Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
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ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2006, vol. 15, nr 4, July-August, p. 599–605

Publication type: original article

Language: English

Anti−Neutrophil Cytoplasmic Antibodies and Autoantibodies to Human Heat Shock Protein 60 in Periodontitis Patients

Autoprzeciwciała dla antygenów cytoplazmatycznych neutrofili oraz ludzkiego białka szoku termicznego 60 u pacjentów z zapaleniem przyzębia

Wojciech Rzeszutko1,, Tomasz Konopka2,, Wacław Kopeć3,

1 Department of Pathological Anatomy, Silesian Piasts University of Medicine in Wrocław

2 Department of Periodontology

3 Laboratory of Immunology, Department of Nephrology, Silesian Piasts University of Medicine in Wrocław, Poland

Abstract

Background. The autoimmune response may contribute to the pathogenesis of periodontitis. Changing levels of anti−neutrophil cytoplasmic autoantibodies (ANCAs) are serologic markers for many infective and connective tissue diseases. Hsp 60 may also be an important factor in the initiation of an autoimmune response.
Objectives. Investigating the presence of ANCAs (p−ANCA to myeloperoxidase and c−ANCA to proteinase 3) and antibodies to human heat shock protein 60 (Hsp 60) in the sera of 73 patients with periodontitis and 13 control subjects.
Material and Methods. The study group consisted of 73 patients aged 19–50 years: 31 with generalized aggressive periodontitis, 13 with localized aggressive periodontitis, and 29 with chronic periodontitis. The control group comprised 13 periodontally healthy subjects. The serum levels of p−ANCA, c−ANCA, and anti−Hsp 60 were detected by ELISA in each subject.
Results. Elevated levels of p−ANCA were demonstrated only in five patients with generalized aggressive periodontitis. Elevated levels of antibodies to Hsp 60 were found only in 12.9% of patients with generalized aggressive periodontitis, 7.6% of patients with localized aggressive periodontitis, and 13.7% of patients with chronic periodontits.
Conclusion. There was no relationship between the significantly elevated levels of p−ANCA and antibodies to Hsp 60 and clinical measurements of periodontitis. These results do not support evidence for a primary role of autoimmunity in periodontal disease. It seems probable that the destruction of periodontal tissues may sometimes be the primary driving factor in the induction of the enhanced autoimmune response in periodontitis.

Streszczenie

Wprowadzenie. Odpowiedź autoodpornościowa może uczestniczyć w etiopatogenezie zapalenia przyzębia. Zmienione stężenia autoprzeciwciał dla cytoplazmy neutrofili (ANCA) są markerami serologicznymi dla wielu chorób zapalnych i tkanki łacznej. Przeciwciała dla białka szoku termicznego 60 (HSP 60) mogą być również istotnym czynnikiem w inicjowaniu reakcji autoimmunologicznej.
Cel pracy. Zbadanie występowania ANCA (p−ANCA antymieloperoksydazie i c−ANCA antyproteinazie 3) oraz przeciwciał dla Hsp 60 w surowicy 73 pacjentów z zapaleniem przyzębia i u 13 osób z grupy kontrolnej.
Materiał i metody. Grupa badana składała się z 73 pacjentów w wieku 19–50 lat: 31 z uogólnionym agresywnym zapaleniem przyzębia, 13 z umiejscowionym agresywnym zapaleniem przyzębia i 29 z przewlekłym zapaleniem przyzębia. Grupa kontrolna liczyła 13 osób ze zdrowym klinicznie przyzębiem. Stężenia surowicze p−ANCA, c−ANCA i przeciwciał dla HSP 60 badano u każdego pacjenta metodą ELISA.
Wyniki. Podwyższone stężenia p−ANCA wykazano tylko u pięciu pacjentów z uogólnionym agresywnym zapaleniem przyzębia. Podwyższone stężenia przeciwciał dla HSP 60 stwierdzono tylko u 12,9% pacjentów z uogólnionym agresywnym zapaleniem przyzębia, 7,6 % z umiejscowionym zapaleniem przyzębia i u 13% pacjentów z przewlekłym zapaleniem przyzębia.
Wnioski. Nie wykazano związku między istotnie podwyższonymi stężeniami p−NCA i przeciwciałami dla HSP 60 a wskaźnikami klinicznymi zapalenia przyzębia. Wyniki te nie potwierdzają pierwotnej roli procesów autoodpornościowych w zapaleniach przyzębia. Wydaje się, że zniszczenie tkanek przyzębia może być niekiedy czynnikiem wywołującym reakcję autoimmunologiczną w zapaleniu przyzębia.

Key words

antibodies, anti−neutrophil cytoplasmic, heat shock protein 60, autoimmunity, periodontitis

Słowa kluczowe

przeciwciała, anty cytoplazmie neutrofili, białko szoku termicznego 60, autoimmunizacja, zapalenie przyzębia

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