Ongoing research in animal models and human populations continues to implicate oral infections like periodontitis in the etiology of systemic conditions such as atherosclerosis and pre-term low birth weight. Indeed, the chronic and septic challenge posed by oral pathogens appears to perpetuate both the local and systemic release of inflammatory mediators leading to manifestations of disease at both levels. The proposed human cohort study aims 1) to determine the extent of systemic inflammatory responses in patients with advanced, end-stage oral injections; and 2) to evaluate changes in these responses following complete elimination and/or treatment of the oral infection. 195 patients meeting inclusion criteria will be recruited from the pool of patients seeking conventional, comprehensive care at UNC School of Dentistry Clinics. At baseline, patients will be categorized on one of four oral disease cohorts: 1) terminal dentition (i.e. most teeth requiring extraction) due to periodontitis (TD-P); 2) terminal dentition due to caries (TD-C); 3) terminal dentition due to periodontitis and caries (i.e., mixed) (TD-M); an 4) moderate to advanced adult periodontitis (AP) but with a salvageable dentition. Baseline data regarding patient demographics, medical and dental histories, oral health impact profile (OHIP) and oral health status (dental, periodontal and gingival crevicular fluid evaluations) will be collected. Thereafter, terminal dentition patients will be treated with prescribed extraction and prosthetic treatments. AP patients will be treated with conventional non-surgical therapy. At baseline (pretreatment) and at 2, 6, 26, and 52 weeks post-treatment, whole blood will be collected for all patients. Serum samples will be analyzed using ELISA techniques for the following groups of mediators: acute phase response reactants (IL-6, haptoglobin, LPS-binding protein and C-reactive protein), oxidative stress markers (8-epi-PGF2a) and homeocystein. In addition, serum fibrinogen levels and while blood counts will be reported as markers of hemostasis and hematology. Inter-group differences in mediator responses secondary to the interventions will be analyzed using repeated measures ANCOVA. If the data indicate a pronounced reduction in systemic inflammatory mediators following oral infection elimination (especially TD-P), protocols evaluating oral disease preventive interventions and systemic, clinical outcomes may be justified.

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Comprehensive Center (P60)
Project #
3P60DE013079-03S1
Application #
6644945
Study Section
Project Start
2001-08-01
Project End
2002-07-31
Budget Start
1998-10-01
Budget End
1999-09-30
Support Year
3
Fiscal Year
2002
Total Cost
$1
Indirect Cost
Name
University of North Carolina Chapel Hill
Department
Type
DUNS #
078861598
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599
Arce, R M; Caron, K M; Barros, S P et al. (2012) Toll-like receptor 4 mediates intrauterine growth restriction after systemic Campylobacter rectus infection in mice. Mol Oral Microbiol 27:373-81
Qian, Li; Wu, Hung-ming; Chen, Shih-Heng et al. (2011) ?2-adrenergic receptor activation prevents rodent dopaminergic neurotoxicity by inhibiting microglia via a novel signaling pathway. J Immunol 186:4443-54
Arce, R M; Diaz, P I; Barros, S P et al. (2010) Characterization of the invasive and inflammatory traits of oral Campylobacter rectus in a murine model of fetoplacental growth restriction and in trophoblast cultures. J Reprod Immunol 84:145-53
Maile, Laura A; Busby, Walker H; Nichols, Timothy C et al. (2010) A monoclonal antibody against alphaVbeta3 integrin inhibits development of atherosclerotic lesions in diabetic pigs. Sci Transl Med 2:18ra11
Lemmon, Christopher A; Chen, Christopher S; Romer, Lewis H (2009) Cell traction forces direct fibronectin matrix assembly. Biophys J 96:729-38
Qian, Li; Hu, Xiaoming; Zhang, Dan et al. (2009) beta2 Adrenergic receptor activation induces microglial NADPH oxidase activation and dopaminergic neurotoxicity through an ERK-dependent/protein kinase A-independent pathway. Glia 57:1600-9
Light, Kathleen C; Bragdon, Edith E; Grewen, Karen M et al. (2009) Adrenergic dysregulation and pain with and without acute beta-blockade in women with fibromyalgia and temporomandibular disorder. J Pain 10:542-52
Williams, Ray C (2008) Understanding and managing periodontal diseases: a notable past, a promising future. J Periodontol 79:1552-9
Qian, Li; Wei, Sung-Jen; Zhang, Dan et al. (2008) Potent anti-inflammatory and neuroprotective effects of TGF-beta1 are mediated through the inhibition of ERK and p47phox-Ser345 phosphorylation and translocation in microglia. J Immunol 181:660-8
Qian, Li; Flood, Patrick M (2008) Microglial cells and Parkinson's disease. Immunol Res 41:155-64

Showing the most recent 10 out of 70 publications