| First Author | Settem RP | Year | 2021 |
| Journal | Front Physiol | Volume | 12 |
| Pages | 722859 | PubMed ID | 34594237 |
| Mgi Jnum | J:312667 | Mgi Id | MGI:6786398 |
| Doi | 10.3389/fphys.2021.722859 | Citation | Settem RP, et al. (2021) B-Cell RANKL Contributes to Pathogen-Induced Alveolar Bone Loss in an Experimental Periodontitis Mouse Model. Front Physiol 12:722859 |
| abstractText | Periodontitis is a bacterially-induced inflammatory disease that leads to tooth loss. It results from the damaging effects of a dysregulated immune response, mediated largely by neutrophils, macrophages, T cells and B cells, on the tooth-supporting tissues including the alveolar bone. Specifically, infiltrating B cells at inflamed gingival sites with an ability to secrete RANKL and inflammatory cytokines are thought to play roles in alveolar bone resorption. However, the direct contribution of B cells in alveolar bone resorption has not been fully appreciated. In this study we sought to define the contribution of RANKL expressing B cells in periodontitis by employing a mouse model of pathogen-induced periodontitis that used conditional knockout mice with B cell-targeted RANKL deletion. Briefly, alveolar bone loss was assessed in the wild-type, B-cell deficient (Jh), or B-cell-RANKL deleted (RANKL(DeltaB)) mice orally infected with the periodontal pathogen Tannerella forsythia. The RANKL(DeltaB) mice were obtained by crossing Cd19-Cre knock-in mice with mice homozygous for conditional RANKL-flox allele (RANKL(flox/flox)). The alveolar bone resorption was determined by morphometric analysis and osteoclastic activity of the jaw bone. In addition, the bone resorptive potential of the activated effector B cells was assessed ex vivo. The data showed that the RANKL producing B cells increased significantly in the T. forsythia-infected wild-type mice compared to the sham-infected mice. Moreover, T. forsythia-infection induced higher alveolar bone loss in the wild-type and RANKL(flox/flox) mice compared to infection either in the B cell deficient (Jh) or the B-cell specific RANKL deletion (RANKL(DeltaB)) mice. These data established that the oral-pathogen activated B cells contribute significantly to alveolar bone resorption via RANKL production. |
