低能量雷射治療對大鼠矯正牙齒移動模式之影響

Abstract

矯正牙齒移動是牙齒受力後，牙周韌帶與齒槽骨組織重塑的結果。包含許多細胞激素參與，RANKL-RANK-OPG系統是調控骨重塑活動的重要一環，也是許多加速牙齒移動機制的主要目標。眾多文獻回顧支持低能量雷射治療有加速矯正牙齒移動功效，可能的機制為透過RANKL-RANK系統活化噬骨細胞、刺激骨生成，以及加快矯正治療中的透明帶移除。 影響RANKL-RANK-OPG系統的因子很多，本實驗使用波長970 nm，功率輸出500 mW之低能量雷射，對大鼠上顎臼齒進行照射，利用IVIS活體影像系統觀察MMP3變化，並針對RANKL、OPG、VEGF、PECAM-1、HIF-1α、PCNA、MCP-1進行免疫化學組織染色分析；亦透過單純照射大鼠下顎臼齒探討單純照射高劑量LLLT對大鼠骨質代謝的影響。結果發現高劑量LLLT刺激並加成RANKL、VEGF、HIF-1α及MCP-1表現，且影響皆相當早期，而噬骨細胞數目的確因雷射刺激而顯著增加；單純照射高劑量LLLT對HIF-1α有明顯刺激作用。 綜合本實驗各項結果推論：LLLT加速牙齒移動機制除了RANKL-RANK系統，可能與HIF-1α→VEGF途徑亦有關，但詳細機轉仍須更進一步研究。

Orthodontic tooth movement (OTM) is the result of periodontium remodeling after mechanical force application. The remodeling includes many cytokines involved. RANKL-RANK-OPG system is one of the important keys to achieve periodontium remodeling, and different approaches were attempted to accelerate tooth movement. Lots of literatures support that low level laser therapy (LLLT) can increase rate of orthodontic tooth movement. The possible mechanisms are activating osteoclasts activity through the RANKL-RANK pathway, stimulating bone formation, and early removal of hyalinization tissue. There are many factors contributing to the RANKL-RANK system. The aim of present study is to explore the LLLT effects on the bone remodeling of OTM in rat model. IVIS living image system was used for detecting luciferase actvitiy under MMP3 promoter at early stages of OTM, and immunohistochemistry was used to analyze the expression RANKL、OPG、VEGF、PECAM-1、HIF-1α、PCNA、MCP-1 at the tissue levels at day 1, day 3, day 7, day day 21 after OTM. The results reveal that MMP3 may be not an appropriate reporter of LLLT acceleration, however, the expression of RANKL、VEGF、HIF-1α及MCP-1 are upgraded early after LLLT stimulation. The number of osteoclasts are significantly higher in the high dose irritation group. And LLLT but without OTM, enhances HIF-1αexpression during physiological molar distal drifting in rats. We suggest that the effects of LLLT on accelerating orthodontic tooth movement are related to RANKL-RANK system and possibly the HIF-VEGF pathway.