Cigarette smoke condensate stimulates urokinase production through the generation of reactive oxygen species and activation of the mitogen activated protein kinase pathways in human gingival fibroblasts

Abstract

Cigarette smoke condensate stimulates urokinase production and plasmin activation in gingival fibroblasts. Moreover, cigarette smoke condensate-stimulated urokinase production depends on both the activation of ERK/JNK pathways and on the generation of intracellular reactive oxygen species. These results show that cigarette smoke may alter connective tissue remodeling by inducing production of the urokinase-type plasminogen activator through specific signaling pathways.

Impact of smoking on inflammation: overview of molecular mechanisms

“…An additive collagen cleavage effect was observed when human gingival fibroblasts were treated with both nicotine and P. gingivalis. More recently, cigarette smoke condensate has been shown to stimulate urokinase production and plasmin activation in human gingival fibroblasts [73]. Although most of these studies used higher concentrations in vitro than those expected in plasma of smokers, the evidence might lead one to believe that tobacco smoking impacts on the inflammatory process in the periodontium through its effect on fibroblasts.…”

Cigarette smoke condensate modulates migration of human gingival epithelial cells and their interactions with Porphyromonas gingivalis

“…Previous studies have explored the role of nicotine on the altered wound healing response described in smokers. However, only recent studies have analyzed the role of the whole mixture of components present in CS that may affect cell responses involved in periodontal tissue repair . In the present study, using a gingival epithelial cell line as a model, we evaluated in vitro the effects of CSC on host cell functions and the potential interaction with a major periodontal pathogen, P. gingivalis .…”

“…Despite these limitations, however, in vitro experiments with CSC have a history of providing useful information . CSC is composed of major toxicants such as nicotine, phenol, anthracyclic hydrocarbons, nitrosamines, heavy metals and chemical carcinogens, such as 4‐(methylnitrosamino)‐1‐(3‐pyridyl)‐1‐butanone .…”

Antioxidants Counteract Nicotine and Promote Migration via RacGTP in Oral Fibroblast Cells

“…A recent study 3 showed that cigarette smoking was one of the risk factors involved in the development and progression of periodontal disease. Smoking promotes a high degree of ROS release that results in heightened oxidative damage to gingival tissues, periodontal ligaments (PDLs), and alveolar bone 4 . Previous studies have documented the effects of smoking including persistent gingival bleeding, 5 vertical bone loss, 6 and poor treatment outcomes 7 .…”

“…These studies 3‐10 evaluated the mode of action that tobacco smoking uses to affect oral health. In addition to an increase in ROS formation, smoking may also decrease antioxidant (AO) levels.…”