UCLA

Background: Periodontitis is a multifactorial inflammatory disease resulting in the destruction of the supporting structures of the teeth. It is currently well established that the host response to bacterial pathogens is the major cause in the pathogenesis and progression of the disease. Moreover, the seminal role of Vitamin D in calcium-phosphate hemostasis and bone metabolism has been well established. More recent studies suggested extraosseous effects of Vitamin D, showing association of Vitamin D deficiency with risk of multiple diseases including cancer, osteoarthritis, cardiovascular disease, autoimmune diseases, infections and more. The immunomodulating effects of vitamin D may explain the reported epidemiological associations between vitamin D status and a large number of autoimmune and inflammatory diseases.

Purpose: To analyze the relationship between Vitamin D deficiency and its effect on LPS-induced periodontal bone loss in mice.

Methods and Materials: Using the P. gingivalis LPS injection model to induce periodontal bone loss, we utilized 32 one month old male mice (C57BL/6J). The mice were divided into four groups. Group 1: Vitamin D adequate diet, No injection; Group 2: Vitamin D adequate diet and LPS injections; Group 3: Vitamin D deficient diet, No injections; Group 4: Vitamin D deficient diet and LPS injections. Test groups received 2 µl (20µg) of P. gingivalis–LPS injections in between the first and second maxillary molars on both sides of the maxilla, two times a week for 6 weeks. Animals were sacrificed one day after last injection,and maxillae were dissected and harvested. The MicroCT analysis was utilized for 3D reconstruction. Periodontal bone loss was measured using linear analysis (Dolphin Software) and volumetric analysis (CTAn Software).

Results: Linear analysis showed statistically significant bone loss when comparing both LPS groups to control groups. However, no statistical significance was seen when comparing Vitamin D deficient and adequate LPS groups, even though slightly more bone loss was seen in the Vitamin D deficient group. Volumetric bone analysis similarly showed no statistical significance when comparing Vitamin D adequate and deficient LPS groups.

Conclusion: In the present study, Vitamin D deficiency alone did not seem to have a strong association with LPS-induced bone loss in our mouse model, however, further investigation is needed to confirm these findings.