Bone Preservation During Ligature-Induced Periodontitis in C1q-Knockout Mice

The serum complement protein C1q of innate immunity accumulates and persists in infected and inflamed tissues. This protein was implicated in the pathogenesis of periodontitis because of in vitro evidence that physiological amounts of C1q stimulate stromal cells to release proinflammatory mediators. This study tested whether in vivo C1q activity might contribute to the bone destruction of periodontitis. Objectives: To compare alveolar bone loss associated with ligature-induced periodontitis in ligated and nonligated sites of C1q-knockout (KO) and normal mice. Methods: Silk ligatures were placed around the right first mandibular molars in six C1q-KO and six wild-type adult mice. Contralateral nonligated molar teeth served as controls. The mice were maintained under identical conditions and sacrificed at 6 weeks postligation. Coded mandibular quadrants and alveolar bone levels were compared radiographically using computer assisted image analysis and the paired t-test. Alveolar bone crest level was expressed as a percentage of the radiographic distance between the root apex and cementoenamel junction (CEJ). Results: In wild type mice, the alveolar bone crest of nonligated sites was located at 73.6 ± 3.6% of the CEJ-root apex distance. Crestal bone levels in ligated contralateral sites were located significantly (P = 0.03) more apically (52.2 ± 22.5%), reflecting alveolar bone loss that ranged from 8% to 53% relative to nonligated sites. Conversely, C1q-KO mice showed no difference (P = 0.63) in crestal height between ligated (70.6 ± 8.4%) and nonligated (72.2 ± 1.1%) sites, which were similar to nonligated wild type sites. Conclusions: These results support the concept that C1q participates in alveolar bone loss in the inflamed periodontium. The C1q-KO mouse model may provide new approaches to role of immunomodulators, including C1q, in alveolar bone loss associated with periodontitis.

This study supported by the University of Washington Hack Estate.