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David A. Scott, Ph.D.


David A. Scott, Ph.D.

Associate Professor
Oral Health and Systemic Disease Research Group
Phone: 502-852-8905
Fax: 502-852-4052

Tobacco smoking, inflammation, and periodontitis

Periodontitis is a common inflammatory disease leading to the destruction of the supporting tissues of the teeth. Tobacco smoking is a critical risk factor. The mechanisms by which smoking contributes to increased susceptibility to periodontitis, and to systemic inflammatory diseases with common etiology, need to be clarified. Thus, novel therapeutic strategies can be identified to treat tobacco-induced diseases, the world’s largest cause of early fatality. Furthermore, identification of key immune mechanisms dysregulated by tobacco smoke will be highly relevant to non-smokers.

The major current research interests of my laboratory are:

- Tobacco-induced genotypic and phenotypc alterations to the immune potential of the periodontal pathogen, Porphyromonas gingivalis (NIH DE019826).

- Mechanisms of tobacco smoke-induced alterations to effector functions of innate immune cells (NIH DE017680).

- Development of Near- and Mid-Infrared Spectroscopy as potential diagnostic, prognostic, and research tools in tobacco-related periodontal diseases (NIH DE017160).

Recent publications

  1. Scott DA and J Krauss. Neutrophils in periodontal inflammation. Frontiers in Oral Biology (invited review, in press, 2011).
  2. Guzik K, Skret J, Smagur J, Bzowska M, Gajkowska B, Scott DA, Potempa JS. Cigarette smoke-exposed neutrophils die unconventionally but are rapidly phagocytosed by macrophages. Cell Death Dis. 2011;2:e131.
  3. Buduneli N, Larsson L, Biyikoglu B, Renaud DE, Bagaitkar J, Scott DA. Fatty acid profiles in smokers with chronic periodontitis. J Dent Res. 2011;90:47-52
  4. Bagaitkar J, Demuth DR, Daep CA, Renaud DE, Pierce DL, Scott DA. Tobacco upregulates P. gingivalis fimbrial proteins which induce TLR2 hyposensitivity. PLoS One. 2010;5:e9323.
  5. Xiang XM, Liu KZ, Man A, Ghiabi E, Cholakis A, Scott DA. Periodontitis-specific molecular signatures in gingival crevicular fluid. J Periodontal Res. 2010;45:345-52.
  6. Bagaitkar J, Williams LR, Renaud DE, Bemakanakere MR, Martin M, Scott DA, Demuth DR. Tobacco-induced alterations to Porphyromonas gingivalis-host interactions. Environ Microbiol. 2009;11:1242-53.
  7. Bagaitkar J, Demuth DR, Scott DA. Tobacco use increases susceptibility to bacterial infection. Tob Induc Dis. 2008;4:12.
  8. Xu M, Scott JE, Liu KZ, Bishop HR, Renaud DE, Palmer RM, Soussi-Gounni A, Scott DA. The influence of nicotine on granulocytic differentiation - inhibition of the oxidative burst and bacterial killing and increased matrix metalloproteinase-9 release. BMC Cell Biol. 2008;9:19.
  9. Rehani K, Scott DA, Renaud D, Hamza H, Williams LR, Wang H, Martin M. Cotinine-induced convergence of the cholinergic and PI3 kinase-dependent anti-inflammatory pathways in innate immune cells. Biochim Biophys Acta. 2008;1783:375-82.


The financial support of the following bodies is gratefully acknowledged:

NIH (National Institute for Dental and Craniofacial Research)

Canadian Institutes for Health Research

Natural Sciences and Engineering Research Council

Centers for Disease Control

University of Louisville


Drs. Jan Potempa and Don Demuth, Oral Health and Systemic Disease Research Group

Dr. Kan-Zhi Liu, National Research Council, Canada

Dr. Nurcan Buduneli, Periodontics, Ege University, Turkey

Drs. Richard Palmer and Ron Wilson, King’s College London, England

Dr. Lennart Larsson, Lund University, Sweden

Graduate students

Graduate students who wish to pursue a M.Sc. in Oral Biology or Ph.D. are periodically accepted. Interested individuals should e-mail me directly.

Clinical graduate students already at University of Louisville who wish to consider undertaking the research component of their program in my laboratory should e-mail or call into the lab in person.


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