PLG and bacterial infectious disease: Without additional bacterial infection, both the tPa/uPa double knockout—that cannot convert plasminogen into plasmin—and the plasminogen-deficient mutant mice, showed to develop periodontitis, as evidenced by alveolar bone loss: the plasminogen-deficient mice showed at any time point significantly more alveolar bone loss that increased with age up to 20 weeks compatible with a clinical picture of spontaneously developing periodontitis.