Andrea Roccuzzo

Smokers employing electronic nicotine delivery systems (ENDS) and heated tobacco products (HTP) are currently the most common types of smoking patients seen in the dental practice. Both types of smoking are currently viewed as less harmful than cigarette smoking. However, many studies already indicate that they could harm oral health. This systematic review and meta-analysis aimed to collect a comprehensive overview of the actual knowledge regarding ENDS and HTP from a clinical and a laboratory perspective. Publications available through PubMed, Embase, the Web of Science, Scopus, and Google Scholar were used to summarize the effects of ENDS and HTP on oral health. Six surveys on self-perceived gum disease (T2 = 9.47 I2 = 99.32%), three cross-sectional studies reporting the BOP score (T2 = 8.68 I2 = 99.13%), and four in vitro studies on apoptosis after vaping exposure in human oral fibroblasts (T 2 = 8.10 I2 = 91.50%) were separately analyzed. The risk of bias ranged from critical to low. Both ENDS and HTP seem to have detrimental effects on periodontal and peri-implant parameters, and laboratory tests confirmed the presence of carcinogenic and inflammatory biomarkers. flavored e-liquids may also be a caries risk factor. Comprehensive smoking counseling should be carried out with all types of smoking patients, investigating the type of habit in terms of duration, nicotine percentage, and additional flavorings. Additional research is necessary to assess the long-term effects of alternative tobacco products on oral health.

Objectives To test the reliability of full zirconia implant‐supported fixed dental prostheses with cantilever extension (FDPCs) after at least 1 year of function. Materials and Methods Thirty‐five patients in need of implant‐supported single unit crowns (SUC) and FDPCs in posterior areas were enrolled. After implant placement, patients were rehabilitated with screw‐retained full‐zirconia FDPCs. Implant survival rate, pocket probing depth (PPD), presence/absence of bleeding on probing (BoP), and presence/absence of mechanical/technical complications were recorded. Mesial and distal radiographic marginal bone levels (mBLs) from baseline (i.e., recall appointment 3–6 months after implant loading [T0]) to the follow‐up examination (i.e., latest recall appointment after at least 12 months after T0 [T1]), were calculated. Results Thirty patients with 34 FDPCs (31 SUCs and 3 FDPs) supported by 37 implants were available for analysis after a mean loading time of 2.6 ± 1.5 years (range: 13–87 months). No implants were lost. MBLs and mean PPD values did not change statistically significantly from T0 to T1 from 0.92 mm ± 0.42 to 0.96 mm ± 0.38 (95% CI: −0.07/0.17; p = .418) and from 2.99 mm ± 0.70 to 3.27 mm ± 0.71 (95% CI: −0.11/0.68; p = .25) respectively. Peri‐implant mucositis was diagnosed in 22 cases. Screw‐loosening and zirconia chipping occurred 1× in 4 patients. Conclusion Within the limitations of the present proof‐of‐principle study, the use of full‐zirconia FDPCs in posterior areas seems a valid and safe short‐term treatment option.

Background Peri‐implant health is characterized by the absence of clinical signs of soft tissue inflammation. Peri‐implant diseases are initiated by the presence of bacterial biofilms and share a similar etiology as that involved in the onset of periodontal diseases. Purpose To summarize available evidence on the physiopathology of peri‐implant diseases with emphasis on similarities and differences with periodontal diseases. Materials and Methods Evidence on the biologic mechanisms involved in the pathogenesis of peri‐implant mucositis and peri‐implantitis were explored in the recent scientific literature. Results Findings of studies in animals and in humans indicate that experimental peri‐implant mucositis leads to a larger inflammatory connective tissue infiltrate and to a higher frequency of bleeding sites around implants compared with teeth. Tissue destruction at experimental peri‐implantitis sites is more pronounced compared with that at experimental periodontitis sites. Although human periodontitis and peri‐implantitis lesions share similarities with respect to etiology and clinical features, they represent distinct entities from a physiopathologic point of view. Conclusions Diagnosis of peri‐implant health requires a clinical examination to confirm absence of peri‐implant soft tissue inflammation. In order to make a correct diagnosis and select the appropriate therapeutic steps to manage peri‐implant diseases, knowledge of their pathogenetic mechanisms is required.