PDF(Pubmed)
Abstract：
Osteoarthritis afflicts millions of individuals across the world resulting in impaired quality of life and increased health costs. To understand this disease, physicians have been studying risk factors, such as genetic predisposition, aging, obesity, and joint malalignment; however have been unable to conclusively determine the direct etiology. Current treatment options are short-term or ineffective and fail to address pathophysiological and biochemical mechanisms involved with cartilage degeneration and the induction of pain in arthritic joints. OA pain involves a complex integration of sensory, affective, and cognitive processes that integrate a variety of abnormal cellular mechanisms at both peripheral and central (spinal and supraspinal) levels of the nervous system Through studies examined by investigators, the role of growth factors and cytokines has increasingly become more relevant in examining their effects on articular cartilage homeostasis and the development of osteoarthritis and osteoarthritis-associated pain. Catabolic factors involved in both cartilage degradation in vitro and nociceptive stimulation include IL-1, IL-6, TNF-α, PGE2, FGF-2 and PKCδ, and pharmacologic inhibitors to these mediators, as well as compounds such as RSV and LfcinB, may potentially be used as biological treatments in the future. This review explores several biochemical mediators involved in OA and pain, and provides a framework for the understanding of potential biologic therapies in the treatment of degenerative joint disease in the future.
摘要：
骨关节炎困扰着全世界数百万人，导致生活质量受损和健康成本增加。为了了解这种疾病，医生一直在研究危险因素，比如遗传易感性，老化，肥胖，和关节不正；然而，无法最终确定直接病因。目前的治疗选择是短期或无效的,并且不能解决与软骨变性和关节炎关节中疼痛的诱导有关的病理生理学和生物化学机制。OA疼痛涉及复杂的感觉整合，情感,和认知过程，整合各种异常的细胞机制在外周和中枢（脊髓和脊柱上）的神经系统水平通过研究人员检查，生长因子和细胞因子的作用在检查它们对关节软骨稳态以及骨关节炎和骨关节炎相关疼痛的发展的影响方面变得越来越重要。参与体外软骨降解和伤害性刺激的分解代谢因子包括IL-1，IL-6，TNF-α，PGE2,FGF-2和PKCδ,和这些介质的药物抑制剂，以及RSV和LfcinB等化合物，将来可能会用作生物治疗。这篇综述探讨了几种参与OA和疼痛的生化介质，并为理解未来退行性关节疾病的潜在生物疗法提供了框架。
