Resistance to Cigarette Smoke Is Increased in Periodontal Ligament Cells by Attachment to Collagen and Fibronectin

• Thomas E. Lallier ^[1] ; Erin Maturin ^[2] ; Matt Brady ^[2] ; Diana Stoute ^[3] ; Tyrous Ward ^[1]
  1. [1] Louisiana State University

     Louisiana State University

     Estados Unidos

     
  2. [2] Department of Pediatric Dentistry, Center of Excellence in Oral and Craniofacial Biology, School of Dentistry, Louisiana State University Health Science Center.
  3. [3] Department of Oral Biology, Center of Excellence in Oral and Craniofacial Biology, School of Dentistry, Louisiana State University Health Science Center.

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• Localización: Journal of periodontology, ISSN 0022-3492, Vol. 86, Nº. 1, 2015, págs. 91-100
• Idioma: inglés
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  • Background: The toxic effects of cigarette smoke often presents in smokers as increased incidence and severity of periodontal disease. These patients demonstrate symptomatic inflammation, increased probing depth, and tooth loss likely attributable to the direct effects of cigarette smoke on periodontal ligament (PDL) fibroblasts. The goal of this in vitro study is to investigate the direct effects of smoking on PDL fibroblasts, focusing on cell–extracellular matrix (ECM) interactions and cell survival.

    Methods: PDL cells were plated for various times on tissue culture plastic, PDL-derived ECMs, collagen Type I, or fibronectin. Cells were exposed to various concentrations of cigarette smoke extract (CSE) at different times during the cell attachment process. Subsequently, cell survival was quantified using calcein-acetoxymethyl ester compound and a fluorescent plate reader.

    Results: After exposure to CSE, PDL cell survival increased with increased cell attachment time to plastic. These observations were independent of soluble factors present in PDL cell–conditioned media. PDL-derived ECMs and collagen Type I–pretreated plates promoted increased cell survival after 1 day of cell attachment. Fibronectin-pretreated plates demonstrated increased cell survival after 3 days of cell attachment.

    Conclusions: Cell–ECM interactions increase survival of PDL cells exposed to CSE. It is suggested that the increased survival is attributable to PDL cells altering their ECM, potentially by depositing collagen and fibronectin. This may imply that cells embedded in an ECM would be more resistant to the toxic effects of cigarette smoke, leading to increased cell death near the exposed edges of a wound.