Fassbender H G
Zentrum für Rheuma-Pathologie (WHO Centre), Mainz, Germany.
Arch Orthop Trauma Surg. 1998;117(1-2):2-7. doi: 10.1007/BF00703430.
The immunological disturbance in rheumatoid arthritis (RA) gives rise to a nonspecific inflammatory reaction mediated by cells and cytokines. This immunological nonbacterial synovitis, however, does not destroy the articular cartilage. The destruction of joint structures is the effect of tumor-like aggressive synoviogenic cell elements (TLP). These TLP formations are not observed in any other type of arthritis. TLP formations are strictly avascular and short-lived. After they have decayed, a collagenous pannus remains. Invasion and destruction of joint structures are brought about by several types of proteases, synthesized and secreted by highly active TLP cells. The TLP formations possess more than twice the affinity for adjacent bone than for the articular cartilage. In these formations, four oncogenes could be identified. In the course of RA disease, TLP formations can recur. Thus, the joint damage can summate with time. The oncological character of the aggressive process in RA demands new therapeutical considerations to protect RA patients from destruction of their joints.
类风湿关节炎（RA）中的免疫紊乱会引发由细胞和细胞因子介导的非特异性炎症反应。然而，这种免疫性非细菌性滑膜炎并不会破坏关节软骨。关节结构的破坏是肿瘤样侵袭性滑膜生成细胞成分（TLP）的作用。在其他任何类型的关节炎中都未观察到这些TLP结构。TLP结构严格无血管且寿命短暂。它们衰变后，会留下胶原性血管翳。关节结构的侵袭和破坏是由高活性TLP细胞合成和分泌的几种蛋白酶引起的。TLP结构对相邻骨骼的亲和力比对关节软骨的亲和力高两倍多。在这些结构中，可以识别出四种癌基因。在RA疾病过程中，TLP结构可能会复发。因此，关节损伤会随着时间累积。RA侵袭性过程的肿瘤学特征需要新的治疗考虑，以保护RA患者的关节不被破坏。
