Causal assessment of smoking and tooth loss: A systematic review of observational studies

<p>Abstract</p> <p>Background</p> <p>Tooth loss impairs oral function. The aim of the present review was to evaluate the causal association between smoking and tooth loss on the basis of high-quality studies.</p> <p>Methods</p> <p>Relevant literature was searched and screened, and the methodological quality was assessed. Information on the strength of the association between smoking and tooth loss, the dose-response relationship and natural experimental data was collected and evaluated with respect to consistency and study design.</p> <p>Results</p> <p>Our literature search yielded 496 citations, and 6 cross-sectional and 2 cohort high-quality studies examining 58,755 subjects in four countries. All studies reported significant associations, although the strength of the association was usually moderate. Four studies reported dose-response relationships between exposure to smoking and the risk of developing tooth loss. A decrease in the risk of tooth loss for former smokers was evident in six studies. Interpretation of evidence for each element was consistent, despite some shortcomings regarding study type and population.</p> <p>Conclusions</p> <p>Based on the consistent evidence found with the existing biological plausibility, a causal association between smoking and tooth loss is highly likely. Further studies using a cohort design and different populations are necessary to confirm this association.</p

Impact of supragingival therapy on subgingival microbial profile in smokers versus non-smokers with severe chronic periodontitis

The aim of this study was to assess subgingival microbiological changes in smokers versus non-smokers presenting severe chronic periodontitis after supragingival periodontal therapy (ST).Non-smokers (n=10) and smokers (n=10) presenting at least nine teeth with probing pocket depth (PPD) (&#x2265;5 mm), bleeding on probing (BoP), and no history of periodontal treatment in the last 6 months were selected. Clinical parameters assessed were plaque index (PI), BoP, PPD, relative gingival margin position (rGMP) and relative clinical attachment level (rCAL). Subgingival biofilm was collected before and 21 days after ST. DNA was extracted and the 16S rRNA gene was amplified with the universal primer pair, 27F and 1492R. Amplified genes were cloned, sequenced, and identified by comparison with known 16S rRNA sequences. Statistical analysis was performed by Student&#x0027;s t and Chi-Square tests (&#x03B1;=5%).Clinically, ST promoted a significant reduction in PI and PPD, and gain of rCAL for both groups, with no significant intergroup difference. Microbiologically, at baseline, data analysis demonstrated that smokers harbored a higher proportion of Porphyromonas endodontalis, Bacteroidetes sp., Fusobacterium sp. and Tannerella forsythia and a lower number of cultivated phylotypes (p&#60;0.05). Furthermore, non-smokers featured significant reductions in key phylotypes associated with periodontitis, whereas smokers presented more modest changes.Within the limits of the present study, ST promoted comparable clinical improvements in smokers and non-smokers with severe chronic periodontitis. However, in smokers, ST only slightly affected the subgingival biofilm biodiversity, as compared with non-smokers

Epigenetic changes caused by diabetes and their potential role in the development of periodontitis

Aims/Introduction Periodontal disease, a chronic inflammation induced by bacteria, is closely linked with diabetes mellitus. Many complications associated with diabetes are related to epigenetic changes. However, the exact epigenetic changes whereby diabetes affects periodontal disease remain largely unknown. Thus, we sought to investigate the role of diabetes-dependent epigenetic changes of gingival tissue in the susceptibility to periodontal disease. Materials and Methods We studied the effect of streptozotocin-induced diabetes in minipigs on gingival morphological and epigenetic tissue changes. Accordingly, we randomly divided six minipigs into two groups: streptozotocin-induced diabetes group, n = 3; and non-diabetes healthy control group, n = 3. After 85 days, all animals were killed, and gingival tissue was collected for histology, deoxyribonucleic acid methylation analysis and immunohistochemistry. Results A diabetes mellitus model was successfully created, as evidenced by significantly increased blood glucose levels, reduction of pancreatic insulin-producing β-cells and histopathological changes in the kidneys. The gingival tissues in the diabetes group presented acanthosis of both gingival squamous epithelium and sulcular/junctional epithelium, and a significant reduction in the number and length of rete pegs. Deoxyribonucleic acid methylation analysis showed a total of 1,163 affected genes, of which 599 and 564 were significantly hypermethylated and hypomethylated, respectively. Immunohistochemistry staining showed that the hypomethylated genes – tumor necrosis factor-α and interleukin-6 – were positively expressed under the junctional epithelium area in the diabetes group. Conclusions Diabetes mellitus induces morphological and epigenetic changes in periodontal tissue, which might contribute to the increased susceptibility of periodontal diseases in patients with diabetes.</p