Comparison of two protocols for early treatment of dentoskeletal Class III malocclusion: Modified SEC III versus RME/FM.

OBJECTIVE: To compare the short-term cephalometric outcomes of the protocols modified splints, Class III elastics, chincup (SEC III) and rapid maxillary expansion and facial mask (RME/FM) for the early treatment of growing subjects with Class III dentoskeletal malocclusion. SETTINGS AND SAMPLE POPULATION: This retrospective observational study included 20 patients (11 males, nine females) treated with the modified SEC III protocol and 31 patients (16 males, 15 females) treated with the RME/FM one. The sample was evaluated before (T1, mean age 7.9 ± 1.0 years) and at the end of treatment (T2, mean age 9.0 ± 1.0 years). Statistical comparisons between the two groups were performed with independent sample t tests. RESULTS: Both the modified SEC III and the RME/FM sample groups showed significantly favourable effects in terms of maxillary advancement (SNA +1.3° and +1.5°, respectively), control of mandibular projection (SNB -0.5° and -0.8°, respectively), and intermaxillary relationships (ANB +1.8° and +2.3°, respectively; Wits +3.4 and +1.9 mm, respectively). The modified SEC III group showed a statistically significant greater control in the intermaxillary divergency considering the SN to Pal. Pl. (P < 0.006) and Pal. Pl. to Mand. Pl. angle (P < 0.002) with a difference of 2.3 mm between the two groups. LIMITATIONS: The main limitations of this study are its retrospective nature and the short-term outcomes. CONCLUSION: Early treatment of growing patients with dentoskeletal Class III disharmonies is efficient using either modified SEC III or RME/FM protocols. However, a higher vertical control is achieved with the modified SEC III.

Antiinflammatory actions of inorganic nitrate stabilize the atherosclerotic plaque.

Reduced bioavailable nitric oxide (NO) plays a key role in the enhanced leukocyte recruitment reflective of systemic inflammation thought to precede and underlie atherosclerotic plaque formation and instability. Recent evidence demonstrates that inorganic nitrate (NO3-) through sequential chemical reduction in vivo provides a source of NO that exerts beneficial effects upon the cardiovascular system, including reductions in inflammatory responses. We tested whether the antiinflammatory effects of inorganic nitrate might prove useful in ameliorating atherosclerotic disease in Apolipoprotein (Apo)E knockout (KO) mice. We show that dietary nitrate treatment, although having no effect upon total plaque area, caused a reduction in macrophage accumulation and an elevation in smooth muscle accumulation within atherosclerotic plaques of ApoE KO mice, suggesting plaque stabilization. We also show that in nitrate-fed mice there is reduced systemic leukocyte rolling and adherence, circulating neutrophil numbers, neutrophil CD11b expression, and myeloperoxidase activity compared with wild-type littermates. Moreover, we show in both the ApoE KO mice and using an acute model of inflammation that this effect upon neutrophils results in consequent reductions in inflammatory monocyte expression that is associated with elevations of the antiinflammatory cytokine interleukin (IL)-10. In summary, we demonstrate that inorganic nitrate suppresses acute and chronic inflammation by targeting neutrophil recruitment and that this effect, at least in part, results in consequent reductions in the inflammatory status of atheromatous plaque, and suggest that this effect may have clinical utility in the prophylaxis of inflammatory atherosclerotic disease.

Inorganic nitrate attenuates cardiac dysfunction: roles for xanthine oxidoreductase and nitric oxide.

BACKGROUND AND PURPOSE: NO is a vasodilator and independent modulator of cardiac remodelling. Commonly, in cardiac disease (e.g., heart failure), endothelial dysfunction (synonymous with NO deficiency) has been implicated in increased BP, cardiac hypertrophy and fibrosis. Currently, no effective therapies replacing NO have succeeded in the clinic. Inorganic nitrate (NO3 - ), through chemical reduction to nitrite and then to NO, exerts potent BP lowering, but whether it might be useful in treating undesirable cardiac remodelling is not known. EXPERIMENTAL APPROACH: We analysed demographics in a nested age- and sex-matched case-control study of hypertensive patients with or without left ventricular hypertrophy (NCT03088514) and assessed the effects of dietary nitrate in mouse models of cardiac dysfunction. KEY RESULTS: Lower plasma nitrite concentrations and vascular dysfunction accompanied cardiac hypertrophy and fibrosis in patients. In mouse models of cardiac remodelling, restoration of circulating nitrite levels using dietary nitrate improved endothelial dysfunction through targeting the xanthine oxidoreductase-driven increase in levels of H2 O2 and superoxide, and decreased cardiac fibrosis through NO-mediated block of SMAD phosphorylation leading to improvements in cardiac structure and function. CONCLUSIONS AND IMPLICATIONS: Dietary nitrate offers easily translatable therapeutic options for delivery of NO and thereby treatment of cardiac dysfunction.