Periodontitis is a prevalent chronic inflammatory disease characterized by alveolar bone resorption mediated by osteoclasts. Pyruvate kinase M2 (PKM2), a key enzyme in glycolysis and pyruvate metabolism, has recently been recognized for its regulatory roles beyond metabolism, including gene expression and protein kinase activity. However, its exact role in osteoclastogenesis remains unclear. This study investigates the function of PKM2 in inflammatory osteoclastogenesis and explores its potential as a therapeutic target for periodontitis.

The chemokine receptor CCR9 coordinates immune cell migration from the thymus to the small intestine along gradients of the chemokine CCL25. Receptor dysregulation is associated with a variety of inflammatory bowel diseases such as Crohn’s and ulcerative colitis, while aberrant CCR9 overexpression correlates with tumor metastasis. Despite being an attractive therapeutic target, attempts to clinically antagonize CCR9 have been unsuccessful. This highlights the need for a deeper understanding of its specific regulatory mechanisms and signaling pathways.