BAX and periodontitis: In vitro:EVs reduced apoptosis in periodontal ligament cells from periodontitis-affected teeth (p-PDLCs)Downregulated pro-apoptotic markers [Caspase-3, BAX], upregulated anti-apoptotic BCL-2Decreased RANKL/OPG ratio and inhibited phosphorylation of JNK and P38In vivo:Reduced alveolar bone loss and osteoclast activityPromoted M2 polarisation [increased CD206, decreased iNOS]Lowered inflammation and bone resorption markersSuggests these EVs modulate inflammation, apoptosis, and osteoclastogenesis via the JNK/P38 MAPK pathway and macrophage polarisation