Ramamurthy Nungavaram S, Greenwald Robert A, Celiker Mohamed Y, Shi Eric Y
Department of Oral Biology and Pathology, School of Dental Medicine, State University of New York at Stony Brook, NY 11794, USA.
J Periodontol. 2005 Feb;76(2):229-33. doi: 10.1902/jop.2005.76.2.229.
Periodontal disease (PD) and rheumatoid arthritis (RA) share many common pathophysiologic features, but a clinical relationship between the two conditions remains controversial, in part because of the confounding effects of anti-inflammatory drug therapy universally used in the latter disease. To further explore this issue, inflammatory arthritis was induced in rats to determine the effect on gingival biomarkers of inflammation and tissue destruction and to investigate the effect of a therapeutic intervention devoid of conventional anti-inflammatory properties.
Adjuvant arthritis (AA) was induced in Lewis male rats by injecting mycobacterium cell wall in complete Freund's adjuvant using standard techniques. One group of animals was treated by induction of systemic tissue inhibitor of matrix metalloproteinases (TIMP-4). At 3 weeks, arthritis severity was recorded and both paw and gingival tissues were collected for matrix metalloproteinase activity (MMP) and cytokine analysis. In addition, the maxillary jaws were removed for assessment of periodontal bone loss.
The development of arthritis was associated with elevated joint tissue MMPs, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1beta levels compared to control rats. In the gingival tissue of the untreated arthritic rats, gelatinase, collagenase, TNF-alpha, and IL-1beta were also elevated compared to control rats. Periodontal bone loss and tooth mobility were also increased significantly (P <0.05) in untreated arthritic rats. All parameters improved after TIMP-4 gene therapy.
To our knowledge, this is the first study to report an association between experimental systemic arthritis in rats and elevated gingival tissue MMPs, cytokine levels, and periodontal disease. Reversal of these changes with TIMP-4 gene therapy strengthens the pathophysiologic correlation between systemic and local disease.
牙周病(PD)和类风湿性关节炎(RA)具有许多共同的病理生理特征,但这两种疾病之间的临床关系仍存在争议,部分原因是后者普遍使用的抗炎药物治疗具有混杂效应。为了进一步探讨这个问题,在大鼠中诱导炎性关节炎,以确定其对牙龈炎症和组织破坏生物标志物的影响,并研究一种缺乏传统抗炎特性的治疗干预措施的效果。
采用标准技术,通过在完全弗氏佐剂中注射分枝杆菌细胞壁,在雄性Lewis大鼠中诱导佐剂性关节炎(AA)。一组动物通过诱导全身性基质金属蛋白酶组织抑制剂(TIMP-4)进行治疗。在3周时,记录关节炎严重程度,并收集爪部和牙龈组织进行基质金属蛋白酶活性(MMP)和细胞因子分析。此外,取出上颌骨以评估牙周骨丧失情况。
与对照大鼠相比,关节炎的发展与关节组织MMP、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β水平升高有关。与对照大鼠相比,未经治疗的关节炎大鼠牙龈组织中的明胶酶、胶原酶、TNF-α和IL-1β也升高。未经治疗的关节炎大鼠的牙周骨丧失和牙齿松动也显著增加(P<0.05)。TIMP-4基因治疗后所有参数均得到改善。
据我们所知,这是第一项报道大鼠实验性全身性关节炎与牙龈组织MMP升高、细胞因子水平升高和牙周病之间存在关联的研究。TIMP-4基因治疗使这些变化逆转,加强了全身性和局部性疾病之间的病理生理相关性。