RESUMO
INTRODUÇÃO: a expansão da maxila induz a formação de novo osso na sutura palatina mediana por um processo de proliferação e diferenciação celular. A força de expansão pode estimular, nas células progenitoras, a produção de citocinas com atividade osteoindutiva, tais como o transforming growth factor β1(TGFβ1). OBJETIVOS: o principal objetivo deste estudo foi determinar a função dessa citocina nos estágios iniciais de expansão da sutura palatina mediana. MÉTODOS: um aparelho ortodôntico foi instalado entre os molares superiores direito e esquerdo de ratos com 4 semanas de idade. A força de expansão inicial foi de 50g. Os grupos controle e experimental foram sacrificados nos dias 0, 2 e 5. Cortes bucais de 6µm foram obtidos e sujeitos à técnica de hibridização in-situ. RESULTADOS: dois dias após a aplicação de força, as células osteocondroprogenitoras, distribuídas no lado interno do tecido cartilaginoso, exibiram altos níveis de transcrição de transforming growth factor β1. No dia 5, o nível de transcrição de TGFβ1 foi observado nos osteócitos e nas células osteoblásticas, na superfície do novo osso. A atividade osteoblástica foi confirmada por meio de um estudo imunohistoquímico utilizando-se Osteocalcina-Pro (OC-Pro). CONCLUSÕES: os dados sugerem que a expansão da sutura palatina induz a diferenciação de células osteocondroprogenitoras em osteoblastos, estimuladas pela produção de citocinas.
INTRODUCTION: The application of an orthodontic expansion force induces bone formation at the midpalatal suture because of cell proliferation and differentiation. Expansion forces may stimulate the production of osteoinductive cytokines, such as transforming growth factor β1 (TGFβ1), in the progenitor cells. OBJECTIVES: This study determined the role of TGFβ1 in the early stage of midpalatal suture cartilage expansion. METHODS: A rectangular orthodontic appliance was placed between the right and left upper molars of 4-week-old rats. The initial expansion force was 50 g. Animals in the control and experimental groups were sacrified on days 0, 2, and 5 and 6 µmm thick sections were prepared for an in situ hybridization technique. RESULTS: Two days after the application of force, prechondroblastic and undifferentiated mesenchymal cells distributed along the inner side of the cartilaginous tissue had high levels of TGFβ1 transcription. On day 5, the TGFβ1 transcription was found in osteocytes and osteoblastic cells on the surface of newly formed bone. Immunohistochemistry using Osteocalcin-Pro (OC-Pro) confirmed osteoblastic activity. Conclusions: Results suggest that the expansion of midpalatal suture cartilage induces differentiation of osteochondroprogenitor cells into osteoblasts after stimulation by cytokine production.
RESUMO
<p><b>OBJECTIVE</b>Alkaline phosphatase (ALP) and osteocalcin (OC) are the markers of new bone formation. Quantitative study of ALP and OC in the process of new bone formation helps to understand the ongoing of this cascade and contributes to make diagnosis in clinical treatment.</p><p><b>METHODS</b>8-week-old male C57BL/6J mice and primary osteoblasts from neonatal C57BL/6J mice calvaria were used in this experiment. HE staining, Northern blot and Real Time PCR methods were employed to detect the histological changes and the expression pattern of ALP and OC.</p><p><b>RESULTS</b>In vivo study showed that after fracture the expressions of both ALP and OC kept on increasing which were peaked on the 10 day, then started decreasing gradually. In vitro study on primary osteoblasts showed that the expressions of ALP and OC reached peak on the 14th day in differentiation culture medium and started decreasing from this time point till the 21st day.</p><p><b>CONCLUSION</b>The expression of ALP and OC in the process of new bone formation parallels with the development of osteoblasts, it increases with the differentiation of osteoblasts and becomes decreasing with the maturation of osteoblasts. The reciprocal relationship between the expression pattern of ALP and OC and development of osteoblast helps to maintain homeostasis.</p>