Soory Mena
Periodontology, King's College London Dental Institute, Denmark Hill, London SE 5 9RW, UK.
Infect Disord Drug Targets. 2012 Aug;12(4):301-15. doi: 10.2174/187152612801319302.
Periodontal pathogens in plaque biofilm initiate periodontitis, which is influenced by genetic and environmental factors. The resultant pro-oxidant status imposed on the periodontium, exacerbated by episodic hyperinflammatory damage contributes to progression of periodontitis and tooth loss in susceptible subjects. Increasing documentation of bi-directional connections between periodontal and cardiometabolic disorders makes it an intriguing area of therapeutic intervention for mutual benefit. Periodontitis and associated comorbidities demonstrate similar risk markers of inflammation during disease progression. Depending on the extent and severity of the inflammatory response, periodontitis could impact significantly on systemic inflammatory loading and influence the progression of endothelial dysfunction, atherosclerotic plaque instability, dyslipidaemia and insulin resistance. Some of the common mechanisms involved are discussed, relevant to periodontal and cardiometabolic disorders which have been documented as having a bidirectional relationship with periodontal disease progression; abating in response to treatment. Periodontal disease may be a useful marker of a susceptible immune system, or directly affect the progression of systemic diseases due to inflammatory loading. These mechanisms mediated by coordinated actions of cytokines, acute phase proteins, enzymes and their sequelae are addressed in the context of conventional periodontal therapy and its outcome with a modulatory role on metabolic diseases. Applications for the role of nutritional and therapeutic antioxidants as adjuncts in diseases with a distinctly prooxidant profile are discussed. Accurate therapeutic targeting as an adjunct to conventional periodontal treatment in this context, for mutual benefit to subjects with periodontitis and cardiometabolic diseases is a challenge.
菌斑生物膜中的牙周病原体引发牙周炎，而牙周炎受遗传和环境因素影响。由此产生的牙周组织促氧化状态，因偶发性的过度炎症损伤而加剧，这会促使易感人群的牙周炎进展和牙齿脱落。越来越多的文献表明牙周疾病与心脏代谢紊乱之间存在双向联系，这使其成为一个互利的有趣治疗干预领域。牙周炎及相关合并症在疾病进展过程中表现出相似的炎症风险标志物。根据炎症反应的程度和严重程度，牙周炎可能会显著影响全身炎症负荷，并影响内皮功能障碍、动脉粥样硬化斑块不稳定、血脂异常和胰岛素抵抗的进展。文中讨论了一些相关的常见机制，这些机制与牙周疾病和心脏代谢紊乱有关，已被证明与牙周疾病进展存在双向关系，并且会随着治疗而减轻。牙周疾病可能是易感免疫系统的一个有用标志物，或者由于炎症负荷直接影响全身性疾病的进展。在传统牙周治疗及其对代谢疾病具有调节作用的结果的背景下，探讨了由细胞因子、急性期蛋白、酶及其后遗症的协同作用介导的这些机制。讨论了营养性和治疗性抗氧化剂作为具有明显促氧化特征疾病辅助治疗的作用。在这种情况下，作为传统牙周治疗辅助手段进行准确的治疗靶向，以造福牙周炎和心脏代谢疾病患者是一项挑战。
