Therapeutic strategy | Agents | Effects | References |
Restoring abnormal subchondral bone remodelling | Bisphosphonate, osteoprotegerin, cathepsin K inhibitor, strontium ranelate | Relieve pain, improve joint structure, and reduce bone and cartilage degradation markers | 96–101 |
Calcitonin | Prevent bone pathology development and promote chondrocyte anabolism | 102 103 | |
TGF-β1 inhibitor | Reform subchondral bone remodelling and inhibit subchondral angiogenesis | 60 | |
Blocking the bridge—subchondral type H vessels | Bevacizumab | Attenuate subchondral angiogenesis | 50 |
Halofuginone | Restore coupled bone remodelling and alleviate type H vessel formation by inhibiting TGF-β1 signalling | 105 | |
Ameliorating OA-related pain by modulating the subchondral bone microenvironment | Tanezumab | Reduce pain and improve joint function by binding NGF specifically | 111 112 |
SB366791, APETx2 | Improve acidic subchondral bone microenvironment and acid-induced pain by inhibiting TRPV1 and ASIC3, respectively | 110 115 | |
COX2 inhibitor, Nav1.8 inhibitor, EP4 receptor inhibitor | Blunt nociceptive signals in subchondral sensory neurons | 11 113 114 |