Sleep Bruxism and Central Sensitization in Myofascial Face Pain

颞下颌关节紊乱病中最常见的肌筋膜面痛（MFP）的发病机制 (TMD)，仍然存在争议。其中一个关键的争议涉及睡眠磨牙症（SB）的作用;而 SB的相对较弱的措施支持SB在至少一些MFP患者中的作用，非实验室- 基于睡眠的研究已经进行了明确的解决这个问题。本申请提出， 主要目的是进行确定性的研究，SB在MFP维护，其中的单独作用， 将检查研磨和紧握。我们还将探讨SB和压力之间的关系- 诱发的磨牙症，以及遗传异常在调节磨牙症患者疼痛风险中的作用 某人第二个目的是评估中枢敏感化（CS）在MFP维持中的作用。 支持CS在MFP中的作用的证据受到两种患者抽样中的偏倚的限制， 解剖部位因此，我们将在更具代表性的MFP样本中研究CS在MFP中的作用 患者和对照组，以及进行评价CS在三叉神经外和三叉神经区域。 CS在这两个领域的差异可能表明不同的疼痛维持机制。收集的数据 在这两个目标的服务，然后允许实现第三个目标，了解的关系， 在MFP中SB和CS之间，包括SB和CS中的升高可能定义亚组的可能性 不同的疼痛维持机制是起作用的。这些目标可以在一个 对120名MFP患者和60名人口统计学匹配的对照进行病例对照研究。实现这些目标将 提供关于SB在MFP中的作用的确凿证据，并将促进对这种关系的理解 在SB和CS之间。这种理解有望支持我们改善临床的长期目标。 通过靶向治疗潜在的疼痛维持机制来治疗MFP。

The pathogenesis of myofascial face pain (MFP), the most prevalent type of temporomandibular disorder (TMD), remains controversial. One of the key controversiesconcerns the role of sleep bruxism (SB); While relatively weak measures of SB have supported a role of SB in at least some MFP patients, nolaboratory- based sleep study has been undertaken to resolvethis issue definitively. This application proposesas its main aim the conduct of the definitive study of SB in MFP maintenance, in which the separate role of grinding and clenching would be examined. We would also explore the relationship between SB andstress- induced bruxism, as well as the role of genetic anomaliesin modulating the risk of pain among thosewith SB. A second aim would evaluate the role of central sensitization (CS) in the maintenanceof MFP. Evidence supporting a role for CS in MFP has been limited by biases in the sampling of both patientsand anatomic sites. Therefore, we would examine the role of CS in MFP in a more representative sample of MFP patients and controls, as well as conduct an evaluationof CS in both extratrigeminal and trigeminal regions. Differences in CS in these two areas might suggest different pain maintenance mechanisms. Data collected in the service of these two aims then allows the achievement a third aim, understanding the relationships between SB and CS in MFP, including the possibility that elevations in SB and CS may define subgroupsin which different pain maintenance mechanisms are operative. These aims can be achieved in the context of a case-control study of 120 MFP patients and 60 demographically-matchedcontrols. Pursuit of these aims will provide firm evidence regarding the role of SB in MFP and will advance understanding of the relationship between SB and CS. This understanding is expectedto support our long-term goal of improving clinical treatment of MFP by targeting treatment to underlying pain-maintenenance mechanisms.