Inflammatory cytokines such as interleukin-1α (IL-1α) are increased in teeth with periapical lesions. Primary teeth with periapical lesions have a propensity for accelerated eruption of the successors. In this study, we asked whether increased levels of IL-1α in the dental follicle (DF) occurring as the result of periapical lesions promote tooth eruption, possibly due to enhanced osteoclastic remodeling of DF cells (DFCs). To this end, we studied the effect and possible mechanism of IL-1α on osteogenic differentiation, osteoclastogenic activity, and matrix remodeling of DFCs. Results demonstrated that DFCs cultured with IL-1α exhibited reduced osteogenic capacity, higher osteoclastogenic activity, and stronger invasive ability. Phosphorylation of JNK and p38 was upregulated, and pretreatment with SB203580 and SP600125 reversed the effect of IL-1α on DFCs. Neonatal rats subjected to subcutaneous injection of an IL-1 receptor antagonist exhibited a reduced number in activated osteoclasts, increased expression of alkaline phosphatase and osteopontin, and delayed tooth eruption. These data support our hypothesis that increased IL-1α cytokine levels as they occur during periodontal and periapical inflammation cause osteoclastic remodeling of the alveolar socket as a requirement for tooth eruption and thus may indirectly promote the vertical eruption of teeth toward the occlusal plane.

中文翻译：

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IL-1α 通过 JNK 和 p38 MAPK 通路调节牙囊细胞的成骨和破骨活性

具有根尖周病变的牙齿中的炎症细胞因子如白细胞介素 1α (IL-1α) 增加。具有根尖周病变的乳牙有加速后牙萌出的倾向。在这项研究中，我们询问了由于根尖周病变导致牙囊 (DF) 中 IL-1α 水平升高是否促进了牙齿萌出，这可能是由于 DF 细胞 (DFC) 的破骨细胞重塑增强。为此，我们研究了 IL-1α 对 DFCs 的成骨分化、破骨细胞活性和基质重塑的影响和可能的机制。结果表明，与 IL-1α 一起培养的 DFCs 表现出降低的成骨能力、更高的破骨细胞活性和更强的侵袭能力。JNK 和 p38 的磷酸化被上调，SB203580 和 SP600125 预处理逆转了 IL-1α 对 DFC 的影响。皮下注射 IL-1 受体拮抗剂的新生大鼠的活化破骨细胞数量减少，碱性磷酸酶和骨桥蛋白的表达增加，牙齿萌出延迟。这些数据支持我们的假设，即在牙周和根尖周炎症期间增加的 IL-1α 细胞因子水平会导致牙槽窝的破骨细胞重塑，这是牙齿萌出的必要条件，因此可能间接促进牙齿向咬合面垂直萌出。