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1.
Eur J Orthod ; 46(6)2024 Dec 01.
Artículo en Inglés | MEDLINE | ID: mdl-39364772

RESUMEN

BACKGROUND: Few prospective investigations have compared direct and indirect techniques through comprehensive and detailed clinical evaluations, considering the impact of all factors. OBJECTIVES: This study aimed to compare and evaluate direct and indirect bonding methods at a single institution and to clarify the selection criteria for the bonding method. MATERIALS AND METHODS: This single-centre, quasi-randomized controlled clinical trial included 153 patients who required fixed orthodontic treatment. They were randomly divided into indirect and direct binding groups by the project lead (K.K.), who was blinded to all clinical data, and performed the allocation using medical record numbers. The chair time for bracket bonding, discomfort during bracket bonding, oral hygiene after bonding, number of bracket failures, number of intentional bracket reattachments, post-treatment occlusal index, and total treatment time were assessed. Outcomes were compared using a two-sample t-test or Mann-Whitney U test (P < .05). RESULTS: Fifty-eight patients were included in the indirect bonding group (20 male, 38 female; mean age: 20.63 ±â€…5.69 years) and 66 (14 male, 52 female; mean age: 23.17 ±â€…8.83 years) in the direct bonding group. Compared to the direct bonding group, the indirect bonding group had shorter chair time (P < .001), a shorter total treatment period (P < .01), and a better final occlusal relationship (P < .001). The number of bracket detachments was higher (P < .001) in the indirect bonding group, but the number of intentional reattachments was lower (P < .001). CONCLUSION: Indirect bonding may improve the efficiency of orthodontic treatment. HARMS: No harm was observed during the study. TRIAL REGISTRATION NUMBER: This trial was approved by the Ethics Review Committee of Okayama University (approval number: d10001), UMIN registration number 000022182.


Asunto(s)
Recubrimiento Dental Adhesivo , Soportes Ortodóncicos , Humanos , Femenino , Masculino , Recubrimiento Dental Adhesivo/métodos , Adulto Joven , Adolescente , Adulto , Estudios Prospectivos , Higiene Bucal , Cementos de Resina/química , Resultado del Tratamiento
2.
Clin Exp Pharmacol Physiol ; 45(1): 75-83, 2018 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-28815657

RESUMEN

Non-steroidal anti-inflammatory drugs (NSAIDs) exert their effects primarily by inhibiting the activity of cyclooxygenase (COX), thus suppressing prostaglandin synthesis. Some NSAIDs are known to perform functions other than pain control, such as suppressing tumour cell growth, independent of their COX-inhibiting activity. To identify NSAIDs with COX-independent activity, we examined various NSAIDs for their ability to inhibit osteoblastic differentiation using the mouse pre-osteoblast cell line MC3T3-E1. Only celecoxib and valdecoxib strongly inhibited osteoblastic differentiation, and this effect was not correlated with COX-inhibiting activity. Moreover, 2,5-dimethyl (DM)-celecoxib, a celecoxib analogue that does not inhibit COX activity, also inhibited osteoblastic differentiation. Celecoxib and DM-celecoxib inhibited osteoblastic differentiation induced by bone morphogenetic protein (BMP)-2 in C2C12 mouse myoblast cell line. Although celecoxib suppresses the growth of some tumour cells, the viability and proliferation of MC3T3-E1 cells were not affected by celecoxib or DM-celecoxib. Instead, celecoxib and DM-celecoxib suppressed BMP-2-induced phosphorylation of Smad1/5, a major downstream target of BMP receptor. Although it is well known that COX plays important roles in osteoblastic differentiation, these results suggest that some NSAIDs, such as celecoxib, have targets other than COX and regulate phospho-dependent intracellular signalling, thereby modifying bone remodelling.


Asunto(s)
Antiinflamatorios no Esteroideos/farmacología , Celecoxib/farmacología , Diferenciación Celular/efectos de los fármacos , Osteoblastos/citología , Osteoblastos/efectos de los fármacos , Animales , Proteína Morfogenética Ósea 2/metabolismo , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Ciclooxigenasa 2/metabolismo , Ratones , Osteoblastos/metabolismo , Transducción de Señal/efectos de los fármacos
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