T he condition first known as ''tennis elbow'' has been recognized for over a century. Typical signs and symptoms include pain and tenderness over the lateral epicondyle, exacerbated by resisted wrist extension and passive wrist flexion, and impaired grip strength. Although many tennis players may experience this condition, most cases are associated with work-related activities or have no obvious precipitating event. As a result, the term now most widely used is lateral epicondylitis. Yet, this name implies a pathological basis that is contrary to longstanding, albeit evolving, evidence that it is not an inflammatory condition. It is therefore recommended that it is time to adopt a new and more appropriate term, such as epicondylalgia (suffix algia means pain), that does not reflect such underlying pathology. This Journal has recently embraced this terminology. A review of the current histopathological evidence as detailed below provides a strong rationale for this change in nomenclature.The traditional view is that this condition is initiated by macroscopic or microscopic tears at the common tendon of the wrist extensor muscles due to chronic overuse. As these tears attempt to unite, the healing surfaces are pulled apart with continued use of the hand, resulting in self-perpetuating and chronic inflammation. This theory was initially put forward by Dr J. Cyriax in 1936 5 and has since been widely accepted as the most plausible pathophysiological mechanism. Consequently, treatment has focused on controlling the inflammatory response through the use of nonsteroidal anti-inflammatory drugs and physical modalities such as ultrasound and ice. This inflammatory model also led to the use of the term epicondylitis, which was considered an improvement over the colloquial term tennis elbow.Yet this theory has never been substantiated and indeed has been refuted as early as the 1970s by Dr R. Nirschl, based on the histopathological examination of over 600 cases of chronic lateral epicondylalgia. 13,17 His studies consistently demonstrated that the affected tendon (usually the extensor carpi radialis brevis [ECRB] tendon) was characterized by a dense population of fibroblasts, disorganized and immature collagen, and an absence of inflammatory cells. These findings are considered characteristic of a degenerative process, which he called ''angiofibroblastic hyperplasia,'' now commonly known as tendinosis. Further histopathological and magnetic resonance imaging studies have revealed similar histological features and have confirmed the absence of an inflammatory process. 4,[19][20][21] Recently, a study using an in vivo microdialysis technique demonstrated normal levels of E2 prostaglandin, a biochemical marker of inflammation, in ECRB tendons of patients with chronic lateral epicondylar pain.1 Histopathological examination of similar chronic tendon conditions (Achilles, rotator cuff, and patellar tendinopathies) provide further support for the tendinosisdegenerative noninflammatory paradigm for chronic overuse tendon injurie...