It has previously been reported that low-energy laser irradiation stimulated the velocity of tooth movement via the receptor activator of nuclear factor kappa B (RANK)/RANK ligand and the macrophage colony-stimulating factor/its receptor (c-Fms) systems. Matrix metalloproteinase (MMP)-9, cathepsin K, and alpha(v) beta(3) [alpha(v)beta3] integrin are essential for osteoclastogenesis; therefore, the present study was designed to examine the effects of low-energy laser irradiation on the expression of MMP-9, cathepsin K, and alpha(v)beta3 integrin during experimental tooth movement. Fifty male, 6-week-old Wistar strain rats were used in the experiment. A total force of 10g was applied to the rat molars to induce tooth movement. A Ga-Al-As diode laser was used to irradiate the area around the moving tooth and, after 7 days, the amount of tooth movement was measured. To determine the amount of tooth movement, plaster models of the maxillae were made using a silicone impression material before (day 0) and after tooth movement (days 1, 2, 3, 4, and 7). The models were scanned using a contact-type three-dimensional (3-D) measurement apparatus. Immunohistochemical staining for MMP-9, cathepsin K, and integrin subunits of alpha(v)beta3 was performed. Intergroup comparisons of the average values were conducted with a Mann-Whitney U-test for tooth movement and the number of tartrate-resistant acid phosphatase (TRAP), MMP-9, cathepsin K, and integrin subunits of alpha(v)beta3-positive cells. In the laser-irradiated group, the amount of tooth movement was significantly greater than that in the non-irradiated group at the end of the experiment (P < 0.05). Cells positively stained with TRAP, MMP-9, cathepsin K, and integrin subunits of alpha(v)beta3 were found to be significantly increased in the irradiated group on days 2-7 compared with those in the non-irradiated group (P < 0.05). These findings suggest that low-energy laser irradiation facilitates the velocity of tooth movement and MMP-9, cathepsin K, and integrin subunits of alpha(v)beta3 expression in rats.

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Recent advances in biologic therapy have enabled reduction of the progression of destructive arthritis in rheumatoid arthritis. Once destroyed, however, the affected bones and cartilage are not fully repaired. We describe the case of an 8-year-old girl with anti-citrullinated peptide antibody (ACPA)-positive polyarticular juvenile idiopathic arthritis (p-JIA). Destructive arthritis progressed during combination therapy with infliximab, methotrexate, mizoribine and prednisolone. Clinical remission was achieved, however, after switching the biologic agent to tocilizumab, a humanized monoclonal antibody to interleukin-6 receptor. Both bone erosion and bone marrow edema on magnetic resonance imaging were repaired in association with restoration of joint spaces. Furthermore, there was no relapse of arthritis on weekly methotrexate alone for 2 years after discontinuation of the tocilizumab. Tocilizumab led to radiological repair of both bone and cartilage destruction and long-term biologics-free remission in a patient with ACPA-positive p-JIA, and should be considered for tumor necrosis factor inhibitor-resistant cases.

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Background: The coronary microvascular vasodilating function is an important determinant of patient outcomes in a number of clinical settings, including coronary artery disease, hypertensive heart disease, or cardiomyopathy. However, the characteristics or the implication of coronary microcirculation in valvular heart disease has not been fully elucidated. The present study was designed to assess coronary vasodilating function and its effects on systolic function in patients with aortic regurgitation (AR) and mitral regurgitation (MR). Methods: Forty-four consecutive patients (66 yrs) with moderate to severe AR and 45 consecutive patients with moderate to severe MR (64 yrs) were enrolled for this study. All patients were free of coronary artery stenosis. Fifty-one age-matched patients without underlying cardiovascular disease served as controls. Endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were assessed by coronary blood flow (CBF) response to acetylcholine and papaverine, respectively. Left ventricular ejection fraction (LVEF) was determined by echocardiography as an indicator of systolic function. Results: In patients with AR, both %change in CBF response to acetylcholine and papaverine were significantly lower than controls (32 ± 61 vs 64 ± 84, 172 ± 87 vs 268 ± 105, p < 0.05, p < 0.01, respectively). Further, %change in CBF response to acetylcholine positively correlated with LVEF (r = 0.45, p < 0.01). In patients with MR, %change in CBF response to papaverine was significantly lower than controls (221 ± 123 vs 268 ± 105, p < 0.05), but %change in CBF response to acetylcholine was comparable with controls. Moreover, neither %change in CBF response to acetylcholine nor CBF response to papaverine had significant correlation with LVEF. Conclusion: In patients with AR, both endothelium-dependent and endothelium-independent vasodilating function of resistance coronary artery were deteriorated. Further, endothelium-dependent vasodilating function may be associated with left ventricular systolic function. Our findings indicate coronary microvascular endothelial dysfunction as a potential target for prevention of systolic heart failure in patients with AR.

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We conducted an in vivo study to clarify the mechanics of the mandibular bone and condyles in pediatric patients with mandibular functional deviation. We experimentally caused lateral displacement of the mandible in 4-week-old rats by attaching a plate to the teeth for 4 (short-term group: ST group) or 12 weeks (long-term group: LT group), and immunohistochemically investigated the pattern of appearance of matrix metalloproteinase-1 (MMP-1), vascular endothelial growth factor (VEGF), and connective tissue growth factor (CTGF) to investigate the changes in the cartilage matrix constitution during the recovery of the condylar morphology. Furthermore, the morphology was observed using micro (μ) -CT.After plate removal, the MMP-1 expression significantly decreased in the both groups. Furthermore the expressions of VEGF and CTGF were increased in the ST group compared to those observed in the LT group. In terms of the morphometry, mandibular asymmetry and deformity of the condyle were noted immediately after removal in the both groups. The mandibular morphology markedly recovered in the ST group compared to that in the LT group. This indicates that correction of occlusal abnormalities during an early stage leads to recovery of the normal mandibular configuration.