Fig. 2

MEVs from inflammatory macrophages transfer mitochondria to BMSCs, exacerbating alveolar bone loss in periodontitis. A Schematic diagram showing the experimental design. The untreated mice served as baseline controls. Periodontitis was induced by ligation combined with P.g coating for 28 days, and PBS, Con-MEVs, or P.g-MEVs were simultaneously injected via the tail vein. B–H Bone resorption was assayed and quantified by the distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC) via Micro-CT (vertical orange lines) (B, C), hematoxylin and eosin (H&E) staining (vertical yellow lines) (E, F), and Masson’s trichrome staining of the maxilla (vertical yellow lines) (G, H). The bone volume fraction was analyzed via Micro-CT (D). I, J To detect mitochondrial transfer in vivo, Con-MEVs and P.g-MEVs were labeled with MitoTracker (red) and then injected into mice, with PBS used as a control. I The average percentage of fluorescence distributed in the heart, liver, spleen, lungs, and kidneys was detected via IVIS Spectrum at 4 and 24 h postinjection. J Cryosections of the maxilla were subjected to immunofluorescence (IF) staining for SCA1 (green) and DAPI (blue), and images were obtained via confocal microscopy. Values were mean ± SD, n = 4 or 6. *P ≤ 0.05, ***P ≤ 0.001, ****P ≤ 0.0001