Abstract
Cigarette smoking is a major lifestyle-related risk factor for periodontal diseases. However, the pathophysiological role of cigarette smoking in periodontal disease has yet to be fully elucidated. Here we report that the systemic administration of cigarette smoke condensate or nicotine, which is the major ingredient of cigarette smoke, augmented alveolar bone loss. Concomitantly, the number of osteoclasts in periodontal tissues increased and the expression of receptor activator of nuclear factor κB ligand was upregulated at the ligated side in mice with periodontitis. Nicotine also attenuated alveolar bone repair after ligature removal. These observations highlight the destruction of periodontal tissue by smoking and the unfavorable clinical course of periodontal disease in patients with a cigarette smoking habit. The present study demonstrates that periodontal disease models are useful for elucidating the pathogenesis of cigarette smoking-related periodontal diseases.
Highlights
Periodontal diseases are inflammatory disorders caused by the accumulation of a bacterial biofilm and characterized by the destruction of periodontal tissues [1, 2]
Additional nicotine treatment on days 8, 9, and 10 reduced the recovery of alveolar bone loss, compared with the mice without nicotine treatment after ligature removal [Fig 8A (e)]. These results suggested that nicotine promoted periodontal destruction and delayed the recovery from periodontal tissue destruction. This is the first study to evaluate the effects of cigarette smoke condensate (CSC) and nicotine on periodontal destruction and bone repair in ligature-induced periodontitis in mice
We have demonstrated that systemic administration of CSC and nicotine accelerated alveolar bone destruction following ligation and delayed alveolar bone recovery after ligature removal
Summary
Periodontal diseases are inflammatory disorders caused by the accumulation of a bacterial biofilm and characterized by the destruction of periodontal tissues [1, 2]. Classified as bacterial infections, epidemiological studies have revealed that cigarette smoking is one of the major lifestyle-related risk factors for periodontal disease [3]. Cigarette smoking significantly increases the risk of developing various diseases including cancer, vascular disease, chronic obstructive pulmonary disease, as well as periodontal diseases [4,5,6,7]. It has been suggested that the increased incidence of these diseases in smokers may be due to chronic inhalation of chemicals in cigarette smoke that eventually alters the immune response [6]. Cigarette smoke contains more than 4000 chemicals, including 69 carcinogens [8]. When cigarette smoke is inhaled, the epithelial surface of the oral cavity, bronchi and lungs are exposed to high localized doses of nicotine [9]. Several in vitro studies have shown that nicotine can impair the migration, attachment and proliferation of gingival fibroblasts and PLOS ONE | DOI:10.1371/journal.pone.0155594 May 20, 2016
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