Archives of oral biology · 2026
Lipocalin-2 inhibition regulates pain-like facial expression associated with neuroinflammation involving the NF-κB/β-catenin pathway during orthodontic tooth movement in a type 2 diabetic model.
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García-Gama Jazhiel Eloy, Cifuentes-Mendiola Saúl Ernesto, Perrusquía-Hernández Elias, González-Alva Patricia, Martínez-Dávalos Arnulfo, Rodríguez-Villafuerte Mercedes, Pérez Martínez Isaac Obed, García-Hernández Ana Lilia
Аннотация
OBJECTIVE: The aim was to explore the role of Lipocalin-2 (LCN-2) in modulating nociceptive and neuroinflammatory signalling during OTM in a murine model of Type 2 diabetes (T2D).
DESIGN: T2D was induced in C57BL/6 mice via a hypercaloric diet combined with low-dose streptozotocin. OTM was achieved by applying orthodontic force to maxillary molars. The experimental groups received either an anti-LCN-2 antibody or an isotype-matched control antibody. Facial-expression changes were quantitatively evaluated using the histogram of oriented gradients (HOG) descriptor and compared with a tail-shock-derived nociceptive facial-expression reference. Periodontal tissue was evaluated by routine histology, and the brain was evaluated by immunofluorescence to assess neuroinflammation in the anterior cingulate cortex (ACC) for microglial activation (Iba-1), interleukin-1β (IL-1β) expression, and the NF-κB/β-catenin pathway.
RESULTS: Compared with control mice, T2D mice presented increased blood glucose levels, tooth displacement, and pain-related facial expression during OTM. In T2D mice undergoing OTM, LCN-2 inhibition reduced tooth displacement and pain-related facial expression. Histological analysis revealed decreased periodontal fibroblast and vascular density in the periodontium; decreased microglial activation (Iba-1) and IL-1β expression; decreased NF-κB/β-catenin signalling; and partially restored Nissl-stained neuronal cell count.
CONCLUSIONS: LCN-2 inhibition was associated with reduced exacerbated tooth movement, altered periodontal remodelling, pain-like facial expression, and neuroinflammation during OTM in T2D. LCN-2 inhibition was associated with changes in these responses and in NF-κB/β-catenin signalling. These findings support further investigation of LCN-2 in the context of OTM under diabetic conditions.
DESIGN: T2D was induced in C57BL/6 mice via a hypercaloric diet combined with low-dose streptozotocin. OTM was achieved by applying orthodontic force to maxillary molars. The experimental groups received either an anti-LCN-2 antibody or an isotype-matched control antibody. Facial-expression changes were quantitatively evaluated using the histogram of oriented gradients (HOG) descriptor and compared with a tail-shock-derived nociceptive facial-expression reference. Periodontal tissue was evaluated by routine histology, and the brain was evaluated by immunofluorescence to assess neuroinflammation in the anterior cingulate cortex (ACC) for microglial activation (Iba-1), interleukin-1β (IL-1β) expression, and the NF-κB/β-catenin pathway.
RESULTS: Compared with control mice, T2D mice presented increased blood glucose levels, tooth displacement, and pain-related facial expression during OTM. In T2D mice undergoing OTM, LCN-2 inhibition reduced tooth displacement and pain-related facial expression. Histological analysis revealed decreased periodontal fibroblast and vascular density in the periodontium; decreased microglial activation (Iba-1) and IL-1β expression; decreased NF-κB/β-catenin signalling; and partially restored Nissl-stained neuronal cell count.
CONCLUSIONS: LCN-2 inhibition was associated with reduced exacerbated tooth movement, altered periodontal remodelling, pain-like facial expression, and neuroinflammation during OTM in T2D. LCN-2 inhibition was associated with changes in these responses and in NF-κB/β-catenin signalling. These findings support further investigation of LCN-2 in the context of OTM under diabetic conditions.