Peri-implantitis fibroblasts respond to host immune factor C1q.
OBJECTIVE
Current therapies for peri-implantitis apply the same clinical protocols as those used for the treatment of periodontitis; however, outcomes remain unpredictable. We hypothesized that resident fibroblasts of the peri-implantitis stroma and periodontitis stroma differ in their phenotype and response to host immune factors. Fibroblasts are highly heterogeneous and comprise discrete subtypes with the potential of modulating inflammatory activities. The aim of the present study was to characterize the expression of receptors for complement C1q of innate immunity on human peri-implantitis fibroblasts and investigate effects of C1q on the proinflammatory properties of the cells.


METHODS
Fibroblasts were cultured from gingival tissues exhibiting peri-implantitis and periodontitis, and from healthy gingivae as a control. Expression of C1q receptors for the collagen (cC1qR) and globular domains (gC1qR) of the protein was determined by flow cytofluorometric analysis (FITC) of specific antibodies bound to the surface of the cells. Secretion of C1q-inducible proinflammatory mediators was quantified after 24 h incubation using array-based ELISAs.


RESULTS
The percentage of fibroblasts FITC-positive for cC1qR was 67, 75 and 12% in peri-implantitis, healthy and periodontitis cultures, respectively, whereas the percentage of gC1qR FITC-positive fibroblasts was 5, 3 and 59%, respectively. The C1q interactions with peri-implantitis and healthy fibroblasts increased secretion of the chemokines interleukin-6 and interleukin-8 twofold, and monocyte chemoattractant protein-1 fourfold over baseline values, whereas periodontitis fibroblasts were unresponsive. Complement C1q increased levels of vascular endothelial growth factor sevenfold and transforming growth factor-β1 12-fold over baseline values in peri-implantitis cultures, only.


CONCLUSIONS
Peri-implantitis fibroblasts differ from periodontitis fibroblasts in phenotypic expression of cC1qR and function, and from healthy fibroblasts in proinflammatory, angiogenic and fibrogenic function. Peri-implantitis fibroblasts may represent a novel subtype.
Department of Periodontics, University of Washington, Seattle, WA 98195-7444, USA.
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Verardi
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Quaranta
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Bordin
D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis; D015922:Complement C1q / Q000235:genetics*; D005347:Fibroblasts / Q000276:immunology* / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D005881:Gingiva / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate; D016130:Immunophenotyping; D018836:Inflammation Mediators / Q000276:immunology*; D015850:Interleukin-6 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D008562:Membrane Glycoproteins / Q000096:biosynthesis / Q000235:genetics*; D057873:Peri-Implantitis / Q000276:immunology* / Q000378:metabolism; D010518:Periodontitis / Q000276:immunology / Q000378:metabolism; D017434:Protein Structure, Tertiary; D011951:Receptors, Complement / Q000096:biosynthesis / Q000235:genetics*; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
D018932:Chemokine CCL2; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D008562:Membrane Glycoproteins; D011951:Receptors, Complement; D053773:Transforming Growth Factor beta1; D042461:Vascular Endothelial Growth Factor A; C032402:complement 1q receptor; D015922:Complement C1q