Disorders of periarticular regions, including painful shoulder syndrome, greater trochanteric pain syndrome, plantar fasciitis, and lateral epicondylitis, represent a heterogeneous group of conditions involving the entheses, tendons, and adjacent soft tissues. While enthesopathies are characterized by pathology at the enthesis, the site where tendons, ligaments, or joint capsules insert into bone, many clinical syndromes also encompass tendinopathies, which involve degenerative or inflammatory changes within the tendon substance, as well as bursitis, defined by inflammation of the bursa adjacent to tendons and entheses.1 These disorders frequently coexist and share overlapping mechanisms, such as repetitive mechanical stress, microtrauma, and variable inflammatory and degenerative responses. For example, in the shoulder, rotator cuff tendinopathy, subacromial bursitis, and enthesopathy often present together, reflecting the integrated function of the “enthesis organ,” which includes the enthesis, adjacent bursa, fat pads, and supporting connective tissues.2 As a result, clinical symptoms and imaging findings may not be isolated to a single structure but instead reflect a spectrum of periarticular soft tissue pathology.3

Enthesopathies, tendinopathies, and bursitis are commonly triggered by repetitive mechanical stress or acute microtrauma, leading to localized pain, impaired function, and tissue degeneration. The response to injury varies: some cases show marked infiltration of immune cells and increased pro-inflammatory cytokines such as IL-1β and TNF-α, while others demonstrate degenerative changes—such as collagen disorganization, fibrosis, or calcification—without significant inflammation.1,4,5,6 Tendinopathies are characterized by tendon degeneration, disorganized collagen, and neovascularization, with inflammation being variable and chronic cases often more degenerative than inflammatory; they frequently coexist with adjacent bursitis or enthesopathy. Bursitis involves inflammation of the bursa, typically resulting from mechanical irritation or overuse, and can be primary or secondary to adjacent tendon or enthesis pathology, with inflammatory cell infiltration and increased fluid within the bursa as typical findings.

The enthesis, adjacent bursa, fat pads, and supporting connective tissues function together as a unit, and stress or injury to one component often affects the others, leading to overlapping clinical syndromes. This integrated model explains why patients frequently present with combined features of enthesopathy, tendinopathy, and bursitis. In clinical practice, symptoms and imaging findings often reflect pathology in multiple structures, making isolated diagnoses rare and a spectrum approach more clinically relevant. Interventions such as low-dose radiotherapy (LDRT) or physical therapy may target shared pathways—such as inflammation, pain, and tissue remodeling—rather than addressing enthesopathy alone.7 Recognizing the interplay among these tissues is essential for comprehensive management and for enhancing quality assurance of the use of LDRT in treating these benign conditions.8 By understanding the overlapping pathophysiology of enthesopathies, tendinopathies, and bursitis, clinicians can better diagnose and treat these common, often coexisting, periarticular disorders.