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Characterization of bone resorbing activity in gingival crevicular fluid from patients with periodontitis
Author(s) -
Rasmussen Lena,
Hänström Lennart,
Lerner Ulf H.
Publication year - 2000
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1034/j.1600-051x.2000.027001041.x
Subject(s) - bone resorption , periodontitis , gingivitis , resorption , osteoclast , prostaglandin e2 , chemistry , stimulation , medicine , rheumatoid arthritis , endocrinology , dentistry , receptor
Background: In attempts to elucidate factors stimulating bone resorption in patients with different inflammatory diseases in the vicinity of the skeleton, e.g., peridontal disease and rheumatoid arthritis, we are investigating the presence of bone‐resorbing activity in a variety of inflammatory exudates. The aim of the present study was to characterize the bone‐resorbing activity present in patients with periodontitis. Methods: Bone‐resorbing activity was assessed in gingival crevicular fluids (GCFs) collected from patients with periodontitis and from patients with no signs of gingivitis. Bone‐resorbing activity was evaluated by analyzing the capacity of GCFs to stimulate the release of minerals and the breakdown of bone matrix proteins in cultured neonatal mouse calvariae. The concentrations of IL‐1α, IL‐1β and PGE 2 were determined with ELISA and RIA techniques, respectively. Results: GCF eluates from 24 different healthy sites caused a 1.23±0.05 fold stimulation of 45 Ca release, whereas GCF eluates from 45 different diseased (periodontitis) sites caused a 2.46±0.10 fold stimulation. The effect on 45 Ca release was time‐ and concentration‐dependent, inhibited by 3 different osteoclast inhibitors and associated with enhanced release of 3 H from [ 3 H]‐proline‐labelled bones. The activity in GCF causing enhanced 45 Ca release was unaffected, or in some samples partially reduced, by ultrafiltration using a filter with a molecular weight cut‐off of 3000 Daltons. The bone‐resorbing activity was temperature sensitive (+90°C, 10 min). The concentrations of prostaglandin E 2 (PGE 2 ) in the diluted GCF eluates, used in the bone resorption bioassay, were too low to be responsible for the release of 45 Ca. Antisera specifically neutralizing human IL‐1α inhibited the stimulatory effect of GCF pooled from several diseased sites. The specific, recombinant human IL‐1 receptor antagonist completely inhibited the effect of pooled GCFs. GCF eluates from diseased sites contained human IL‐1α and IL‐1β at concentrations of 1838±294 pg/ml and 512±91 pg/ml, respectively. Conclusions: These data show that GCF contains activity(ies) stimulating osteoclastic bone resorption in vitro. The factor primarily responsible for this activity seems to be IL‐1α, but IL‐1α is not the sole activator of bone resorption in GCF.