The adult K/BxN transgenic mouse develops spontaneous autoimmune arthritis with joint remodeling and profound bone loss. We report that both males and females display a severe sustained tactile allodynia which is reduced by gabapentin but not the potent cyclooxygenase inhibitor ketorolac. In dorsal horn, males and females show increased GFAP⁺ astrocytic cells; however, only males demonstrate an increase in Iba1⁺ microglia. In dorsal root ganglia (DRG), there is an increase in CGRP⁺, TH⁺, and Iba1⁺ (macrophage) labeling, but no increase in ATF3⁺ cells. At the ankle there is increased CGRP⁺, TH⁺, and GAP-43⁺ fiber synovial innervation. Thus, based on the changes in dorsal horn, DRG and peripheral innervation, we suggest that the adult K/BxN transgenic arthritic mice display a neuropathic phenotype, an assertion consistent with the analgesic pharmacology seen in this animal. These results indicate the relevance of this model to our understanding of the nociceptive processing which underlies the chronic pain state that evolves secondary to persistent joint inflammation.

成年 K/BxN 转基因小鼠会发展为自发性自身免疫性关节炎，伴有关节重塑和严重的骨质流失。我们报告说，男性和女性都表现出严重的持续触觉异常性疼痛，加巴喷丁可以减轻这种疼痛，但强效环氧合酶抑制剂酮咯酸却不能。在背角，雄性和雌性均表现出 GFAP ⁺星形胶质细胞增多；然而，只有男性表现出 Iba1 ⁺小胶质细胞的增加。在背根神经节 (DRG) 中，CGRP ⁺、TH ⁺和 Iba1 ⁺（巨噬细胞）标记增加，但 ATF3 ⁺细胞没有增加。在脚踝处，CGRP ⁺、TH ⁺和 GAP-43 ^{+ 增加}纤维滑膜神经支配。因此，基于背角、背根神经节和外周神经支配的变化，我们建议成年 K/BxN 转基因关节炎小鼠表现出神经性表型，这一断言与在该动物中看到的镇痛药理学一致。这些结果表明该模型与我们对疼痛处理的理解相关，疼痛处理是继发于持续性关节炎症的慢性疼痛状态的基础。