Award Date


Degree Type


Degree Name

Master of Science (MS)


Dental Medicine

First Committee Member

Brian Chrzan

Second Committee Member

Katherine Howard

Third Committee Member

Bob Martin

Fourth Committee Member

Jennifer Pharr

Number of Pages



Orthodontic tooth movement requires coordinated bone resorption and deposition in response to mechanical stimuli. Underlying this process is a complex network of biological signaling to activate osteoclasts and osteoblasts. The broad category of small proteins known as cytokines include many potential mediators involved in complex interactions to initiate tooth movement. One of the signaling factors is interleukin-1β (IL-1β), which plays a critical role in inflammation and bone erosion via the activation of osteoclasts. IL-1β is a key cytokine involved in osteoclast differentiation, multinucleation, and overall survival. Recently, interleukin-17 (IL-17) has been identified as a potent inducer of inflammation that influences bone homeostasis. IL-17 affects a broad range of cell types and enhances the production of other pro-inflammatory cytokines, including IL-1β, IL-6 and TNF-α. To date, few studies have examined the role of IL-17 in orthodontic tooth movement. However, studies focusing on the role of IL-17 in bone homeostasis suggest that IL-17 may be a key mediator of bone resorption during orthodontic tooth movement. The present study expanded upon previous research by Faulkner (2011) which demonstrated elevated IL-6 levels in GCF within 24 hours of orthodontic force activation. The aim of this study was to evaluate whether increased levels of bone resorptive cytokines (IL-17 and IL-1β) can be detected in GCF from the compression (resorptive) sites after application of orthodontic force. This study also evaluated the expression of IL-17 and IL-1β at various time points to determine if there was a temporal relationship between the expressions of these two cytokines. GCF samples were collected 1, 6, and 24 hours after initial activation from mesiobuccal (MB) and distolingual (DL) sites of experimental and control teeth from 9 patients undergoing orthodontic treatment. Control teeth were not bonded, thus no force was applied. Patients returned in 5-7 weeks for their 1st retie activation visit. GCF iv samples were collected again at the same time intervals. GCF was sampled three times for each site and time point and pooled for volume analysis. A Bradford assay was performed to obtain total protein levels of each pooled sample at each time point. MILLIPLEX® MAP (multianalyte profiling) assays were used to detect IL-1β and IL-17 in the GCF samples from both the tension and compression sites. IL-1β and IL-17 levels for both experimental and control sites were compared with a paired t-test. Levels of IL-1β at the mesiobuccal sites peaked at 6 hours after orthodontic force application at both the initial and retie visits. While all previous studies reported peak expression of IL-1β at 24 hours, this present study was the only study to measure cytokine levels at 6 hours post force activation. Levels of IL-1β peaking at 6 hours may imply that the inflammatory response is most reactive at 6 hours post force application. Levels of IL17 peaked at the mesiobuccal site 24 hours after force application at both the initial and retie visits. There seems to be no correlation between the temporal expression of IL-1β and IL-17. It is possible that better detection methods or additional patients and sites may help to determine smaller variations in IL-17 at compression and tension sites. This may also help with defining a temporal relationship between the expressions of IL-1β and IL-17.



File Format


Degree Grantor

University of Nevada, Las Vegas




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