Hydroxyapatite deposition disease beyond the shoulder: A case series on unusual musculoskeletal locations

Case 1

A 44-year-old woman presented with acute right thigh pain for 5 days without trauma or fever. Magnetic resonance imaging (MRI) hip and thigh [Figure 1] revealed small amorphous calcifications along the posterior aspect of the proximal femoral diametaphysis, at the attachment of the vastus lateralis muscle onto the linea aspera. Adjacent soft-tissue and fascial edema were evident, with no periosteal reaction or bone marrow involvement. Findings were consistent with acute calcific tendinitis (HADD) of the linea aspera. The patient was managed conservatively with non-steroidal anti-inflammatory drugs (NSAIDs) and rest, showing symptomatic improvement.

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Figure 1:

(a) Axial GRE image of the right thigh showing tiny hypointense foci (calcific deposits) along the posterior aspect of the proximal femur at the attachment of the vastus lateralis (green arrow). (b and c) Axial STIR and Coronal T2 weighted images showing localized peritendinous inflammation along linea aspera with surrounding soft tissue and fascial edema (green arrow). (d) Axial computed tomography confirming amorphous calcific foci at the muscle insertion (green arrow).

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Case 2

A 28-year-old woman presented with acute neck pain and right upper limb paresthesia for 5 days. MRI cervical spine [Figure 2] demonstrated a small amorphous calcific focus (7 × 6 mm) involving the central fibers of the right longus colli muscle at the C5–C6 level, with associated soft-tissue edema and thin prevertebral fluid extending from C1 to C5. Computed tomography (CT) correlation confirmed calcification without evidence of infection or abscess. These findings supported acute calcific tendinitis of the longus colli muscle (HADD). The patient responded well to NSAIDs and physiotherapy within 10 days.

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Figure 2:

(a) Axial STIR image showing prevertebral soft-tissue edema at the C5–C6 level with focal hyperintensity in the right longus colli, (green arrow). (b) post-contrast T1-weighted image demonstrating thin linear prevertebral enhancement extending from C1 to C5, (green arrow). (c and d) axial computed tomography (CT) and sagittal radiograph images showing a small amorphous calcific focus within the right longus colli muscle at C5-6 level, (green arrow) and (e) sagittal CT image confirming central calcification with surrounding soft-tissue swelling (green arrow).

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Case 3

An 81-year-old male presented with pain and swelling over the left 1^st metatarsophalangeal (MTP) joint for one week. Serum uric acid was normal. MRI foot [Figure 3] revealed a small amorphous calcific focus in the periarticular region of the 1^st MTP joint involving the medial capsuloligamentous structure, with mild marrow edema and subtle cortical erosion. Dual-energy CT (DECT) excluded uric acid deposition. Imaging features were consistent with acute calcific periarthritis (HADD). The patient improved with conservative management and short-term NSAIDs.

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Figure 3:

(a) Axial short tau inversion recovery (STIR) image showing hyperintensity around the first metatarsophalangeal joint with surrounding soft-tissue edema, (green arrow). (b) Axial post-contrast T1-weighted image showing enhancement of periarticular soft tissues along the medial capsule (green arrow). (c) Axial computed tomography (CT) showing amorphous calcific focus in the periarticular region of the first MTP joint (green arrow). (d) Dual-energy CT showing absence of uric acid deposition (urate-negative signal) (green arrow).

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Background

HADD encompasses a group of conditions involving hydroxyapatite crystal deposition in soft tissues, tendons, and periarticular structures. Commonly affecting the rotator cuff, HADD may occur at atypical sites such as the hip, neck, or extremities, leading to diagnostic confusion. The pathogenesis likely involves microtrauma, ischemia, and tendon necrosis, leading to calcium crystal deposition. The disease progresses through pre-calcific, calcific, and post-calcific stages, with symptoms typically most severe during the resorptive phase.^[1,2]

Clinical and imaging perspective

When occurring in atypical locations, HADD can mimic infection, trauma, or neoplasm, especially in the acute inflammatory phase. Plain radiography and CT remain first-line modalities, showing amorphous or cloud-like calcifications near tendons or capsule insertions. MRI may reveal low-signal foci (calcific deposits) with surrounding soft-tissue edema and enhancement. The “arc and ring” sign or gradient echo (GRE) blooming supports the diagnosis. DECT is valuable in differentiating HADD from gout by demonstrating the absence of urate deposition. The correlation of imaging findings with absence of systemic inflammatory markers and clinical improvement under conservative therapy confirms the diagnosis.^[3-5]

Ultrasonography is also a valuable tool for evaluating HADD. In most cases, calcifications appear as hyperechoic foci with or without acoustic shadowing. During the symptomatic resorptive phase, Color Doppler imaging often reveals increased vascularity. Unlike degenerative calcifications in non-viable tendons, HADD-related calcifications are typically vascular.^[3-5]

Outcome and management

Acute HADD is self-limiting, resolving within 2–3 weeks. Conservative measures – NSAIDs, rest, and physiotherapy – are first-line. Ultrasound-guided barbotage or aspiration may be considered for persistent cases, while surgery is reserved for refractory ones.^[6]

MCQs

1. In differentiating HADD from HO on CT, which finding favors HADD?

   1. Presence of peripheral cortical bone formation

   2. Amorphous, cloud-like calcification without cortication

   3. Mature trabecular bone within soft tissue

   4. Central lucent zone with surrounding ossification

   Answer Key: b

2. On ultrasonography, which feature differentiates HADD from degenerative (non-HADD) calcification?

   1. Presence of hyperechoic foci

   2. Absence of posterior acoustic shadowing

   3. Associated vascularity on color Doppler

   4. Location near tendon insertion

   Answer Key: c

3. HADD at atypical sites, such as the hip or neck, may commonly be misdiagnosed as:

   1. Fibromyalgia

   2. Infective or neoplastic lesion

   3. Stress fracture

   4. Rheumatoid arthritis

   Answer Key: b