J. Gamonal et al., Characterization of cellular infiltrate, detection of chemokine receptor CCR5 and interleukin-8 and RANTES chemokines in adult periodontitis, J PERIOD RE, 36(3), 2001, pp. 194-203
Leukocyte migration is essential fur immune surveillance of tissues by focu
sing immune cells to sites of antigenic challenge. The control of leukocyte
migration depends on the combined actions of adhesion molecules and a vast
array of chemokines and their receptors. The purpose of the present study
was to investigate the involvement of Interleukin-8 (IL-8). RANTES, the ass
ociated infiltrating cells and expression of CCR5 chemokine receptors in pe
riodontitis: furthermore. the effect of periodontal therapy on these parame
ters was evaluated. Patients included in the study had moderate to advanced
periodontal disease with at least 5-6 teeth with probing depth > 6 mm, att
achment loss greater than or equal to3 mm and extensive radiographic bone l
oss. The inflammatory infiltrate was analyzed by immunohistochemistry in gi
ngival biopsies obtained from subjects at the beginning of the study and 2
months after periodontal treatment. Gingival crevicular fluid (GCF) was col
lected for 30 seconds using periopaper strips, and chemokines were quantifi
ed by ELISA. The cellular components of the inflammatory infiltrate include
d B (CD19) and T (CD3, CD4+ and CD8 +) lymphocytes and monocytes/macrophage
s (CD11c). CCRS chemokine receptor expressing cells were exclusively found
in periodontitis gingiva. IL-8 and RANTES were detected in the periodontiti
s group, obtaining a total amount of 212.5 pg and 42.0 pg, respectively. Ho
wever. IL-8 was also detectable in the GCF of the healthy group (total amou
nt of 44.8 pg). Periodontal therapy reduced the cell number in the infiltra
te and the levels of IL-8 and RANTES, suggesting a relationship between the
se chemokines and periodontal status. We propose that the presence of these
chemokines and the expression of chemokine receptors may represent a marke
r of lymphocyte subsets with the ability to migrate to inflammatory sites.