Aspirin Blocks Orthodontic Relapse via Inhibition of CD4+ T Lymphocytes.

Immunologic response plays an important role in orthodontic tooth movement (OTM) and relapse. Nonsteroidal anti-inflammatory drugs, such as aspirin, affect immune cells and clinical orthodontic treatment. However, the mechanisms by which nonsteroidal anti-inflammatory drugs regulate immune cells to affect orthodontic relapse are unclear. In this study, male Sprague-Dawley rats were grouped as relapse and relapse + aspirin for 10 d after 14 d of OTM. Silicone impressions of the rats' maxillary dentitions were obtained to record the distance of OTM at the indicated time point. CD4+ T lymphocytes in spleen were examined by flow cytometry. Serum levels of type 1 T-helper (Th1) cell-associated cytokines tumor necrosis factor α (TNF-α), and interferon γ (IFN-γ) were determined through enzyme-linked immunosorbent assay. The effects of aspirin on CD4+ T and Th1 cells were also analyzed in vitro. Aspirin treatment significantly reduced the relapse rate. More interestingly, injection of CD25 neutralizing antibody basiliximab or TNF-α inhibitor etanercept can significantly reduce the relapse rate as well. Correspondingly, aspirin treatment significantly accelerated the decrease of orthodontic force-induced secretion of TNF-α and IFN-γ in serum and the expression of TNF-α and IFN-γ in periodontal ligament during relapse. Furthermore, aspirin treatment in vitro significantly repressed the differentiation of CD4+ T and Th1 cells. Overall, results indicated that aspirin treatment can block orthodontic relapse by regulating Th1 cells.

Estrogen aggravates iodoacetate-induced temporomandibular joint osteoarthritis.

Temporomandibular joint osteoarthritis (TMJOA) is clinically characterized by female preponderance, with a female-to-male ratio of more than 2:1; however, the underlying mechanism remains obscure. We examined the effects of estrogen on TMJOA induced by monosodium iodoacetate. Female rats were randomly and equally divided into 5 groups: control, sham-ovariectomized, and ovariectomized rats treated, respectively, with 17ß-estradiol (E2) at doses of 0 µg, 20 µg, and 80 µg/day until the end of the experiment. After induction of TMJOA, TMJs were evaluated by histopathology and microCT, and the expression of Fas, FasL, caspase 3, and caspase 8 was evaluated by real-time polymerase chain-reaction or immunohistochemistry. Another 5 groups of female rats were used to evaluate the effect of estrogen receptor antagonist ICI 182780 on E2 effects on TMJOA, when injected intraperitoneally into the control, sham-ovariectomized, and 80-µg-E2-treated groups. We found that E2 potentiated cartilage degradation and subchondral bone erosion in iodoacetate-induced TMJOA. E2 also potentiated mRNA expression of Fas, FasL, caspase 3, and caspase 8 in the condylar cartilage. Moreover, the estrogen receptor antagonist partially blocked E2 effects on TMJOA. These findings suggest that E2 could aggravate TMJOA, which may be an important mechanism underlying the sexual dimorphism of TMJOA.