Effects of Cotinine on Human Gingival Fibroblast Migration.
It is well known that tobacco smoking impairs wound healing; a systematic review
and meta analysis concluded that smoking cessation in surgical patients was associated with
significantly decreased rates of post-surgical complications.
Tobacco use is a prime behavioral contributor to periodontal disease with accompanying poor oral wound healing and potential tooth loss.2 As a phase in the wound healing process, fibroblasts transition to myofibroblasts and form granulation tissue by secreting and remodeling the extracellular matrix.
Fibroblasts are located in gingival, lingual, buccal, labial and palatal structures as well as the periodontal ligament fiber groups, and thus are central to production and maintenance of the connective tissue underlying the surface epithelium of the oral mucosa and periodontium. Indeed fibroblasts are the main cell type of the periodontium.
Additional mechanisms to explain nicotine-inhibited cell migration may be through effects on cell adhesion. Nicotine in the range of 5 ng/ml to 10 mg/ml inhibited the attachment and growth of human periodontal ligament fibroblasts.
Nicotine-induced decrease of beta1 integrin expression suggests an impairment of human gingival fibroblast ability to adhere to extracellular matrix.10,11 Conversely whole cigarette smoke
inhibited fibroblast migration and correlated with an increased level of focal adhesions, suggesting that nicotine-inhibited cell migration was due to increased cell adhesion.
Using nicotine alone, increasing nicotine concentrations correlated to increased
human gingival fibroblast adhesion.
Dent Open J. 2015; 2(1): 25-31. doi: 10.17140/DOJ-2-106
