Detection of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 2(PAI-2) in gingival crevicular fluid from healthy, gingivitis and periodontitis patients.
BACKGROUND
The regulation of plasminogen activation is a key element in controlling proteolytic events in the extracellular matrix. Our previous studies had demonstrated that in inflamed gingival tissues, tissue-type plasminogen activator (t-PA) is significantly increased in the extracellular matrix of the connective tissue and that interleukin 1beta(IL-1beta) can up regulate the level of t-PA and plasminogen activator inhibitor-2 (PAI-2) synthesis by human gingival fibroblasts.


METHODS
In the present study, the levels of t-PA and PAI-2 in gingival crevicular fluid (GCF) were measured from healthy, gingivitis and periodontitis sites and compared before and after periodontal treatment. Crevicular fluid from106 periodontal sites in 33 patients were collected. 24 sites from 11 periodontitis patients received periodontal treatment after the first sample collection and post-treatment samples were collected 14 days after treatment. All samples were analyzed by enzyme-linked immunosorbent assay (ELISA) for t-PA and PAI-2.


RESULTS
The results showed that significantly high levels of t-PA and PAI-2 in GCF were found in the gingivitis and periodontitis sites. Periodontal treatment led to significant decreases of PAI-2, but not t-PA, after 14 days. A significant positive linear correlation was found between t-PA and PAI-2 in GCF (r=0.80, p<0.01). In the healthy group, different sites from within the same subject showed little variation of t-PA and PAI-2 in GCF. However, the gingivitis and periodontitis sites showed large variation. These results suggest a good correlation between t-PA and PAI-2 with the severity of periodontal conditions.


CONCLUSIONS
This study indicates that t-PA and PAI-2 may play a significant rôle in the periodontal tissue destruction and tissue remodeling and that t-PA and PAI-2 in GCF may be used as clinical markers to evaluate the periodontal diseases and assess treatment.
Yin
X
X
Department of Dentistry, The University of Queensland, Brisbane, Australia.
Bunn
C L
CL
Bartold
P M
PM
D000328:Adult; D000704:Analysis of Variance; D015415:Biomarkers / Q000032:analysis; D015331:Cohort Studies; D003238:Connective Tissue / Q000737:chemistry; D004797:Enzyme-Linked Immunosorbent Assay; D005109:Extracellular Matrix / Q000737:chemistry; D005260:Female; D005347:Fibroblasts / Q000378:metabolism; D005500:Follow-Up Studies; D005883:Gingival Crevicular Fluid / Q000737:chemistry*; D005891:Gingivitis / Q000378:metabolism* / Q000628:therapy; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000378:metabolism / Q000628:therapy; D010518:Periodontitis / Q000378:metabolism* / Q000628:therapy; D017396:Plasminogen Activator Inhibitor 2 / Q000032:analysis*; D010959:Tissue Plasminogen Activator / Q000032:analysis*; D015854:Up-Regulation
D015415:Biomarkers; D007375:Interleukin-1; D017396:Plasminogen Activator Inhibitor 2; D010959:Tissue Plasminogen Activator