Nonsteroidal Anti-Inflammatory Drugs Effects on Tendinosis and Tendon Healing

Abstract

Tendon injuries at the bone-tendon junction are frequently encountered in both general and orthopedic clinical practice. These injuries are disabling and typically painful, often requiring the use of some type of analgesic in their management. More successful results can be achieved in many of these injuries with surgical management, necessitating some form of postoperative analgesia. Commonly prescribed analgesics for these types of injuries include acetaminophen, nonselective, nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase-2 (COX-2), selective NSAIDs, and opiates. However, despite the benefits of these drugs in terms of pain management, their side-effects must also be kept in mind. The effect mechanism of NSAIDs involves inhibition of cyclooxygenase (COX) enzymes in the arachidonic acid (ArA) pathway to reduce the synthesis of prostaglandins. The ArA pathway and prostaglandins regulate and are potent inducers of inflammation. NSAIDs are therefore commonly used to control pain and swelling associated with skeletal injuries and chronic skeletal diseases such as osteoarthritis. However, prostaglandins and other lipid mediators produced in the ArA pathway regulate numerous physiological processes in addition to inflammation, such as blood clotting, vascular tone, stomach lining maintenance, kidney functions, ocular pressure, and smooth muscle contraction associated with airway dilation and parturition. Among their many uses, COX inhibitors are widely employed for musculoskeletal system indications, including post-surgical orthopedic analgesia. It has been hypothesized that these drugs may modulate bone, ligament, or tendon healing by inhibiting prostaglandin production. This chapter discusses the effect of NSAIDs on tendon healing in light of the current literature. © 2021 by Nova Science Publishers, Inc. All rights reserved.