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Background
Hydroxyapatite deposition disease (HADD) refers to the deposition of calcium hydroxyapatite crystals within tendons and periarticular tissues. While these findings may be incidental, some patients experience acute, debilitating joint pain. HADD most commonly affects the rotator cuff muscles and presents as calcific tendinitis, though may affect virtually any joint in the body. Given its ability to involve many structures, HADD is an important differential consideration in acute joint pain and, most importantly, must be differentiated from septic arthritis and malignancy. The purposes of this exhibit are to detail the wide spectrum of multimodality imaging findings in HADD, differentiate it from other disease states, and discuss how to treat it.

Educational Goals / Teaching Points
Readers will learn about the natural progression of HADD and how it commonly presents in patients. After reviewing key multimodality imaging features of HADD, readers will review selected HADD cases, which will include common and uncommon sites of disease, as well as classic and advanced disease manifestations. After the reader has reviewed several cases, we will discuss common disease mimickers and important differential considerations, offering diagnostic clues to assist in excluding other entities. Finally, we will discuss treatment options, particularly the use of ultrasound-guided barbotage, and review additional ultrasound cases to illustrate its utility as a therapeutic intervention.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Radiographs will show calcification in the region correlating to patients’ symptoms. Depending on the phase of HADD, calcifications may appear homogenous and well-defined, or amorphous and ill-defined. CT effectively localizes calcification to specific tendons and delineates the extent of any bony involvement. MRI can also depict osseous involvement, though excels at evaluating the extent of soft tissue involvement of the tendon, muscle, joint space, and bursae. Ultrasound, primarily reserved for therapeutic intervention, will show echogenic calcification with varying degrees of posterior acoustic shadowing. Associated tendon thickening can also be appreciated, as well as occasional increased color Doppler flow due to acute inflammation.

Conclusion
HADD can affect virtually any tendon in the body. Given its ubiquitous involvement, it is important to keep this diagnosis in the differential for acute onset joint pain, which often includes other important differentials such as septic arthritis and malignancy. As illustrated throughout the exhibit, HADD can affect multiple sites aside from tendons, including joint spaces, bursae, bone, and muscle. Despite the heterogeneity of disease extent, hallmark findings consistently include calcific deposits on radiographs, which correlate to T1/T2 hypointense crystal deposition on MRI in the region of patients’ symptoms. For severe symptoms, ultrasound-guided barbotage is a minimally invasive, effective option to accelerate the healing process, circumventing the need for more painful and invasive therapy, including surgery.