细菌感染作为慢性风湿性疾病的潜在诱因的作用是有据可查的。口腔感染如牙周炎可能在自身免疫性疾病的发展中起着特别重要的作用。口腔作为致病菌的储库。这些细菌可能通过分子模仿等机制引发失调的免疫反应,其中细菌肽类似于自身肽。遗传因素也可能使个体易患特定的自身免疫性疾病,在强直性脊柱炎以及其他风湿性疾病的情况下,最值得注意的是人类白细胞抗原B27(HLA-B27)。我们介绍了一例23岁的女性,患有术后感染引起的反应性关节炎。患者表现为双侧肩部疼痛,运动范围减小,下背部疼痛恶化,和最近第三磨牙拔除部位的下颌疼痛。虽然最初被诊断为类风湿性关节炎,在未解决的感染的手术治疗后,患者经历了快速和戏剧性的改善,证明口腔感染与慢性系统性自身免疫性疾病之间存在因果关系或时间相关性。这个案例提供了关于慢性自身免疫性疾病和口腔细菌感染之间联系的因果机制的有用证据。说明口腔感染如何成为反应性关节炎的致病因素。我们认为,这表明口腔微生物群落中通常存在的细菌是引发全身性炎症的抗原的潜在来源。尤其是那些已经与其他自身免疫性疾病相关的疾病,如强直性脊柱炎的肺炎克雷伯菌。根据先前的出版物将自身肽与此类细菌中的同源性联系起来,我们推测这种联系背后的机制,特别注意分子模仿。临床医生应该意识到某些风湿性疾病(如反应性关节炎)与细菌感染之间的密切联系,特别是口腔;这种意识应该为关节炎疾病的治疗和预防提供指导。
The role of bacterial infections as potential triggers for chronic rheumatic diseases is well-documented. Oral infections such as periodontitis may play a particularly important role in the development of autoimmune diseases, with the oral cavity serving as a reservoir for pathogenic bacteria. These bacteria may trigger dysregulatory immune responses through mechanisms like molecular mimicry, whereby bacterial peptides resemble self-peptides. Genetic factors may also predispose individuals to specific autoimmune diseases, most notably human leukocyte antigen B27 (HLA-B27) in the
case of ankylosing spondylitis as well as other rheumatic diseases. We present a
case of a 23-year-old woman with reactive arthritis resulting from a postoperative infection. The patient presented with bilateral shoulder pain, decreased range of motion, worsening lower back pain, and mandibular pain at the site of a recent third molar extraction. Though initially diagnosed with rheumatoid arthritis, the patient experienced rapid and dramatic improvements following surgical treatment of the unresolved infection, demonstrating a causative or temporally related association between oral infections and chronic systemic autoimmune disease. This
case provides useful evidence regarding causal mechanisms for the connections between chronic autoimmune diseases and oral bacterial infection, illustrating how oral infection may serve as a causative factor for reactive arthritis. We suggest that this implicates bacteria normally present in oral microflora as a potential source of the antigens involved in triggering systemic inflammation, especially those already associated with other autoimmune diseases, such as Klebsiella pneumoniae in the
case of ankylosing spondylitis. Based on prior publications linking self-peptides with homologies in such bacteria, we speculate on mechanisms underlying this connection, with particular attention to molecular mimicry. Clinicians should be aware of the close connection between certain rheumatic diseases (such as reactive arthritis) and bacterial infection, particularly of the oral cavity; such awareness should inform strategies for treatment and prevention of arthritic disease.