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Cytokine and matrix metalloproteinase expression in fibroblasts from peri‐implantitis lesions in response to viable P orphyromonas gingivalis
Author(s) -
Irshad M.,
Scheres N.,
Anssari Moin D.,
Crielaard W.,
Loos B. G.,
Wismeijer D.,
Laine M. L.
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.12051
Subject(s) - porphyromonas gingivalis , periodontitis , matrix metalloproteinase , fibroblast , inflammation , chronic periodontitis , cytokine , chemistry , chemokine , immunology , medicine , in vitro , dentistry , biochemistry
Background and Objective To assess inflammatory reactions of fibroblasts in the pathophysiology of peri‐implantitis, we compared the pro‐inflammatory and matrix‐degrading responses of gingival and granulation tissue fibroblasts from periodontally healthy controls, peri‐implantitis, and periodontitis lesions to an in vitro challenge with P orphyromonas gingivalis . Methods Fibroblasts from periodontally healthy, peri‐implantitis and periodontitis donors were challenged with viable P . gingivalis . The inflammatory reactions of fibroblasts were analyzed before and after 6 h P . gingivalis challenge, and 2.5 and 18 h after removal of the challenge. Gene expression and induction of pro‐inflammatory mediators, and matrix metalloproteinases ( MMP s) were assessed by real‐time polymerase chain reaction. Protein expression was measured by enzyme‐linked immunosorbent assay. Results Non‐challenged fibroblasts from peri‐implantitis and periodontitis lesions expressed higher levels of interleukin ( IL )‐1β , IL ‐8 , and monocyte chemotactic protein ( MCP )‐1 than fibroblasts from periodontally healthy individuals. The P . gingivalis challenge induced expression of IL ‐1β , IL ‐8 , IL ‐6 , MCP ‐1 , and MMP ‐1 in periodontitis and peri‐implantitis fibroblasts, but not in fibroblasts from periodontally healthy individuals. MMP ‐8 expression was higher in non‐challenged peri‐implantitis fibroblasts than in fibroblasts from periodontally healthy individuals. However, the P . gingivalis challenge downregulated MMP ‐8 gene expression in peri‐implantitis fibroblasts. After removal of the P . gingivalis challenge, peri‐implantitis fibroblasts sustained higher induction of IL ‐1β, MCP ‐1 , and MMP ‐1 compared to periodontitis fibroblasts. Conclusions Fibroblasts from peri‐implantitis and periodontitis lesions gave a more pronounced inflammatory response to the P . gingivalis challenge than fibroblasts from healthy donors. They may therefore be involved in the development of inflammation in peri‐implantitis and periodontitis. Moreover, the sustained upregulation of inflammatory mediators and MMP ‐1 in peri‐implantitis fibroblasts may play a role in the pathogenesis of peri‐implantitis.