Chen Rensa, Schwander Martin, Barbe Mary F, Chan Marion M
Department of Microbiology and Immunology, Lewis Katz School of Medicine-Temple University, Philadelphia, PA, 19140, United States of America.
Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, 08854, United States of America.
PLoS One. 2016 Sep 30;11(9):e0164078. doi: 10.1371/journal.pone.0164078. eCollection 2016.
Globally, a body of comparative case-control studies suggests that rheumatoid arthritis (RA) patients are more prone to developing hearing loss (HL). However, experimental evidence that supports this hypothesis is still lacking because the human auditory organ is not readily accessible. The aim of this study was to determine the association between bone damage to the ossicles of the middle ear and HL, using a widely accepted murine model of collagen-induced arthritis (RA mice). Diarthrodial joints in the middle ear were examined with microcomputer tomography (microCT), and hearing function was assessed by auditory brainstem response (ABR). RA mice exhibited significantly decreased hearing sensitivity compared to age-matched controls. Additionally, a significant narrowing of the incudostapedial joint space and an increase in the porosity of the stapes were observed. The absolute latencies of all ABR waves were prolonged, but mean interpeak latencies were not statistically different. The observed bone defects in the middle ear that were accompanied by changes in ABR responses were consistent with conductive HL. This combination suggests that conductive impairment is at least part of the etiology of RA-induced HL in a murine model. Whether the inner ear sustains bone erosion or other pathology, and whether the cochlear nerve sustains pathology await subsequent studies. Considering the fact that certain anti-inflammatories are ototoxic in high doses, monitoring RA patients' auditory function is advisable as part of the effort to ensure their well-being.
在全球范围内，一系列比较性病例对照研究表明，类风湿性关节炎（RA）患者更容易出现听力损失（HL）。然而，由于人类听觉器官不易进行研究，支持这一假设的实验证据仍然缺乏。本研究的目的是利用广泛认可的胶原诱导性关节炎小鼠模型（RA小鼠），确定中耳听小骨的骨质损伤与HL之间的关联。通过微型计算机断层扫描（microCT）检查中耳的滑膜关节，并通过听性脑干反应（ABR）评估听力功能。与年龄匹配的对照组相比，RA小鼠的听力敏感性显著降低。此外，观察到砧镫关节间隙明显变窄，镫骨孔隙率增加。所有ABR波的绝对潜伏期延长，但平均峰间潜伏期无统计学差异。观察到的中耳骨质缺损伴有ABR反应变化，这与传导性HL一致。这种情况表明，在小鼠模型中，传导性损伤至少是RA诱导的HL病因的一部分。内耳是否存在骨质侵蚀或其他病理变化，以及耳蜗神经是否存在病理变化，有待后续研究。考虑到某些抗炎药在高剂量时有耳毒性，建议对RA患者的听觉功能进行监测，作为确保其健康的一部分努力。
