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Periodontal health and serum, saliva matrix metalloproteinases in patients with mild chronic obstructive pulmonary disease
Author(s) -
Yildirim E.,
Kormi I.,
Başoğlu Ö. K.,
Gürgün A.,
Kaval B.,
Sorsa T.,
Buduneli N.
Publication year - 2013
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/jre.12004
Subject(s) - copd , medicine , saliva , matrix metalloproteinase , outpatient clinic , gastroenterology , pulmonary disease , case control study , periodontal disease , pathology
Background and Objectives The present case–control study aimed to evaluate comparatively the salivary and serum levels of matrix metalloproteinases ( MMP )‐8 and‐ 13 and tissue inhibitor of matrix metalloproteinase‐1 ( TIMP ‐1) in patients with mild chronic obstructive pulmonary disease ( COPD ) and non‐ COPD controls. Material and Methods Clinical periodontal measurements were recorded before any periodontal intervention in 36 patients with mild COPD and 20 non‐ COPD controls admitted to Ege University Department of Chest Diseases COPD outpatient clinic (İzmir, Turkey). Salivary and serum levels of MMP ‐8, MMP ‐13, and TIMP ‐1 were determined by immunofluorometric assay ( IFMA ) and enzyme‐linked immunosorbent assay ( ELISA ). Data were analyzed with non‐parametric statistical tests. Results Patients with COPD were significantly older than the control group ( p < 0.05). The COPD group showed significantly higher serum levels of MMP ‐8 IFMA , MMP ‐8/ TIMP ‐1 IFMA than the control group ( p < 0.005). By ELISA , serum MMP ‐8, MMP ‐8/ TIMP ‐1, TIMP ‐1, and MMP ‐13 levels were similar in both groups ( p > 0.05). Salivary MMP ‐8, MMP ‐13, and TIMP ‐1 levels were similar in both groups ( p > 0.05). Conclusions The present findings suggest that immunodetection of MMP ‐8 is dependent on the selected techniques and even with mild COPD some systemic inflammatory markers such as MMP ‐8 tend to increase. However, the present clinical periodontal and biochemical findings do not provide support for the previously proposed interaction between COPD and periodontal diseases.