Thein vivomodel was performed by LPS to induce inflammation model,48osteoporosis,49, 50osteonecrosis,51, 52and arthritis.53, 54, 55, 56In the bone inflammation and osteoporosis model, GSE maintained the bone structure,49by increasing the trabecular thickness48, 50and bone mineral content.50The exact mechanism decreased the number of osteoclasts.48The proanthocyanidins are responsible for this mechanism because this active substance is able to inhibit the osteoclast through inhibition of activation of NF-kB and JNK signaling pathways.29 Here, NFKB1 is linked to arthritic joint disease.