Impact of Smoking Cessation on Periodontal Tissues.

There is cumulative evidence supporting the negative effects of smoking on periodontal tissues. Smoking cessation can be successfully accomplished through specific programs, including behaviour modification and medications, and has been suggested as a suitable way to reduce the risk of several diseases, including periodontitis. The aim of this review is to provide a concise overview of the current knowledge about the impact of smoking cessation on periodontal tissues and therapy, with data from studies published in the last 15 years. Literature was searched using Medline database from 2005 up to and including September 2020 using medical subject heading (MeSH) terms and other search terms, restricted to the English language. Studies were evaluated and summarised in a narrative review format. Results demonstrated that there is convincing evidence to support the benefits of tobacco cessation in reducing the risk of periodontitis and tooth loss. In addition, the harmful effects of smoking on periodontal tissues seem to be assuaged as the number of years since quitting increases. The existing current evidence, even limited, also shows that smoking cessation may result in additional benefits to the outcome of nonsurgical periodontal treatment. Periodontal care providers should not only check their patient's smoking habit for estimating risk of disease progression and predictability of periodontal therapy, but they should also help smokers improve their oral and systemic health by providing efficient and personalised tobacco-cessation counselling and treatment.

Levels of Gene Expression of Immunological Biomarkers in Peri-Implant and Periodontal Tissues.

This study compared the gene expression of the immunoinflammatory markers interleukin (IL)-6, IL-1ß, and tumor necrosis factor alpha (TNF-α), the matrix metalloproteinases (MMP)-1, -2, -8, and -9, and the tissue inhibitors of matrix metalloproteases (TIMP)-1 and -2 in the gingival tissue of individuals with periodontal and peri-implant disease. The study population included individuals with four periodontal statuses: periodontal health (PH group, n = 20); periodontitis (P group, n = 20); peri-implant health (PIH group, n = 20), and peri-implantitis (PI group, n = 20). Gingival biopsies were collected from one tooth per patient according to the inclusion criteria of each group. The mRNA levels of IL-6, IL-1ß, TNF-α, MMP-1, MMP-2, MMP-8, MMP-9, TIMP-1, and TIMP-2 were evaluated by qPCR. The levels of IL-1ß were significantly higher in the PI group when compared to the other groups (p < 0.05), while the levels of IL-6 were significantly higher in the groups with periodontal and peri-implant disease when compared with the healthy groups (p < 0.05); however, the levels of IL-6 did not differ between the PI and P groups (p > 0.05). For all other studied biomarkers, no significant differences were observed between groups (p > 0.05). IL-6 and IL-1ß presented higher levels of mRNA in diseased periodontal and peri-implant tissues. However, the expression of metalloproteinases and their inhibitors did not differ between the different periodontal statuses.