Gaurilcikaite E, Renton T, Grant A D
Wolfson Centre for Age-Related Diseases, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Department of Oral Surgery, Dental Institute, King's College London, London, UK.
Oral Dis. 2017 May;23(4):451-463. doi: 10.1111/odi.12537. Epub 2016 Aug 1.
Periodontal diseases, primarily gingivitis and periodontitis, are characterised by progressive inflammation and tissue destruction. However, they are unusual in that they are not also accompanied by the pain commonly seen in other inflammatory conditions. This suggests that interactions between periodontal bacteria and host cells create a unique environment in which the pro-algesic effects of inflammatory mediators and factors released during tissue damage are directly or indirectly inhibited. In this review, we summarise the evidence that periodontal disease is characterised by an accumulation of classically pro-algesic factors from bacteria and host cells. We then discuss several mechanisms by which inflammatory sensitisation of nociceptive fibres could be prevented through inactivation or inhibition of these factors. Further studies are necessary to fully understand the molecular processes underlying the endogenous localised hypoalgesia in human periodontal disease. This knowledge might provide a rational basis to develop future therapeutic interventions, such as host modulation therapies, against a wide variety of other human pain conditions.
牙周疾病，主要是牙龈炎和牙周炎，其特征是进行性炎症和组织破坏。然而，它们不同寻常之处在于，它们不像其他炎症性疾病那样伴有常见的疼痛。这表明牙周细菌与宿主细胞之间的相互作用创造了一个独特的环境，在这个环境中，组织损伤期间释放的炎症介质和因子的促痛作用被直接或间接抑制。在这篇综述中，我们总结了牙周疾病以细菌和宿主细胞中经典促痛因子积累为特征的证据。然后，我们讨论了几种通过使这些因子失活或抑制来预防伤害性纤维炎症敏化的机制。有必要进行进一步研究，以充分了解人类牙周疾病内源性局部痛觉减退背后的分子过程。这些知识可能为开发未来的治疗干预措施提供合理依据，例如宿主调节疗法，以应对多种其他人类疼痛状况。
