Granulocyte elastase activity and PGE 2 levels in gingival crevicular fluid in relation to the presence of subgingival periodontopathogens in subjects with untreated adult periodontitis
1999; Wiley; Volume: 26; Issue: 8 Linguagem: Inglês
10.1034/j.1600-051x.1999.260807.x
ISSN1600-051X
AutoresLJ Jin, Per‐Östen Söder, WK Leung, EF Corbet, LP Samaranayake, Birgitta Söder, W. I. R. Davies,
Tópico(s)Oral and gingival health research
ResumoAbstract . This study aimed to determine the association between the levels of granulocyte elastase and prostaglandin E 2 (PGE 2 ) in GCF, and the concomitant presence of periodontopathogens in untreated adult periodontitis (AP). GCF and subgingival plaque were sampled by paper strips and paper points respectively, from various periodontal sites in 16 AP subjects. Granulocyte elastase activity in GCF was analyzed with a low molecular weight substrate specific for granulocyte elastase, pGluProVal‐pNA, and the maximal rate of elastase activity (MR‐EA, mAbs/min/site) was calculated. PGE 2 levels in GCF were determined by radioimmunoassay. 5 species‐specific DNA probes were used to detect the presence of A. actinomycetemcomitans ( A.a. , ATCC 43718 ), B. forsythus ( B.f., ATCC 43037 ), P. gingivalis ( P.g., ATCC 33277 ), P. intermedia ( P.i., ATCC 33563 ), and T. denticola ( T.d., ATCC 35405 ), with a sensitivity of 10 3 cells/paper point. No A.a . was detectable from all sites sampled. The predominant combination of species detected was B.f., P.g ., P.i. & T.d . and it was significantly higher at periodontitis sites (68%) than at healthy (7%) or gingivitis sites (29%) ( p <0.05). Overall, MREA values were strongly correlated with PGE 2 levels ( r =0.655, p <0.001), especially at these periodontitis sites co‐infected by B.f., P.g., P.i. & T.d . ( r =0.722, p <0.001). The periodontitis sites co‐infected by the 4 species were observable from 15 subjects. These sites were sub‐grouped into 8 subjects with a high MREA and 7 subjects with a low MR‐EA. The PGE 2 levels in the high MR‐EA group were significantly higher than in the low MR‐EA group ( p <0.05). No significant differences in clinical or bacterial data were found between the two groups. While within the high MR‐EA group, similar results were found between the paired periodontitis sites in each subject with highest and lowest MR‐EA values. This study shows that the local host response to bacterial challenge in untreated periodontal pockets is diverse in terms of the intensity of inflammatory response measured by granulocyte elastase and PGE 2 levels in GCF. A more thorough evaluation of the risk for active periodontal disease may involve the combined approaches to the test of the dynamic bacteria‐host relations.
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