Androgens modulate interleukin-6 production by gingival fibroblasts in vitro

Citation
Ra. Gornstein et al., Androgens modulate interleukin-6 production by gingival fibroblasts in vitro, J PERIODONT, 70(6), 1999, pp. 604-609
Citations number
44
Categorie Soggetti
Dentistry/Oral Surgery & Medicine","da verificare
Journal title
JOURNAL OF PERIODONTOLOGY
ISSN journal
00223492 → ACNP
Volume
70
Issue
6
Year of publication
1999
Pages
604 - 609
Database
ISI
SICI code
0022-3492(199906)70:6<604:AMIPBG>2.0.ZU;2-1
Abstract
Background: Pregnancy and puberty gingivitis have been attributed to increa sed concentrations of circulating sex hormones. This inflammatory gingival condition is accompanied by the local production of cytokines. The aims of this in vitro study were to assess, in the presence or absence of testoster one (T) or dihydrotestosterone (DHT), the production of interleukin-6 (IL-6 ) by human gingival fibroblasts (hGF), and to evaluate the effects of fluta mide (a common anti-androgen) in this system. Methods: The effects of the androgens, T and DHT, on IL-6 production were m easured in vitro in serum-free, phenol red-free medium. Cells were incubate d with or without androgens for 72. hours; the concentration of IL-6 secret ed into the medium after an additional 24-hour challenge with IL-1 beta plu s hormones was estimated by radioimmunoassay. The reverse transcription pol ymerase chain reaction was used to examine hGF and periodontal ligament cel ls (PDL) for the presence of androgen receptor. Results: In serum-free medium, T and DHT at concentrations of 5 x 10(-8) to 10(-7)M significantly (P < 0.05) inhibited IL-6 production by hGF Flutamid e, up to concentrations of 2 x 10(-5)M, did not reverse this inhibition. Th e androgen receptor was identified in both hGF and PDL. Conclusions: We concluded that elevated levels of androgens, specifically t estosterone and dihydrotestosterone, could affect the stromal cell response to an inflammatory challenge by downregulation of IL-6 production. This in vitro study lends support to the hypothesis that increased hormones during pregnancy or puberty could modulate the development of localized inflammat ion.