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Relationship between substance P and interleukin-1β in gingival crevicular fluid during orthodontic tooth movement in adults

Metabolism by peptidases plays an important role in modulating the levels of biologically-active neuropeptides, while that of substance P (SP), a component of gingival crevicular fluid (GCF), may potentiate the inflammatory process in orthodontic tooth movement. The aim of this study was two-fold: (...

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Bibliographic Details
Published in:European journal of orthodontics 2006-06, Vol.28 (3), p.241-246
Main Authors: Yamaguchi, Masaru, Yoshii, Mizuho, Kasai, Kazutaka
Format: Article
Language:English
Online Access:Get full text
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Summary:Metabolism by peptidases plays an important role in modulating the levels of biologically-active neuropeptides, while that of substance P (SP), a component of gingival crevicular fluid (GCF), may potentiate the inflammatory process in orthodontic tooth movement. The aim of this study was two-fold: (1) to investigate GCF levels of SP and interleukin-1β (IL-1β) during human orthodontic tooth movement, and (2) to determine the correlation coefficients between SP and IL-1β levels in the GCF. The subjects were 3 males, with a mean age of 21.3 ± 2.8 years old, and 6 females, with a mean age of 23.1 ± 2.4 years, undergoing orthodontic movement of a single tooth, with the contralateral tooth used as the control. GCF was sampled at the control and treatment (compression) sites before and 1, 4, 8, 24, 72, 120, and 168 hours after initiation of orthodontic treatment. Prevention of plaque-induced inflammation allowed assessment of the dynamics of mechanically stimulated SP and IL-1β levels in the GCF, which were determined using enzyme-linked immunosorbent assay (ELISA) kits. GCF levels of SP and IL-1β for the treated teeth were significantly higher (P < 0.001) than for the corresponding control teeth from 8 to 72 hours, and peaked at 24 hours. These results show that the amounts of SP and IL-1β in GCF increase with orthodontic tooth movement, and indicate that such increases may be involved in inflammation in response to mechanical stress.
ISSN:1460-2210
DOI:10.1093/ejo/cji100