Irwin C R, Myrillas T T
Department of Restorative Dentistry, School of Clinical Dentistry, Queen's University, Belfast, UK.
Oral Dis. 1998 Mar;4(1):43-7. doi: 10.1111/j.1601-0825.1998.tb00255.x.
The mechanisms underlying periodontal disease involve complex interactions between bacterial products, host cells and locally produced, biologically active factors. The umbrella term cytokine has been used to include a variety of such factors, including the interleukin family. The role of one cytokine, IL-1 beta, in periodontal disease pathogenesis has been widely reported. More recent studies have focused on a potential role for IL-6 in driving the destructive processes. Most of these reports have suggested a pro-inflammatory role for IL-6 alongside IL-1 and TNF-alpha. This manuscript reviews the biological functions of IL-6, specifically related to tissue destruction at the periodontal site. We would suggest that the activity of IL-6 in periodontal disease differs from IL-1 and TNF-alpha, and may, in part, play a protective role.
牙周病的潜在发病机制涉及细菌产物、宿主细胞以及局部产生的生物活性因子之间的复杂相互作用。细胞因子这一统称涵盖了多种此类因子，包括白细胞介素家族。细胞因子白细胞介素-1β（IL-1β）在牙周病发病机制中的作用已有广泛报道。最近的研究聚焦于IL-6在驱动破坏过程中的潜在作用。这些报告大多表明IL-6与IL-1和肿瘤坏死因子-α（TNF-α）一样具有促炎作用。本文综述了IL-6的生物学功能，特别是与牙周组织破坏相关的功能。我们认为IL-6在牙周病中的活性不同于IL-1和TNF-α，并且可能在一定程度上发挥保护作用。
