Habu Manabu, Tominaga Kazuhiro, Sukedai Miho, Alstergren Per, Ohkawara Susumu, Kopp Sigvard, Fukuda Jinichi
First Department of Oral and Maxillofacial Surgery, Kyushu Dental College, Kokurakita, Kitakyushu, Japan.
J Oral Pathol Med. 2002 Jan;31(1):45-54. doi: 10.1046/j.0904-2512.2001.10057.x.
In temporomandibular joint (TMJ) arthritis, there is limited knowledge of the relationship between interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1ra), as well as the source of these cytokines. We investigated the development of an antigen-induced arthritis in the rabbit TMJ immunohistochemically.
Unilateral TMJ arthritis was induced in 32 adult New Zealand White rabbits. From 6 h to 12 weeks after induction of arthritis, topology of IL-1beta and IL-1ra were observed.
The acute stage of induced arthritis lasted for one week after induction, thereafter it became chronic. In the early phase of the acute stage, infiltrating inflammatory cells, as well as synovial cells, produced IL-1beta and IL-1ra. In the late phase of the acute stage, the main source of these cytokines was subsynovial fibroblasts. In this phase of arthritis, IL-1beta and IL-1ra did not appear to be produced by synovial cells. From the early to intermediate phase of the chronic stage, proliferating synovial cells produced IL-1beta and IL-1ra. In this phase of the arthritis, these cytokines were also observed in a cluster formation in chondrocytes.
This arthritis model shows a staging of the joint inflammation process with time. IL-1beta and IL-1ra are produced by a certain kind of cells depending on the stage of inflammation.
在颞下颌关节(TMJ)关节炎中,关于白细胞介素-1β(IL-1β)与白细胞介素-1受体拮抗剂(IL-1ra)之间的关系以及这些细胞因子的来源,目前了解有限。我们通过免疫组织化学方法研究了兔颞下颌关节抗原诱导性关节炎的发展过程。
对32只成年新西兰白兔诱导单侧颞下颌关节炎。在诱导关节炎后的6小时至12周内,观察IL-1β和IL-1ra的分布情况。
诱导性关节炎的急性期在诱导后持续一周,此后变为慢性期。在急性期早期,浸润的炎性细胞以及滑膜细胞产生IL-1β和IL-1ra。在急性期后期,这些细胞因子的主要来源是滑膜下成纤维细胞。在关节炎的这个阶段,滑膜细胞似乎不产生IL-1β和IL-1ra。从慢性期的早期到中期,增殖的滑膜细胞产生IL-1β和IL-1ra。在关节炎的这个阶段,软骨细胞中也观察到这些细胞因子呈簇状形成。
该关节炎模型显示了关节炎症过程随时间的分期。IL-1β和IL-1ra由特定类型的细胞产生,这取决于炎症阶段。