Levels of cytokine receptor activator of nuclear factor κB ligand in gingival crevicular fluid in untreated chronic periodontitis patients
Author
dc.contributor.author
Vernal Astudillo, Rolando
Author
dc.contributor.author
Chaparro, Alejandra
Author
dc.contributor.author
Graumann, Rebecca
Author
dc.contributor.author
Puente, Javier
Author
dc.contributor.author
Valenzuela, Maria Antonieta
Author
dc.contributor.author
Gamonal Aravena, Jorge Antonio
Admission date
dc.date.accessioned
2018-12-20T15:22:34Z
Available date
dc.date.available
2018-12-20T15:22:34Z
Publication date
dc.date.issued
2004
Cita de ítem
dc.identifier.citation
Journal of Periodontology, Volumen 75, Issue 12, 2004, Pages 1586-1591.
Identifier
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00223492
Identifier
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10.1902/jop.2004.75.12.1586
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/158913
Abstract
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Background: Receptor activator of nuclear factor κB ligand
(RANK-L) is a cytokine involved in the regulation of osteoclastogenesis in bone remodeling and inflammatory osteolysis. One
of the major causes of tooth loss in humans is bone destruction.
The aim of our study was to determine the presence of RANK-L
in gingival crevicular fluid (GCF) samples from adult patients with
untreated chronic periodontitis and in healthy controls. We also
identified the RANK-L present in lesions undergoing episodic
attachment loss from GCF.
Methods: GCF samples were collected from two periodontally
affected sites (probing depth ≥5 mm, attachment loss ≥3 mm)
in 20 patients (N = 40). After monitoring for 4 months, seven
patients showed active periodontal disease, and GCF samples
were collected from one active and one inactive site (N = 14
samples). The comparison with healthy controls was carried out
by collecting GCF samples from 12 healthy volunteers (N = 24
samples). GCF was collected using a paper strip, and enzymelinked immunosorbent assay (ELISA) was performed to determine the total amount of RANK-L.
Results: RANK-L was found in a higher proportion (85%) of
samples from patients than from controls (46%). The total amount
of RANK-L was significantly higher in patients (115.53 ± 78.18
picograms [pg]) than in healthy subjects (63.08 ± 55.08 pg) (P =
0.003). Active sites, presumably associated with tissue destruction, had significantly higher levels of RANK-L than their inactive
counterparts (125.95 pg versus 91.80 pg, P = 0.007).
Conclusion: GCF total amount of RANK-L is significantly
increased in periodontal disease, supporting its role in the alveolar bone loss developed in this disease.