6月29日讯/生物谷BIOON/--患有牙周疾病的患者，往往有心血管疾病。牙周疾病是心脏疾病的一个风险因子，就像吸烟和高血压一样。来自阿尔波特大学的研究人员们的最新研究发现，口腔的清洁是如何影响心脏疾病的发病风险的。此项研究结果于近日发表在PLOS ONE杂志上。
许多人们没有意识到口腔健康可以影响到全身的器官。此项研究结果表明，患有牙周疾病的患者，有较高的风险发生心血管疾病。研究人员利用临床前小鼠模型，发现了一种新的细胞受体，CD36/SR-B2，这种受体可以与口腔中的细菌相互作用，从而引起牙周疾病。CD36/SR-B2可以与Toll样受体相互作用（Toll样受体是免疫系统早期的警戒防线），并产生出一种名为IL-1 beta的蛋白。这种蛋白可以引起炎症，最终导致牙周疾病和动脉粥样硬化。这项发现提供了牙周疾病与心血管疾病相互联系的理论基础。
之前的研究已经证明，Toll样受体是涉及到牙周疾病及心血管疾病的相互关系中的。此项研究发现了CD36/SR-B2是一个新的，共同作用的受体，从而促进了炎症及疾病发生。下一步，研究人员们将开展研究，如何靶向这两种受体，从而阻止心脏疾病的发生。
因此，早期诊断和治疗牙周疾病，对于降低和预防炎症和心脏病风险，至关重要。然而，人们常常在牙周病的早期，由于没有影响到日常生活，所以并不重视，直到牙齿出现松动或是异常才去看牙科医生。事实上，常规的牙齿检查及转业的牙齿清洁，对保持口腔卫生及身体健康，都十分关键。因为许多疾病，早期的诊断和治疗比晚期的治疗简单而且便宜得多。（生物谷)
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CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model.
Paul M.Braun, et al.
There is strong epidemiological association between periodontal disease and cardiovascular disease but underlying mechanisms remain ill-defined. Because the human periodontal disease pathogen, Porphyromonas gingivalis (Pg), interacts with innate immune receptors Toll-like Receptor (TLR) 2 and CD36/scavenger receptor-B2 (SR-B2), we studied how CD36/SR-B2 and TLR pathways promote Pg-mediated atherosclerosis. Western diet fed low density lipoprotein receptor knockout (Ldlr°) mice infected orally with Pg had a significant increase in lesion burden compared with uninfected controls. This increase was entirely CD36/SR-B2-dependent, as there was no significant change in lesion burden between infected and uninfected Ldlr° mice. Western diet feeding promoted enhanced CD36/SR-B2-dependent IL1β generation and foam cell formation as a result of Pg lipopolysaccharide (PgLPS) exposure. CD36/SR-B2 and TLR2 were necessary for inflammasome activation and optimal IL1? generation, but also resulted in LPS induced lethality (pyroptosis). Modified forms of LDL inhibited Pg-mediated IL1? generation in a CD36/SR-B2-dependent manner and prevented pyroptosis, but promoted foam cell formation. Our data show that Pg infection in the oral cavity can lead to significant TLR2-CD36/SR-B2 dependent IL1? release. In the vessel wall, macrophages encountering systemic release of IL1?, PgLPS and modified LDL have increased lipid uptake, foam cell formation, and release of IL1?, but because pyroptosis is inhibited, this enables macrophage survival and promotes increased plaque development. These studies may explain increased lesion burden as a result of periodontal disease, and suggest strategies for development of therapeutics.
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