</p><p>c</p><p>2009 Quintessence Publishing Co, Inc.All Rights Reserved</p></li><li><p>This case impressively shows the efficacy</p><p>of the full-mouth disinfection treatment regi-</p><p>men for the therapy of severe aggressive</p><p>periodontitis.4 Despite high disease progres-</p><p>sion over 7 years, the therapy stopped the</p><p>progression, and a long-term tooth preserva-</p><p>tion of the severely affected maxillary premo-</p><p>lars was achieved. Narrow and deep 3-wall</p><p>bony defects have the highest regenerative</p><p>potential,5 and the selection of those sites for</p><p>surgical procedures may be one cause for</p><p>the impressive regenerations at the</p><p>mandibular first molars.</p><p>REFERENCES</p><p>1. Tonetti MS, Mombelli A. Early-onset periodontitis.</p><p>Ann Periodontol 1999;4:3953.</p><p>2. van Winkelhoff AJ, Rodenburg JP, Goene RJ, Abbas F,</p><p>Winkel EG, de Graaff J. Metronidazole plus amoxy-</p><p>cillin in the treatment of Actinobacillus actino-</p><p>mycetemcomitans associated periodontitis. J Clin</p><p>Periodontol 1989;16:128131.</p><p>3. Sculean A, Schwarz F, Becker J, Brecx M. The applica-</p><p>tion of an enamel matrix protein derivative</p><p>(Emdogain) in regenerative periodontal therapy: A</p><p>review. Med Princ Pract 2007;16:167180.</p><p>4. Buchmann R, Nunn ME, Van Dyke TE, Lange DE.</p><p>Aggressive periodontitis: 5-year follow-up of treat-</p><p>ment. J Periodontol 2002;73:675683.</p><p>5. Cortellini P, Bowers GM. Periodontal regeneration of</p><p>intrabony defects: An evidence-based treatment</p><p>approach. Int J Periodontics Restorative Dent</p><p>1995;15:128145.</p><p>VOLUME 40 NUMBER 4 APRIL 2009 273</p><p>QUINTESSENCE INTERNATIONAL</p><p>Pelka/Petschel t</p><p>Figs 3a to 3c Detailed radiographic status and clinical situation in 2007 after full-mouth disinfection therapy and surgicalregenerative procedures.</p><p>a</p><p>b c</p><p>2009 Quintessence Publishing Co, Inc.All Rights Reserved</p></li></ul>
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<p>SINDROM NEFRITIK VS SINDROM NEFROTIK</p><p>Preseptor : dr. Santoso Chandra. SpPd</p><p>GLOMERULAR DISEASESindrom Nefritik Azotemia, Hipertensi, Edema, Hematuria (RBC cast), proteinuria (< 3 g/hr), terkadang oliguria. Sindrom Nefrotik Proteinuria masif (> 3.5 gram / 24 jam / 1,73 m2 atau 40-50 mg/kg/hari / +3-+4 ) Hipoalbuminemia, Edema anasarka, Hiperlipidemia, Lipiduria.</p><p>Sindroma NefritikGlomerulonefritis akut (GNA) Sindroma Nefritik / GNA adalah sindroma klinik yg ditandai kelainan : </p><p>Azotemia, Hipertensi, Edema, Hematuria (RBC cast), proteinuria (< 3 g/hr), terkadang oliguria.</p><p>3</p><p>Etiologi :1. Glomerulopati (GP) idiopatik /primer a. GP akut proliferatif b. GP mesangio proliferatif (IgA) (penyakit Burger) c. GP membranoproliferatif. Infeksi : a. post-infection streptococcus Fhaemolitik b. Non Streptococcal : endokarditis bakterialis (nefritis Lohlein) sepsis, pneumococcal pneumonia, thypoid fever, etc. c. parasit : malaria, toxoplasmosis, etc. d. Viral : hepatitis B, mumps, measles, varicella, etc. Sistemik : Lupus Nephritis, Vaskulitis, Good pasteur syndrome.4</p><p>2.</p><p>3.