Yoo T J, Shea J J, Floyd R A
Division of Allergy-Immunology, University of Tennessee, Memphis 38163.
Am J Otolaryngol. 1987 Sep-Oct;8(5):317-24. doi: 10.1016/s0196-0709(87)80050-9.
Collagen autoimmunity has been suggested as one etiologic mechanism to otosclerosis. Although substantial studies relating this disease to collagen autoimmunity have been reported, a basic understanding of the pathogenic mechanism involved is lacking. Some otosclerosis patients have a high level of antibody to type II collagen. In addition, complement and antibody were deposited in the stapes from otosclerosis patients. Furthermore, the otic capsule and stapes have been found to contain type II collagen by immunohistologic studies and biochemical analysis. Otospongiosis-like lesions have also been produced in rats by immunizing them with type II collagen. This finding led us to postulate a hypothesis of an autoimmunity to type II collagen as an etiopathogenesis of this illness. Our initial hypothesis has been updated to incorporate new findings in the field of cell biology. The role of interleukin 1, osteoclasts, osteoblasts, bone resorption, and other factors such as minor collagens, calcitonin, vitamin D, parathyroid hormone, collagenase, and prostaglandins are incorporated in this updated hypothesis.
胶原自身免疫被认为是耳硬化症的一种病因机制。尽管已经报道了大量将这种疾病与胶原自身免疫相关联的研究，但对于所涉及的致病机制仍缺乏基本认识。一些耳硬化症患者具有高水平的抗II型胶原抗体。此外，补体和抗体沉积在耳硬化症患者的镫骨中。而且，通过免疫组织学研究和生化分析发现，耳囊和镫骨含有II型胶原。通过用II型胶原免疫大鼠，也在大鼠中产生了耳海绵化样病变。这一发现使我们提出了一种针对II型胶原的自身免疫作为该疾病发病机制的假说。我们最初的假说已更新，纳入了细胞生物学领域的新发现。白细胞介素1、破骨细胞、成骨细胞、骨吸收以及其他因素（如微小胶原、降钙素、维生素D、甲状旁腺激素、胶原酶和前列腺素）的作用被纳入了这个更新后的假说中。
