Contribution of orthodontic load to inflammation-mediated periodontal destruction.

AIM

Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation.

MATERIALS AND METHODS

PDL cells (from six donors) grown on BioFlex(®) plates were treated with interleukin (IL) 1β, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student's t-test and ANOVA were applied (p<0.05).

RESULTS

In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals.

CONCLUSION

These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation.