Diabetes mellitus is one of the most prevalent chronic diseases in the United States and worldwide. The persistent hyperglycemic state that characterizes type 1 diabetes leads to a number of significant complications that increase morbidity and mortality in affected individuals. Periodontal disease has been established as one of these complications. Recent research has begun to unravel some of the mechanisms involved in the development of diabetes-associated periodontal infections, but the basic underlying pathogenic mechanisms remain poorly understood. Interestingly, some supporting data also exist for an association between periodontal infections and atherosclerosis, and for an effect of periodontal therapy on the level of metabolic control in poorly controlled diabetic adults. However, additional evidence is needed, and the involved mechanisms need to be explored. In the context of advancing the diagnosis, prevention and treatment of periodontal disease in patients with type 1 diabetes, and taking advantage of an established relationshipwith the Naomi Berrie Diabetes Center on the Columbia Presbyterian Medical Center campus, we propose to examine a cohort of adult type 1 diabetic patients with a disease duration of 10 years. Non-diabetic individuals matched for gender, race, age and periodontal disease severity will be used as controls. We intend to investigate two key features of periodontal infections, namely the specific bacteria of the periodontal lesion and the systemic antibody responses to his bacterial challenge. We will examine the prevalence of a number of periodontal bacteria in subgingival plaque samples, including both putative pathogens and beneficial species, by means of the checkerboard DNA-DNA hybridization assay. We will further assess levels of serum antibodies to the above bacteria by the checkerboard immunoassay. Microbial and antibody profiles will be related to importantdiabetes-associated variables. In a subset of diabetes patients who exhibit the most severe periodontal conditions, we will investigate whether periodontal infection is associated with peripheral blood mononuclear cell activation. We will specifically assess levels of pro-inflammatory mediator of particular importance in atherogenesis, prior to and after mechanical periodontal therapy. Theses studies will markedly enhance our understanding of the oral microbiology and immunology in type 1 diabetes.
Roth, Georg A; Moser, Bernhard; Roth-Walter, Franziska et al. (2007) Infection with a periodontal pathogen increases mononuclear cell adhesion to human aortic endothelial cells. Atherosclerosis 190:271-81 |
Lalla, E; Kaplan, S; Yang, J et al. (2007) Effects of periodontal therapy on serum C-reactive protein, sE-selectin, and tumor necrosis factor-alpha secretion by peripheral blood-derived macrophages in diabetes. A pilot study. J Periodontal Res 42:274-82 |
Lalla, Evanthia; Kaplan, Selma; Chang, Shu-mei J et al. (2006) Periodontal infection profiles in type 1 diabetes. J Clin Periodontol 33:855-62 |