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Gingival crevicular fluid levels of calprotectin and myeloperoxidase during therapy for generalized aggressive periodontitis
Author(s) -
Kaner Doğan,
Bernimoulin JeanPierre,
Kleber BerndMichael,
Heizmann Wolfgang R.,
Friedmann Anton
Publication year - 2006
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2005.00849.x
Subject(s) - calprotectin , myeloperoxidase , medicine , periodontitis , aggressive periodontitis , bleeding on probing , gastroenterology , gingival and periodontal pocket , inflammation , pathology , immunology , inflammatory bowel disease , disease
Background:  Levels of the inflammation marker calprotectin in gingival crevicular fluid correspond to clinical and biochemical parameters of periodontal inflammation. Neutrophil granulocytes (polymorphonuclear neutrophils: PMNs) are supposed to be the main source of calprotectin in gingival crevicular fluid, but evidence is still lacking. The influence of periodontal therapy on gingival crevicular fluid levels of calprotectin has not yet been determined. Objectives:  Gingival crevicular fluid levels of calprotectin were monitored during therapy for generalized aggressive periodontitis. Interrelations between calprotectin and the PMN marker myeloperoxidase (MPO) were evaluated. Material and methods:  Gingival crevicular fluid samples were collected from 23 patients with generalized aggressive periodontitis before and 3 months after non‐surgical therapy with an adjunctive antimicrobial medication. Clinical parameters were recorded with a pressure‐calibrated electronic probe. Levels of calprotectin and MPO in gingival crevicular fluid were analysed by enzyme‐linked immunosorbent assay (ELISA) procedures. Results:  At baseline, levels of calprotectin and MPO were highly correlated. Bleeding and suppurating sites showed significantly higher levels of calprotectin and MPO than non‐bleeding, non‐suppurating sites. Therapy significantly decreased levels of both biomarkers. These changes of calprotectin and MPO were highly correlated and also related to probing‐depth reduction. Three months after therapy, the levels of both markers still showed significant correlations in initially deep sites, whereas in initially shallow sites no significant correlation was found. After therapy, levels of markers in bleeding and non‐bleeding sites were comparable. Conclusion:  The correlations between calprotectin and MPO indicate that PMNs are a major contributor to the calprotectin content in gingival crevicular fluid of severely affected sites. Calprotectin levels in gingival crevicular fluid and their changes reflect periodontal inflammation as well as the clinical treatment outcome. A prognostic potential of this marker substance remains to be determined.

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