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THE BIOLOGY OF ORTHODONTIC TOOTH MOVEMENT AND THE IMPACT OF ANTI-INFLAMMATORY DRUGS

机译:正畸牙齿运动的生物学和抗炎药的影响

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Orthodontic tooth movement (OTM) results from complex biological mechanisms, more knowledge of which is needed for optimized orthodontic treatment. The biology of OTM is characterized by a cascade of events, triggered by the strain of the periodontal ligament fibers, leading to an inflammatory process that allows appropriate tissue remodeling. However, this inflammatory process may evoke side effects, such as pain, for which the use of non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol (acetaminophen) has been advocated. In vitro and in vivo studies have demonstrated that the arachidonic acid (AA) pathway represents a main step of the molecular events governing tissue remodeling during OTM. Through this pathway, important pro-inflammatory prostaglandins (PGs) are synthesized by three isoforms of a key enzyme referred as cyclooxygenase (COX), which catalyzes the conversion of AA into prosta-glandin G_2 (PGG_2), the precursor of all of the other PGs. Interestingly, among the downstream effects of these PGs also are the main side effects of OTM, pain and root resorption. The NSAIDs thus act by non-specifically blocking either all of the COX isoforms or the isoform 2 (COX-2), while paracetamol specifically blocks the isoform 3 (COX-3). The different tissue distribution and action of these COX isoforms likely would be responsible for some differences in the clinical effects produced by NSAIDs and paracetamol. Current animal and human studies show that all NSAIDs, including paracetamol, generally are useful in controlling pain associated to OTM while not affecting root resorption. However, only paracetamol does not appear to inhibit OTM and, therefore, may represent the drug of choice to control pain during OTM. Moreover, specific inhibitors for the COX-2 have not been reported to have significantly different effect on OTM as compared to all the non-specific inhibitors. The choice between these two classes of drugs, therefore, should be made on the basis of whether the patient has other systemic conditions, such as gastric or cardiovascular diseases. Although general indications for the use of these NSAIDs during OTM now are available, future investigations on both the basic biology underlying OTM and on the mechanisms of action of these drags are warranted to further optimize orthodontic treatments.
机译:正畸牙齿运动(OTM)由复杂的生物机制产生,更多的知识,优化的正畸治疗需要这一切。 OTM的生物学的特征在于由牙周韧带纤维的菌株引发的级联事件,导致炎症过程,允许适当的组织重塑。然而,这种炎症过程可以引起副作用,例如疼痛,其中倡导了使用非甾体抗炎药(NSAID)和乙酰氨基酚(乙酰氨基酚)。体外和体内研究表明,花生素酸(AA)途径代表了在OTM期间治疗组织重塑的分子事件的主要步骤。通过该途径,重要的促炎前列腺素(PGS)由作为环氧氢酶(COX)的三种同种型合成,其催化AA转化为普罗辛(PGG_2),所有其他的前体PGS。有趣的是,这些PGS的下游效果也是OTM,疼痛和根部吸收的主要副作用。因此,NSAID通过非特异性地阻断所有COx同种型或同种型2(COX-2)而起作用,而扑热酰胺特别阻断同种型3(COX-3)。这些COX同种型的不同组织分布和作用可能会对NSAIDs和扑热息痛产生的临床效果的一些差异负责。目前的动物和人类研究表明,所有NSAID(包括扑热息痛)通常可用于控制与OTM相关的疼痛,同时不影响根部吸收。然而,只有扑热息痛似乎没有抑制OTM,因此,可以代表在OTM期间控制疼痛的选择药物。此外,与所有非特异性抑制剂相比,尚未涉及COX-2的特异性抑制剂对OTM具有显着不同的影响。因此,这两类药物之间的选择应基于患者是否具有其他全身状况,例如胃或心血管疾病。虽然现在在OTM期间使用这些NSAID的一般指示现在是可用的,但未来对基本生物学的未来调查依据的基本生物学和这些拖累的行动机制,以进一步优化正畸治疗。

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