</p><p>Patogenesis Inflamatory process Degree of glomerular inflamation the sverity of renal dysfunction and associated clinical manifestations. Poststreptococcal glomerulonephritis tissue injury or result in inflammatory reaction.</p><p>Patofisiologi1. Kel. urinalisis: ok. Kerusakan dd. Kapiler glomerulus selektif proteinuri < 3 g/hr, hematuria disertai silinder eritrosit. 2. LFG menurun, disertai reabsorbsi Na. dan air sehingga terjadi oliguri ,edema, edema paru dan hipertensi.</p><p>6</p><p>Gejala klinis:1. 2. 3. 4. hipertensi (malignant in some cases). Edema Oliguria Physical examination : a. SLE Malar Rash, Oral ulcers b. Henoch-schonlein purpura and cryoglobulinemia palpable purpura7</p><p>LaboratoriumUrinalisis Macroscopic hematuria (tea cola colored urine) Microscopic urine reveals RBCs Proteinuria (< 3gr/hari)</p><p> Hematologi Anemia Underlying disease : Trombocytopenia or leukopenia (SLE) Blood cultures fever & murmur Streptozyme & ASO sore throat etc</p><p>ImagingPulmonary Edema Wagener s Granulomatosis & good pasteur disease Echocardiogram pericardia effusion or endocarditis USG Renal Kidney Size ( 3.5 gram / 24 jam / 1,73 m2) atau 40-50 mg/kg/hari Hipoalbuminemia, Edema anasarka, Hiperlipidemia, dan Lipiduria.</p><p>ETIOLOGIGlomerular disease : Membranous Nephropathy(40%) Minimal change disease (15%) Focal glomerulosclerosis (15%) Membarnoproliferative GN (7%) Masangioproliferatif GN (5%) Immunotactoid and Fibrilary GN</p><p>Systemic Causes Diabetes mellitus, SLE, Amyloidosis, HIV-associated nephropathy Drugs : Gold, Penicillamine, probenecid, street heroin, captopril, NSAIDs Infection : bacterial endocarditis, hepatitis B, shunt Infection, shypilis, malaria, hepatic schistosomiasis Malignancy : multiple myeloma, light chain deposition disease, hodgkin s and other lymphomas, leukemia, carcinoma of breast, GI tract.</p><p>Patogenesis Reflects noninflammatory damage glomerular capillary wall. Proteinuria from alterations in the charge or size selectivity of the glomerular capillary wall.</p><p>Patofisiologi</p><p>Gejala Klinik Proteinuria Asymptomatic Edema Edem (High Intravascular hydrostatic pressure and tissue hydrostatic pressure) edem anasarka.</p><p>LaboratoriumUrinalisis Proteinuria (urine dipstick +3 to +4 dan 24 hour urine collection >3.5 g protein/1.73 m2) Few cells or cast and Urinary lipid in sediment</p><p> Polarized light maltese crosses</p><p>Hematologi Serum albumin , GFR normal. Anemia, Elevated erythrocyte sedimentation Rate (ESR), Hypocalcemia nad Vit. D deficiency.</p><p> Biopsi Kontroversi Standar procedure determining the cause of proteinuria.</p><p>TERIMA KASIH</p><p> From Current diagnosis & treatment Nephrology & Hypertension Chapter 23. nephrotic syndrome vs nephritic Harrison manual of medicine</p>
Epidemiologi Pada Glomerulonefritis sering ditemukan pada anak berumur antara 3-7 tahun dan lebih sering mengenai anak laki-laki dibandingkan anak perempuan. Perbandingan antara anak laki-laki dan perempuan adalah 2:1 dan jarang menyerang anak dibawah usia 3 tahun. Askep Glomerulonefritis 0 comments Posted in Labels: Materi Kuliah BAB I. Latar Belakang. Glomerulonefritis merupakan penyebab utama terjadinya gagal ginjal tahap akhir dan tingginya angka morbiditas baik pada anak maupun pada dewasa ( Buku Ajar Nefrologi Anak, edisi 2, hal.323, 2002).