Laboratory of David A. Scott, PhD

Part-time Faculty - Department Oral Immunology & Infectious Diseases

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Research interests

Tobacco, marijuana, inflammation and periodontal diseases

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Illustration of how GSK3β inhibition abrogates pathogen-induced bone loss
GSK3β inhibition abrogates pathogen-induced bone loss: 8-12 week old B6129SF2/J mice were randomly divided into three control groups and two experimental groups (n = 5 per group). The control groups were treated with cellulose (sham infected), 0.02% DMSO, or SB216763 (10 mg/kg) respectively. The experimental groups were orally infected with P. gingivalis 33277 with or without pretreatment of the GSK3 inhibitor, SB216763 (10 mg/kg). Alveolar bone loss was visualized by methylene blue / eosin staining six weeks later. Typical maxillae from (A) sham-infected, (B) P. gingivalis-infected, and (C) SB216763-treated, P. gingivalis-infected mice are presented. (D) The distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC) was measured 6 weeks post infection at 14 predetermined maxillary buccal sites, marked by yellow diamonds, in 8-12 week old B6129SF2/J mice divided into three control (cellulose; DMSO; or SB216763 treated) and two experimental (P. gingivalis-infected; and SB216763-treated, P. gingivalis-infected mice) groups. Data are presented as mean distance CEJ-ABC in mm ± s.d. where there are 5 mice per group. Symbols: * p < 0.05 compared to P. gingivalis treated group; ** p < 0.01 compared to P. gingivalis treated group. (Molecular Medicine 2012, 18: 1190-6).

Periodontitis is a common inflammatory disease defined by the irreversible destruction of the supporting tissues of the teeth. Tobacco and cannabis smoking are critical risk factors for this and other chronic bacterial-induced inflammatory diseases. 

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. We are particularly interested in (a) how oral bacteria, primarily Porphyromonas gingivalis, survive in a tobacco-rich environments; (b) how tobacco-induced genotypic and phenotypic alterations to oral bacterial pathogens change how such microbes are recognized by the immune system; and (c) how tobacco- and marijuana-derived molecules erroneously activate endogenous anti-inflammatory pathways, such as nicotinic cholinergic signaling, and thus suppresses the ability of the immune system to fight off periodontal pathogens.

Current funding

  • P. gingivalis genes essential for tobacco smoke survival, R01DE026963 (P.I.)
  • SGK1 and the control of periodontal inflammation, R01DE026727 (Co-I)

Frequent collaborators

  • Drs. Richard Lamont, Jan Potempa and Huizhi Wang (Oral Immunology and Infectious Diseases, UofL)
  • Dr. Debbie Yoder-Himes (Biology, UofL)
  • Dr. Nurcan Buduneli (Periodontics, Ege University, Turkey)
  • Dr. Jackie Singleton (Dental Hygiene, UofL)

Graduate students

Graduate students who wish to pursue a MS in Oral Biology or PhD (Microbiology & Immunology; Pharmacology & Toxicology; or Interdisciplinary Studies) are periodically accepted. Interested individuals should email 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 email or call into the lab (School of Dentistry, Room 260) in person.

Publications 

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