Anti-Inflammatory Drug Effects on Bone Healing

The repair of bone following injury is a finely tuned interplay between inflammation, cellular recruitment and matrix synthesis. Anti-inflammatory drugs, particularly non-steroidal anti-inflammatory agents and glucocorticoids, modulate key mediators of the early inflammatory response that mobilises osteoprogenitor cells. By inhibiting cyclooxygenase enzymes and thus reducing prostaglandin production, these drugs can attenuate pain and swelling but may also delay the transition from soft to hard callus, alter osteoblast and osteoclast activity and compromise the quality of the newly formed bone. Low-dose regimens of certain agents have been shown to support osteoblastic differentiation and suppress excessive osteoclast-driven resorption, whereas higher doses or prolonged administration frequently impair mechanical strength and callus microarchitecture. Understanding the dose- and timing-dependent effects of anti-inflammatory therapy is essential for optimising fracture management and ensuring robust bone regeneration without exacerbating systemic inflammation or impairing long-term bone health.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Anti-Inflammatory Drug Effects on Bone Healing publication trend

The graph below shows the total number of articles in anti-inflammatory drug effects on bone healing across all publications each year (not limited to Nature Index journals).

Technical terms

Non-steroidal anti-inflammatory drug (NSAID): A class of medications that reduce inflammation and pain by inhibiting cyclooxygenase enzymes.

Cyclooxygenase (COX): An enzyme family (COX-1 and COX-2) that catalyses prostaglandin synthesis during inflammation and healing.

Prostaglandin: Lipid mediators produced by COX that regulate inflammation, vasodilation and bone cell activity.

Osteoblast: A bone-forming cell responsible for synthesising new bone matrix and mineralisation.

Osteoclast: A bone-resorbing cell that breaks down mineralised tissue during remodelling.

Callus: The initial fibrocartilaginous or mineralised tissue that bridges a fracture site during early healing.

References

1. Dose-dependent roles of aspirin and other non-steroidal anti-inflammatory drugs in abnormal bone remodeling and skeletal regeneration. Cell & Bioscience (2019).
2. Effect of Non-Steroidal Anti-Inflammatory Drugs on Bone Healing. Pharmaceuticals (2010).
3. A biomechanical, micro-computertomographic and histological analysis of the influence of diclofenac and prednisolone on fracture healing in vivo. BMC Musculoskeletal Disorders (2016).