Gunson Michael J, Arnett G William, Milam Stephen B
Arnett and Gunson Facial Reconstruction, Santa Barbara, CA 93101, USA.
J Oral Maxillofac Surg. 2012 Aug;70(8):1918-34. doi: 10.1016/j.joms.2011.07.018. Epub 2011 Oct 19.
When osseous mandibular condylar resorption occurs there can be many different diagnoses: inflammatory arthritis, TMJ compression, trauma, hormone imbalances, and others. While each diagnosis has its own original inciting event, the pathophysiological pathway for articular bone loss is the same. The aim of this article is to review the relevant literature on condylar resorption and the use of pharmacotherapy to control arthritic erosions and resorption.
The literature search was performed using PubMed database with various combinations of related keywords. Preference was given to clinical trials when reviewing articles.
The literature reveals that common cellular level events associated with articular resorption include the activation of osteoblasts by cytokines, free radicals, hormone imbalances and/or potent phospholipid catabolites. The osteoblast then activates the recruitment of osteoclasts and promotes the release of matrix degrading enzymes from the osteoclast. Research into articular erosions has focused on elucidating the important steps in the bone destructive pathways and interfering with them by pharmacological means. The use of antioxidants, tetracyclines, omega-3 fatty acids, non-steroidal anti-inflammatories and inflammatory cytokine inhibitors to aid in preventing and controlling articular bone loss including osseous mandibular condylar resorption has been successful.
By understanding the known pathways that lead to condylar resorption and the individual patient's susceptibilities, targeted pharmacotherapy might be able to disturb these pathways and prevent further condylar resorption. Basic clinical investigations and randomized clinical trials are still required, but the present science is encouraging.
当发生骨性下颌髁突吸收时,可能存在多种不同的诊断:炎性关节炎、颞下颌关节受压、创伤、激素失衡等。虽然每种诊断都有其最初的诱发事件,但关节骨丢失的病理生理途径是相同的。本文的目的是综述有关髁突吸收以及使用药物治疗来控制关节炎性侵蚀和吸收的相关文献。
使用PubMed数据库,通过相关关键词的各种组合进行文献检索。在综述文章时优先选择临床试验。
文献表明,与关节吸收相关的常见细胞水平事件包括细胞因子、自由基、激素失衡和/或强效磷脂分解代谢产物对成骨细胞的激活。然后,成骨细胞激活破骨细胞的募集,并促进破骨细胞释放基质降解酶。对关节侵蚀的研究集中在阐明骨破坏途径中的重要步骤,并通过药理学手段对其进行干预。使用抗氧化剂、四环素、ω-3脂肪酸、非甾体抗炎药和炎性细胞因子抑制剂来帮助预防和控制包括骨性下颌髁突吸收在内的关节骨丢失已取得成功。
通过了解导致髁突吸收的已知途径以及个体患者的易感性,有针对性的药物治疗或许能够干扰这些途径并防止髁突进一步吸收。仍需要基础临床研究和随机临床试验,但目前的科学研究令人鼓舞。