Abstract: Objective  To evaluate the different responses in immunodeficient mice and immunocompetent mice during incisor homeostasis maintenance and injury repair. Methods  The mice aged 8-10 weeks were used, which include male BALB/c Nude mice (n=10), BALB/c mice (n=10), and C57BL/6J mice (n=10). A mechanical injury model was established in the incisors, and the length of the incisors was measured at a fixed time every day for three consecutive days, and their growth rate was calculated. Comparisons were made between clipped and non-clipped sides, as well as normal controls. Immunological responses were assessed, and histological analyses were conducted to evaluate mineralization in dental hard tissues. Real-time quantitative reverse transcription  polymerase chain reaction (RT-qPCR), immunohistochemistry (IHC), and immunofluorescence (IF) staining were employed to detect the expression of immune-related cytokine receptors and to assess stem cell proliferation in the cervical loop. Results  BALB/c Nude mice demonstrated significantly lower incisor growth rates under both homeostatic maintenance and injury conditions compared to BALB/c and C57BL/6J mice (P<0.05), suggesting that immune responses may contribute to incisor regeneration. Growth rates were markedly higher at night than during the day. The injury stimulated an accelerated incisor growth (P<0.05), with increased proliferation of cervical loop stem cells, as indicated by elevated numbers of SOX2⁺ and Ki-67⁺ cells (P<0.05). Histological staining revealed reduced mineralization on the clipped side compared to the unclipped and normal control side (P<0.05). Additionally, expression levels of Dspp, Ambn, genes involved in dentin and enamel formation, were significantly upregulated (P<0.05). IF staining showed that the expression of the Th2 cytokine receptor interleukin 4 receptor alpha（IL4rα）was significantly increased on the clipped side, consistent with mRNA expression levels. Conclusion  The incisor injury promotes growth and enhances stem cell proliferation and differentiation in the cervical loop. Early repair is characterized with reduced mineralization of hard tissues. This study suggests that T cell deficiency may affect the homeostatic repair and regeneration ability of incisors, and the high expression of type Ⅱ immune cytokine receptor IL4rα is closely related to the repair process. Further, it is necessary to study the specific functional mechanism to delineates the role of immune participation, thereby providing a novel theoretical framework for clinical regenerative medicine.

Key words: injury repair, mouse incisor growth, cervical loop, mineralization, immunity, regeneration