Human beta-defensin-1 and -2 and matrix metalloproteinase-25 and -26 expression in chronic and aggressive periodontitis and in peri-implantitis.
OBJECTIVE
Aberrant matrix metalloproteinase (MMP) and human beta-defensin (HBD) functions have been found in inflammatory diseases. The objectives of this study were to investigate the immunolocalisation, mRNA expression and molecular forms of MMP-25, MMP-26, HBD-1 and HBD-2 in chronic and aggressive periodontitis and in peri-implantitis. The expression of MMP-25 by cultured human plasmacytoma cells and macrophages, and the effects of MMP-26 and Porphyromonas gingivalis trypsin-like proteinase on HBD-1 and -2 were also studied.


METHODS
Immunohistochemistry, immunofluorescent analysis, reverse transcriptase polymerase chain reaction and immunoblotting were used to assess localisation, mRNA expression and molecular forms of MMP-25, MMP-26, HBD-1 and HBD-2. HBD degradation by MMP-26 and P. gingivalis proteinase was studied by sodium dodecyl sulphate-polyacrylamide gel electrophoresis.


RESULTS
MMP-25 was present in plasma cells and polymorphonuclear leucocytes, and MMP-26 was present in oral and sulcular basement membrane zones. HBD-1 was distributed perivasculary in gingival connective tissue and in oral and sulcular epithelium, and HBD-2 was found to a lesser extent in the perivascular space. Low MMP-25, MMP-26, HBD-1 and HBD-2 mRNA expression was found. Immunoblot revealed 29-57-kDa MMP-25 in myeloma cell lysates, but not in macrophages, and partly activated MMP-25 and -26 in diseased gingival crevicular fluid and peri-implant sulcular fluid. P. gingivalis trypsin-like proteinase degraded HBD-1 and -2.


CONCLUSIONS
Both MMP-25 and -26 were expressed more strongly in extensively inflamed gingiva compared with healthy gingiva. The expression of HBD-1 was stronger than that of HBD-2 in periodontitis and peri-implantitis. De-novo expression of MMP-25 and -26 is associated with periodontal and peri-implant inflammation. Furthermore, P. gingivalis trypsin-like proteinase, but not MMP-26, can degrade HBD-1 and -2, which could lead to a weakened innate immune response.
Kuula
Heidi
H
Biomedicum Helsinki, Institute of Dentistry, University of Helsinki, PO Box 63, FIN-00014 Helsinki, Finland. heidi.kuula@helsinki.fi
Salo
Tuula
T
Pirilä
Emma
E
Hagström
Jaana
J
Luomanen
Marita
M
Gutierrez-Fernandez
Ana
A
Romanos
Georgios E
GE
Sorsa
Timo
T
D000293:Adolescent; D000328:Adult; D000368:Aged; D000890:Anti-Infective Agents / Q000378:metabolism*; D002908:Chronic Disease; D015921:Dental Implants; D005260:Female; D015870:Gene Expression; D005891:Gingivitis / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D020782:Matrix Metalloproteinases / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D010518:Periodontitis / Q000378:metabolism*; D016133:Polymerase Chain Reaction / Q000379:methods; D016966:Porphyromonas gingivalis / Q000235:genetics / Q000378:metabolism*; D023083:beta-Defensins / Q000235:genetics / Q000378:metabolism*
D000890:Anti-Infective Agents; D015921:Dental Implants; D023083:beta-Defensins; D020782:Matrix Metalloproteinases