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Background Probiotic lozenges have been developed to harvest the benefits of probiotics for oral health, but their long-term consumption may encourage the transfer of resistance genes from probiotics to commensals, and eventually to disease-causing bacteria. Aim To screen commercial probiotic lozenges for resistance to antibiotics, characterize the resistance determinants, and examine their transferability in vitro . Results Probiotics of all lozenges were resistant to glycopeptide, sulfonamide, and penicillin antibiotics, while some were resistant to aminoglycosides and cephalosporins. High minimum inhibitory concentrations (MICs) were detected for streptomycin (>128 µg/mL) and chloramphenicol (> 512 µg/mL) for all probiotics but only one was resistant to piperacillin (MIC = 32 µg/mL). PCR analysis detected erythromycin ( erm(T), ermB or mefA ) and fluoroquinolone ( parC or gyr(A) ) resistance genes in some lozenges although there were no resistant phenotypes. The dfrD, cat-TC, vatE, aadE, vanX , and aph(3”)-III or ant(2”)-I genes conferring resistance to trimethoprim, chloramphenicol, quinupristin/dalfopristin, vancomycin, and streptomycin, respectively, were detected in resistant probiotics. The rifampicin resistance gene rpoB was also present. We found no conjugal transfer of streptomycin resistance genes in our co-incubation experiments. Conclusion Our study represents the first antibiotic resistance profiling of probiotics from oral lozenges, thus highlighting the health risk especially in the prevailing threat of drug resistance globally.

Aim The underlying mechanisms connecting obesity and periodontal diseases remain unclear. This study investigates the potential causal association of obesity with periodontal diseases using Mendelian randomization (MR). Materials and Methods Single‐nucleotide polymorphisms of obesity traits including body mass index (BMI), waist circumference (WC), and WC adjusted for BMI (WCadjBMI) from large‐scale genome‐wide association studies were screened for instrumental variables. The single trait periodontitis and the combined trait comprising periodontitis and loose teeth were adopted as surrogates for periodontal diseases. Inverse‐variance weighted (IVW), series of sensitivity analyses and multivariable MR were employed to determine the association of obesity with periodontal diseases. Results IVW results showed that per 1‐SD increment in BMI (odds ratio, OR = 1.115; 95% confidence interval [CI] = 1.064–1.169; p < .001) and WC (OR = 1.117; 95% CI = 1.052–1.185; p < .001), but not WCadjBMI, were significantly associated with an increased risk of periodontitis/loose teeth. Moreover, the MR estimates were consistent across other MR sensitivity analyses and multivariable MR. However, a causal association of obesity with the single trait periodontitis was not identified. Conclusions The presented evidence supports previous epidemiological findings by showing a potential causal association of genetic liability to obesity with periodontal diseases. The biological mechanisms underlying this association warrant further investigation.

ObjectiveObservational studies indicated that individuals with osteoporosis could be at an increased risk of periodontitis. This study aimed to investigate whether there is a causal association of bone mineral density (BMD) with periodontitis using Mendelian randomization (MR).Materials and MethodsSummary statistics were sourced from genome‐wide association study on BMD measured at different skeletal sites, including estimated heel BMD (eBMD, N = 426,824), forearm BMD (FA‐BMD, N = 8143), femoral neck BMD (FN‐BMD, N = 32,735), and lumbar spine BMD (LS‐BMD, N = 28,498). Genetic variants of periodontitis (N = 45,563) and loose teeth (N = 461,031) were used as outcome surrogates. Inverse variance weighted meta‐analysis (IVW) was adopted as main analyses. Other sensitivity MR approaches were used to boost power and account for pleiotropy.ResultsIVW results suggested no evidence for a causal association of any phenotypes of BMD with periodontitis (eBMD, odds ratio [OR] = 0.984, 95% confidence interval [CI] = 0.885–1.083; FA‐BMD, OR = 1.028, 95%CI = 0.864–1.193; FN‐BMD, OR = 1.033, 95%CI = 0.896–1.169; LS‐BMD, OR = 0.991, 95%CI =0.878–1.103; all P > 0.65). Such null associations were consistent through other sensitivity MR approaches. Similarly, no significant causal effects of BMD on loose teeth were found.ConclusionsWithin the limitation of the study, our MR estimates suggested that a decreased BMD is unlikely to substantially increase the risk of periodontitis.