Echocardiography performed using a standardized protocol, which included quality control of the measurements, is an added strength. However, these findings should be considered within the context of some limitations: this is a cross-sectional analysis and hence temporal associations and causality cannot be inferred; biomarkers were measured at one time point only; and some echocardiographic parameters were not available in a subset of study participants due to technical difficulties. The overall suspected relationship between periodontal disease and glycemic control provides a strong rationale for our central hypothesis that increased inflammatory burden and quantitative biomarkers of periodontal disease will be associated with decreased glycemic control. To our knowledge, this has never been evaluated in a T1D cohort. Saliva is a clear mucoserous exocrine derived liquid containing a mixture of secretions from the submandibular, parotid, sublingual and minor glands that provides a representation of overall health status and oral inflammatory burden. Saliva can be obtained noninvasively, safely and economically with minimal processing and required training by personnel. Inflammatory molecules within the saliva are derived from the periodontium via influx of gingival crevicular fluid and from the mucosa. This bio-collection serves as a highly accessible and useful general measurement of oral inflammatory and periodontal burden. Despite the tremendous potential and utility of the saliva for the examination of biomarkers related to systemic disease, limited studies have been conducted in understanding and evaluating the salivary inflammatory burden specifically in T1D. This study demonstrated that specific salivary inflammatory markers in T1D subjects are associated with decreased glycemic control. Two principal components were associated with decreased glycemic control. The inflammatory markers that loaded strongly on these components were MMP-8, MMP-9, and TNF-��. This is the first study that we are aware of to examine the association of multiple salivary inflammatory biomarkers with glycemic control and self-reported gingival condition in T1D subjects. Prior studies examining salivary inflammatory levels within general systemic diseases, T1D, and type 2 diabetes have demonstrated that specific mediators of inflammation are elevated within the saliva of these respective cohorts. Another investigation demonstrated that poor glycemic control was significantly associated with increased IL-1�� levels in gingival crevicular fluid in T2D. In a later report, IL-8 levels did not associate with increased HbA1c. Taken together, these findings solidify the central hypothesis that salivary inflammatory burden can be associated with diseases of autoimmunity, metabolic control and periodontitis. However, the specific relationship between certain cytokines such as IL-1�� and either glycemic or periodontal status can be contradictory and requires further characterization. Proteomic and peptidomic analysis has revealed significant Abmole MK-2206 differences in the saliva between those subjects with T1D and periodontitis versus those with T1D and without periodontitis. A recent report by Engebretson et al. revealed that periodontal intervention failed to promote glycemic control in T2D subjects displaying moderate to advanced chronic periodontitis. These findings would be somewhat discordant with our conclusions indicating that increased inflammatory burden is association with decreased glycemic control.