Introduction

Over the last decade, periodontitis, a chronic bacterial infection of the oral cavity, has emerged as a novel risk factor for cardiovascular disease (CVD). Biofilms in the oral cavity on soft and hard tissues contain greater than 1010 organisms, many of which are pathogenic in that they can evade local host defenses to elicit local inflammation, as well as gain access to the circulation to induce systemic inflammation. Within the local periodontal tissues, monocytes and other immune cells recognize lipo-polysaccharides in the bacterial cell wall and other toll-

KAR.GEII

Steven Offenbacher, DDS PhD, MMSc

Center for Oral and Systemic Diseases, UNC School of Dentistry University of North Carolina at Chapel Hill, CB No. 7455, DRC Rm 222 Chapel Hill, NC 27599-7455 (USA)

Tel. +1 919 962 7081, Fax +1 919 966 7537, E-Mail [email protected]

like receptor agonists and secrete various inflammatory mediators, including prostaglandin E 2 (PGE 2), interleu-kin (IL)-1p, IL-6, and tumor necrosis factor-a (TNFa) [1, 2]. The effects of systemic dissemination of these bacteria results in hepatic activation of the acute phase response with increases in C-reactive protein (CRP) and IL-6 [24]. Furthermore, oral organisms are capable of invading the endothelial lining of the major elastic arteries [5] and have both nucleotide signals and viable bacteria within atheromatous plaques [6, 7]. Consequently, these bacteria in combination with inflammatory cytokines and acute phase reactants are believed to contribute to an acceleration of systemic atherosclerosis [8-10], and the development of clinical CVD. Indeed, several studies, cross-sectional [11, 12], case-control [13-16], and longitudinal [17-22], have demonstrated an association between the clinical signs of periodontitis and atherosclerotic cardiovascular disease. A smaller number of reports did not show a significant association [19, 23, 24].

Recently, studies have shown that systemic antibody to specific oral pathogens has even stronger associations with cardiovascular risk for events other than clinical signs of disease [25-29]. (This result has been suggested to perhaps reflect the fact that the elevated titers reflect a greater systemic exposure to these pathogens, which is not necessarily related to traditional signs of local peri-odontal disease.)

Chronic kidney disease (CKD) shares many risk factors with CVD. We had previously postulated that peri-odontitis may be associated with CKD, and demonstrated this association in two independent population-based surveys [30, 31], and a cohort of patients with end-stage kidney disease [32-34]. These studies used traditional measures of periodontal disease, including a historical definition such as the extent of bone loss around the teeth, but did not consider microbial etiology. Yet the link between periodontal disease and CKD may be more likely attributable to concomitant infection and inflammation that is not readily measured by the clinical evaluation of periodontal disease. In the present study we explored the relationship between serum antibodies to periodontal pathogens and renal insufficiency. We examined the association of serum Immunoglobulin-G (IgG) antibody titers to a specific panel of periodontal bacteria in the Dental Atherosclerosis Risk in Communities population to examine whether increased titers were associated with reduced kidney function.

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