Osteoporosis is a common disease characterized by bone mass reduction, leading to an increased risk of bone fracture, and it is caused by an imbalance of osteoblastic bone formation and osteoclastic bone resorption. Current osteoporosis drugs aim to reduce the risk of bone fracture, either by increasing osteoblastic bone formation or decreasing osteoclastic bone resorption. However, osteoblasts and osteoclasts are closely coupled, such that any reagent altering the differentiation or activity of one eventually affects the other. This tight coupling between osteoblasts and osteoclasts not only limits the therapeutic efficacy but also threatens the safety of osteoporosis drugs. This review will discuss the biological mechanisms of action of currently approved medications for osteoporosis treatment, focusing on the osteoblast–osteoclast coupling.

Introduction
 Anti-resorptive Drugs
  1. Bisphosphonates
  2. Receptor activator of nuclear factor kappa-B ligand antibody (Denosumab)
  3. Hormone replacement therapy: estrogen therapy
  4. Selective estrogen receptor modulators Anabolic Drugs
  1. Parathyroid hormone receptor agonists
 Conclusions
 References

• Sung-Jin Kim(Department of Oral Biology, Yonsei University College of Dentistry) Correspondence to
• Seok Jun Moon(Department of Oral Biology, Yonsei University College of Dentistry)
• Jeong Taeg Seo(Department of Oral Biology, Yonsei University College of Dentistry)