The impact of smoking on peri-implant microbiota: A systematic review.

OBJECTIVES: Peri-implantitis is associated with bacterial plaque biofilms and with patients who have a history of periodontitis. Smoking is a risk factor for periodontitis, but the relationship between smoking and peri­implantitis is unclear. The aim of this systematic review was to assess evidence ascertaining the relationship between smoking and peri­implant microbiota. DATA SOURCES: An electronic search was conducted in the MEDLINE/PubMed, Embase and Scopus® databases in duplicate up to January 2023 without language restrictions. Studies were considered eligible for inclusion if they involved evaluation of the peri­implant microbiota of smokers and nonsmokers. Methodological quality was assessed with the adapted Newcastle-Ottawa scale. STUDY SELECTION: Fourteen studies were identified for inclusion in the present study, and 85.7% of the studies were defined as medium to high methodological quality. Overall, the evidence presented in this review was limited to medium to high methodological quality. The data indicates that significantly higher frequencies of anaerobic pathogens are detectable in healthy peri­implant tissues of smokers. A lower diversity of microbiota was observed in healthy peri­implant sites of smokers. In the transition from clinically healthy to a diseased status, smoking shaped a reduced peri­implant microbiota by depleting commensal and enriching pathogenic species. CONCLUSIONS: The composition of peri­implant microbiota may be influenced by smoking. More studies are needed to determine the impact of smoking on peri­implant microbiota. CLINICAL SIGNIFICANCE: In the transition from clinically healthy to a diseased status, smoking shaped a reduced peri­implant microbiota by depleting commensal and enriching pathogenic species. The composition of peri­implant microbiota may be influenced by smoking.

Silibinin alleviates inflammation-induced bone loss by modulating biological interaction between human gingival fibroblasts and monocytes.

BACKGROUND: Silibinin has shown various pharmacological effects that could be attributed to its antioxidant, anti-inflammatory, and immunoregulatory properties. However, the therapeutic potential of silibinin for periodontitis has not been investigated. METHODS: The therapeutic effects of silibinin in ligation-induced experimental periodontitis were investigated using biochemical, histological, and immunohistochemical methods. The effects of silibinin on the osteoclastogenesis of RAW264.7 cells were investigated using TRAP staining, quantitative polymerase chain reaction (qPCR), pit formation, and immunoblotting. Moreover, its effects on inflammatory cytokine production, RANKL expression, and oxidative stress in lipopolysaccharide (LPS)-stimulated human gingival fibroblasts (HGFs) were evaluated using qPCR and flow cytometry. A coculture system was established to elucidate the effects of silibinin on the crosstalk between LPS-stimulated HGFs and undifferentiated monocytes. RESULTS: Silibinin significantly reduced the alveolar bone loss, decreased the gingival inflammation and RANKL expression, and decreased the RANKL/osteoprotegerin ratio in gingival tissues in experimental periodontitis. The in vitro results showed that silibinin inhibited RANKL-induced osteoclast differentiation and function of RAW264.7 cells and suppressed RANKL-induced nuclear factor of activated T cells 1 (NFATc1) induction and translocation through the nuclear factor-κB and mitogen-activated protein kinase signaling pathways. Silibinin decreased the inflammatory cytokine level and oxidative stress production in LPS-stimulated HGFs; significantly suppressed membrane-bound RANKL expression on LPS-stimulated HGFs; and significantly disrupted TRAP+ cell differentiation in the coculture system. CONCLUSIONS: Silibinin effectively inhibits inflammation-induced bone loss in experimental periodontitis based on the regulation of stimulated HGFs by inhibiting the expression of inflammatory and osteoclastogenic mediators. Collectively, targeting the inflamed HGF resolution that mediates osteogenesis may use silibinin as a potential drug-repurposing candidate for modulating alveolar bone destruction in periodontitis. SUMMARY: Silibinin effectively inhibits inflammation-induced bone loss in experimental periodontitis based on the regulation of stimulated HGFs by inhibiting the expression of inflammatory and osteoclastogenic mediators.