Protease inhibitor levels in periodontal health and disease.
OBJECTIVE
Our previous study showed that protease inhibitors were attenuated by the periodontal pathogen Porphyromonas gingivalis in cultured gingival epithelial cells. We hypothesize that fewer protease inhibitors would be present in more advanced periodontal disease sites, where the level of P. gingivalis may be high. The goal of this study was to investigate the relationship between the protease inhibitor [secretory leukocyte protease inhibitor (SLPI), elastase-specific inhibitor (ELAFIN) and squamous cell carcinoma antigen (SCCA)] levels in gingival crevicular fluid and the number of P. gingivalis micro-organisms in subgingival plaque.


METHODS
Plaque samples from subjects without (n = 18) and with moderate to advanced periodontitis (n = 41) were used to quantify P. gingivalis using real-time PCR. Protease inhibitor levels in the gingival crevicular fluid of all the subjects were determined by ELISA.


RESULTS
P. gingivalis was detected in 68.3% of patients with periodontitis, while 16.7% of subjects without periodontitis had a detectable level of P. gingivalis. Patients with periodontitis and P. gingivalis in their plaque exhibited lower SLPI and ELAFIN levels (p < 0.001) compared with control subjects without periodontitis. Secretory leukocyte protease inhibitor was also reduced (p < 0.05) in gingival crevicular fluid of periodontitis patients without a detectable level of P. gingivalis. Periodontitis patients with high vs. low levels of P. gingivalis exhibited reciprocal mean levels of SLPI and ELAFIN concentrations.


CONCLUSIONS
The reduced concentrations of SLPI and ELAFIN may contribute to the loss of host protective capacity and increase susceptibility to breakdown from chronic infection. The work of this investigation may aid in finding diagnostic and prognostic markers in periodontal health and disease and may also help in finding pharmacological targets directed against periodontal inflammation.
Department of Oral Health Sciences, University of Washington, Seattle, WA, USA.
S
S
Kretschmar
L
L
Yin
F
F
Roberts
R
R
London
T T
TT
Flemmig
D
D
Arushanov
K
K
Kaiyala
W O
WO
Chung
D000328:Adult; D000951:Antigens, Neoplasm / Q000032:analysis; D058491:Bacterial Load; D055113:Chronic Periodontitis / Q000201:enzymology* / Q000382:microbiology; D003773:Dental Plaque / Q000382:microbiology; D003774:Dental Plaque Index; D053492:Elafin / Q000032:analysis; D005260:Female; D005883:Gingival Crevicular Fluid / Q000201:enzymology; D005884:Gingival Hemorrhage / Q000201:enzymology / Q000382:microbiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000201:enzymology / Q000382:microbiology; D010512:Periodontal Index; D010514:Periodontal Pocket / Q000201:enzymology / Q000382:microbiology; D010519:Periodontium / Q000201:enzymology*; D016966:Porphyromonas gingivalis / Q000254:growth & development; D011480:Protease Inhibitors / Q000032:analysis*; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000032:analysis; D015843:Serpins / Q000032:analysis
D000951:Antigens, Neoplasm; D053492:Elafin; D011480:Protease Inhibitors; D053481:Secretory Leukocyte Peptidase Inhibitor; D015843:Serpins; C051072:squamous cell carcinoma-related antigen