| 1. |
- Dionigi, Carlotta, et al.
(author)
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Cellular expression of epigenetic markers and oxidative stress in periodontitis lesions of smokers and non-smokers
- 2022
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In: Journal of Periodontal Research. - : Wiley. - 0022-3484 .- 1600-0765. ; 57:5, s. 952-959
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Journal article (peer-reviewed)abstract
- Objective To evaluate differences in the cellular expression of epigenetic markers and oxidative stress in periodontitis lesions between current smokers and non-smokers. Background Tobacco smoking is recognized as one of the major risk factors for periodontitis. However, the mechanisms by which smoking affects the progression of the disease remain to be determined. Methods Twenty-five current smokers and 21 non-smokers with generalized severe periodontitis were included. From each patient, one soft tissue biopsy from a periodontitis site was harvested and prepared for histological analysis. The infiltrated connective tissue (ICT) was selected as the region of interest to assess the cellular expression of epigenetic markers and reactive oxygen/nitrogen species (RONS) by immunohistochemistry. Results Although the ICT of smokers and non-smokers did not differ in size or in the expression of markers for DNA damage or oxidative stress, current smokers presented with significantly lower area proportions and densities of cells positive for the epigenetic markers DNMT1 and AcH3. In addition, periodontitis lesions in current smokers presented with a diminished antimicrobial activity, as indicated by significantly lower densities and area proportions of NOX2- and iNOS-positive cells. Conclusions Components of the host response and epigenetic mechanisms in periodontitis lesions in smokers are downregulated as opposed to lesions of non-smokers.
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| 2. |
- Lindhe, Jan, et al.
(author)
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Peri-implant diseases : consensus report of the Sixth European Workshop on Periodontology.
- 2008
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In: Journal of Clinical Periodontology. - 0303-6979 .- 1600-051X. ; 35:8 Suppl, s. 282-285
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Journal article (peer-reviewed)abstract
- Issues related to peri-implant disease were discussed. It was observed that the most common lesions that occur, i.e. peri-implant mucositis and peri-implantitis are caused by bacteria. While the lesion of peri-implant mucositis resides in the soft tissues, peri-implantitis also affects the supporting bone. Peri-implant mucositis occurs in about 80% of subjects (50% of sites) restored with implants, and peri-implantitis in between 28% and 56% of subjects (12-40% of sites). A number of risk indicators were identified including (i) poor oral hygiene, (ii) a history of periodontitis, (iii) diabetes and (iv) smoking. It was concluded that the treatment of peri-implant disease must include anti-infective measures. With respect to peri-implant mucositis, it appeared that non-surgical mechanical therapy caused the reduction in inflammation (bleeding on probing) but also that the adjunctive use of antimicrobial mouthrinses had a positive effect. It was agreed that the outcome of non-surgical treatment of peri-implantitis was unpredictable. The primary objective of surgical treatment in peri-implantitis is to get access to the implant surface for debridement and decontamination in order to achieve resolution of the inflammatory lesion. There was limited evidence that such treatment with the adjunctive use of systemic antibiotics could resolve a number of peri-implantitis lesions. There was no evidence that so-called regenerative procedures had additional beneficial effects on treatment outcome.
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| 3. |
- Lindhe, Jan, et al.
(author)
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Peri-implant diseases : consensus report of the Sixth European Workshop on Periodontology.
- 2008
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In: Journal of Clinical Periodontology. - : Blackwell Munksgaard. - 0303-6979 .- 1600-051X. ; 35:8 Suppl, s. 282-285
-
Journal article (peer-reviewed)abstract
- Issues related to peri-implant disease were discussed. It was observed that the most common lesions that occur, i.e. peri-implant mucositis and peri-implantitis are caused by bacteria. While the lesion of peri-implant mucositis resides in the soft tissues, peri-implantitis also affects the supporting bone. Peri-implant mucositis occurs in about 80% of subjects (50% of sites) restored with implants, and peri-implantitis in between 28% and 56% of subjects (12-40% of sites). A number of risk indicators were identified including (i) poor oral hygiene, (ii) a history of periodontitis, (iii) diabetes and (iv) smoking. It was concluded that the treatment of peri-implant disease must include anti-infective measures. With respect to peri-implant mucositis, it appeared that non-surgical mechanical therapy caused the reduction in inflammation (bleeding on probing) but also that the adjunctive use of antimicrobial mouthrinses had a positive effect. It was agreed that the outcome of non-surgical treatment of peri-implantitis was unpredictable. The primary objective of surgical treatment in peri-implantitis is to get access to the implant surface for debridement and decontamination in order to achieve resolution of the inflammatory lesion. There was limited evidence that such treatment with the adjunctive use of systemic antibiotics could resolve a number of peri-implantitis lesions. There was no evidence that so-called regenerative procedures had additional beneficial effects on treatment outcome.
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| 4. |
- Schmidt, J. C., et al.
(author)
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Periodontitis lesions in smokers and non-smokers
- 2020
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In: European Journal of Oral Sciences. - : Wiley. - 0909-8836 .- 1600-0722. ; 128:3, s. 196-203
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Journal article (peer-reviewed)abstract
- Differences in the progression of periodontitis have been observed between smokers and non-smokers. The aim of the present study was to compare vascular and inflammatory cell densities in periodontitis lesions from smokers and non-smokers to gain further understanding of the influence of smoking on histopathological characteristics of the disease. Two groups of patients with generalized severe periodontitis were recruited. One group consisted of 25 current smokers, aged 33-69 yr, while the second group comprised 21 non-smokers, aged 35-76 yr. From each patient, gingival biopsies were harvested from one periodontitis site (probing pocket depth >= 6 mm and bleeding on probing) and one site without clinical signs of gingival inflammation (reference site). Immunohistochemical analyses were performed to assess the density of vessels and inflammatory cells. Small differences existed between smokers and non-smokers regarding the size, proportion, number, and density of cells in periodontitis lesions. However, the vascular density in periodontitis lesions was significantly higher in non-smokers than in smokers. In clinically healthy reference sites, lesions were considerably smaller than in periodontitis sites and presented with similar vascular densities in smokers and non-smokers.
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