After 29 years of clinical practice treating odontogenic infections of the head, neck and oral cavity, my co-contributors and I sought to determine by a review of the literature and three clinical cases if Prevotella species were significant opportunistic pathogens in odontogenic infections of all kinds in the oral and maxillofacial region. We performed a PubMed review of 40 articles using terms associated with odontogenic infections, pericoronitis, Prevotella and antibiotics used to treat common oral and maxillofacial infections. Three cases were reported, and the treatment was discussed. An additional 26 articles were reviewed to describe the pathogenesis of Prevotella. Given the opportunity to become virulent—such as post-extraction wound healing of an extraction site adjacent to an intact dentition, excessive plaque and calculus, nearby gingivitis or periodontitis, or an immunocompromised host—we wondered if Prevotella could be targeted with antimicrobials mitigating, or even resolving, odontogenic infections in those cases of refractory to conservative surgical therapy that includes source control. We found that Prevotella is a significant opportunistic pathogen in odontogenic infections. Prevotella is susceptible to Metronidazole (Flagyl), and it is effective in mitigating the disease process when basic principles of the treatment of odontogenic infections are employed. Infections not responsive to this empiric therapy should be cultured to determine the opportunistic organism’s sensitivity and susceptibility to specific antibiotic therapy.

Background: primary sclerosing cholangitis (PSC) is a chronic cholestatic disease characterized by inflammation and fibrosis of the bile ducts. Cholestasis may lead to hepatic inflammation and fibrosis, and amelioration of cholestasis may allow recovery from inflammatory and fibrotic pathological damage. Prevotella copri (P. copri) intervention have been reported could significantly improve cholestasis and liver fibrosis in DDC-induced PSC mice model. Despite alone P. copri treatment could not recover DDC-induced inflammation, it increased the abundance of Lactobacillus murinus (L. murinus) compared to DDC treatment, which has been reported to have anti-inflammatory effects. The abundance of L. murinus still not recover to normal level may underlie hepatic inflammation in P. copri+DDC mice. Method: alone or in combination interventions of P. copri and L. murinus were used to investigate the molecular mechanism of improvement of PSC inflammation and fibrosis. Results: P. copri and L. murinus significantly reduced the hepatic inflammatory cell aggregation and inflammatory factor expression, as well as the hepatic collagen content and fibrin factor expression in PSC mice. Further analysis of phosphorylation and dephosphorylation levels revealed that P. copri and L. murinus combined intervention in PSC mice inhibited the activity of DDC-activated TGF-β1/Smad pathway, thereby reducing liver inflammation and fibrosis. Conclusion: combination of P. copri and L. murinus inhibits the TGF-β1/Smad pathway and reduces inflammation and fibrosis in PSC.