Hydroxyapatite Deposition Disease

Notes

Overview

Hydroxyapatite Deposition Disease (HADD) is a crystal-induced tendinopathy caused by the deposition of hydroxyapatite (HA) crystals, typically in periarticular soft tissues, especially tendons and bursae. The shoulder (supraspinatus tendon) is most commonly affected. It often presents between ages 30–60, more frequently in women. While often asymptomatic, it can cause acute pain and functional limitation during resorptive phases.

Definition

Hydroxyapatite (HA): A calcium phosphate crystal naturally found in bone but pathologically deposited in soft tissues.
HADD: Disease resulting from abnormal deposition of HA crystals in tendons or bursae, leading to pain and inflammation.
Calcific tendinitis: Clinical term describing symptomatic HADD, often in the shoulder.
Periarticular: Refers to structures surrounding a joint (e.g. tendons, bursae).

Anatomy and Physiology

The rotator cuff (supraspinatus, infraspinatus, subscapularis, teres minor) stabilizes the glenohumeral joint.
The subacromial-subdeltoid bursa reduces friction between the rotator cuff and overlying structures.
Tendons are poorly vascularized, especially near insertion zones (enthesis), which may predispose to crystal deposition.

Aetiology and Risk Factors

Aetiology

Unknown in most cases (idiopathic)
Possibly due to cell necrosis, hypoxia, or local mechanical stress causing crystal precipitation
May be related to disordered healing of tendon microtears

Risk Factors

Age 30–60
Female sex
Diabetes mellitus
Hypothyroidism
Repetitive overuse or trauma (especially shoulder)
Chronic renal disease (rare)

Remember

HADD = middle-aged women + shoulder pain + calcification.

Pathophysiology

Pre-calcific stage: Fibrocartilaginous metaplasia occurs in tendon → prone to mineralization
Calcific stage:
- Formative phase: Deposition of HA crystals
- Resorptive phase: Inflammatory reaction with macrophage and giant cell infiltration → severe pain
Post-calcific stage: Remodeling and healing with tendon reconstitution

Think

Symptoms typically arise in the resorptive phase due to intense local inflammation.

Clinical Manifestations

Often asymptomatic during formative phase
Acute calcific tendinitis
- Sudden, severe shoulder pain, often nocturnal
- Limited active ROM, especially abduction and external rotation
- Pain on palpation over greater tuberosity
Chronic phase
- Dull ache
- Stiffness and impingement signs
Bursitis or tenosynovitis if crystals rupture into adjacent structures
- Less common sites: hip, elbow, wrist, knee

Think

Shoulder pain + calcification on X-ray + intact ROM = HADD.

Diagnosis

No formal criteria, diagnosis is clinical + radiologic

X-ray
- Homogeneous, dense calcific deposit in tendon (e.g. supraspinatus)
- Location: 1–2 cm from insertion
Ultrasound
- Hyperechoic calcification with posterior shadowing
- May show signs of bursitis or tendon rupture
MRI
- Shows soft tissue edema, inflammation, may mimic rotator cuff tear
Aspiration (rarely done)
- HA crystals are non-birefringent, not visualized on polarised microscopy
- Can stain with Alizarin red (calcium-binding dye)

Crystal Arthropathy Clinical Comparison Table

Feature	Gout	Pseudogout (CPPD)	BCP / Milwaukee Shoulder	HADD (Hydroxyapatite)
Typical Age	30–50 (M > F)	>60	>70 (F > M)	30–60 (F > M)
Crystal Type & Shape	Monosodium urate, needle	Calcium pyrophosphate, rhomboid	BCP (hydroxyapatite), amorphous	Hydroxyapatite, amorphous
Birefringence	Strongly negative	Weakly positive	None	None
Common Joint Involved	1st MTP, midfoot, ankle	Knee, wrist	Shoulder (glenohumeral joint)	Shoulder (supraspinatus tendon)
Synovial Fluid WBC	High (2,000–50,000+)	Moderate (2,000–50,000)	Low (<2,000), non-inflammatory	Normal to mildly elevated

Differential diagnoses

Rotator cuff tear
Subacromial bursitis
Adhesive capsulitis
Septic arthritis (if systemic signs present)
Gout/pseudogout (if intra-articular)

Remember

HADD calcific deposits are dense, homogeneous on X-ray and non-birefringent.

Remember

If unsure on ultrasound, confirm with X-ray – classic finding is curvilinear or oval dense calcification near tendon insertion.

Treatment

Acute phase

NSAIDs (first-line)
Rest and ice
Physiotherapy (after acute pain subsides)
Local corticosteroid injection if significant inflammation
Needle lavage/barbotage (ultrasound-guided): break up and aspirate calcification
Ultrasound therapy for pain control
Surgery (arthroscopic removal) if refractory after 6–12 months

Chronic phase

Ongoing physiotherapy and ROM exercises
Treat contributing factors (e.g. diabetes, thyroid dysfunction)

Complications and Prognosis

Complications

Rotator cuff tear
Adhesive capsulitis
Chronic pain or impingement syndrome
Bursal rupture or inflammation

Prognosis

Excellent prognosis in most with conservative management
Most resolve spontaneously within 1–3 weeks during resorptive phase

Poor Prognostic Factors

Large deposits
Chronic symptoms >6 months
Recurrent episodes
Poor compliance with rehab

References

Harvie P, Pollard TC, Carr AJ. Calcific tendinitis: natural history and association with endocrine disorders. J Shoulder Elbow Surg. 2007;16(2):169–173.
Uhthoff HK, Loehr JW. Calcific tendinopathy of the rotator cuff: pathogenesis, diagnosis, and management. J Am Acad Orthop Surg. 1997;5(4):183–191.
Chianca V, et al. Calcific tendinopathy: imaging findings and therapeutic options. Radiol Med. 2020;125(5):431–447.
Jiménez-Martín A, et al. Calcific tendinopathy of the shoulder: clinical and radiological analysis of 100 patients. Clin Rheumatol. 2022;41(3):821–828.
de Witte PB, et al. Therapeutic options for calcific tendinitis of the rotator cuff: a state-of-the-art review. Br J Sports Med. 2016;50(15):884–890.