A 72-year-old female patient presented with a 6-month history of left knee pain, not relieved by anti-inflammatories. Physical examination revealed a moderate sized joint effusion with medial joint line pain. On follow-up three weeks later, the patient was completely unable to flex or extend the left knee.
Fig. 1: Plain radiograph findings: Irregular density demonstrated in the left intercondylar notch.
Fig. 2: MRI - Sagittal proton density (A), axial T2 with fat saturation and (B) and coronal T2 with fat saturation (C) images.
Fig. 2a: Sagittal Proton Density weighted image: demonstrates a low signal intensity mass anterior to and contiguous with the most anterior fibres of the ACL.
Fig. 2b: axial T2 FSE with fat saturation and Fig. 2c: coronal T2 FSE with fat saturation. These images demonstrate the low signal mass in the intercondylar notch anterior to and contiguous with the most anterior fibres of the ACL. There is also a very small knee joint effusion present.
Fig. 3: Arthroscopic debridement of the hypervascular mass.
Calcium hydroxyapatite deposition disease (HADD), gout and calcium pyrophosphate dihydrate deposition disease (CPPD) are the three most common of all the crystal-induced arthropathies [1].
Clinical perspective: HADD is typically associated with periarticular deposits of hydroxyapatite in tendons and soft tissues resulting in tendinosis, tendinitis and bursitis. It most commonly affects the shoulder joint with calcification in the supraspinatus tendon [2]. HADD has also been demonstrated in the soft tissues surrounding the elbow, hip, hands and feet [2, 3, 4]. Bursitis and calcific tendinosis related to the knee have been described in relation to the fibular head, prepatellar region and femoral condyles [2, 5, 6, 7, 8]. In comparison to periarticular HADD, the intraarticular form is less common.
Imaging perspective: Intra-articular HADD results in subchondral bone destruction, joint space narrowing, intra-articular debris and the development of subchondral sclerosis [3, 9]. Calcification and arthropathy are the two classical features of intra-articular HADD [2].
On plain radiographs calcium hydroxyapatite deposits may initially be thin and poorly defined but can become denser and more homogeneous over time [2].
MRI demonstrates the inflammatory response associated with HADD with T2 signal hyperintensity in regions of inflammation, low signal within calcified segments and marked enhancement post gadolinium [2].
It is important to interpret the MRI findings in conjunction with the plain radiographic findings to ensure that calcification in the adjacent tendon, which is more readily appreciated on the radiograph, is identified [9].
Outcome: Following MRI, a decision was made to perform arthroscopy. A very large highly vascular synovial reaction was demonstrated in the intercondylar notch (Fig. 3). Further probing of the mass demonstrated white gelatinous material within it consistent with calcium deposition (Fig. 4). Complete resection was then performed using the arthroscopic shaver.
Fig. 4: Pathology findings: inflammatory cells and amorphous calcium hydroxyapatite. The patient’s symptoms resolved post-operatively.
Take home message: Calcium hydroxyapatite deposition disease (HADD), gout and calcium pyrophosphate dihydrate deposition disease are the three most common of all the crystal-induced arthropathies [1].
HADD can be differentiated from CPPD by the absence of pathognomonic cartilagionous calcifications seen in CPPD but the two conditions can co-exist [1, 2, 3].
The differential diagnosis includes but is not limited to idiopathic tumoural calcinosis, milk-alkali syndome, hypervitaminosis D, hypoparathyroidism, CPPD, sarcoidosis, synovial chondromatosis, synovial sarcoma, collagen vascular disease, and gout [2].
Before a diagnosis of idiopathic HADD is made, secondary causes of hydroxyapatite deposition including collagen vascular diseases, end stage kidney failure, tumoural calcinosis and vitamin D intoxication should be excluded [6].
Calcium hydroxyapatite deposition disease (HADD) – intra-articular
1. Plain Film (X-ray): The left knee joint space appears narrowed, with local bony sclerosis (sclerotic margins) and irregular dense shadows suggesting possible calcium salt deposits. Mild thickening of the surrounding soft tissues is noted, and slight bony destruction or localized defect is observed at the inferior border of the joint surface.
2. Magnetic Resonance Imaging (MRI): On T2-weighted images, certain areas within and around the joint exhibit hyperintense signals, indicating inflammatory exudation or synovial thickening. Regions of calcification appear as hypointense or mixed signals on corresponding sequences. After contrast enhancement, there is marked synovial enhancement within the joint, indicating local inflammation and proliferation.
3. Arthroscopic Findings: Under arthroscopy, the intercondylar notch area shows proliferative synovial tissue with pronounced vascularity. A white gel-like substance, consistent with the deposition of calcium salts (mainly hydroxyapatite), is noted during probing.
4. Pathological Examination: Reveals inflammatory cell infiltration in the tissue and amorphous calcium salt deposits (hydroxyapatite), corroborating the calcifications observed in the imaging and arthroscopic findings.
Based on the patient’s knee pain, radiological evidence of calcification and inflammation, as well as arthroscopic/pathological findings, the following differential diagnoses are considered:
Considering the patient’s advanced age, history of knee pain, radiological findings, and confirmation by arthroscopy/pathology, the most likely diagnosis is Hydroxyapatite Deposition Disease (HADD).
This diagnosis is supported by intra-articular white gel-like material identified as hydroxyapatite crystals on pathological examination, and by ruling out classic CPPD cartilage calcification as well as gout-related urate crystals.
1. Treatment Strategy:
2. Rehabilitation/Exercise Prescription: Follow a gradual approach (FITT-VP principle), tailored to postoperative status:
3. Safety and Individualized Precautions:
Disclaimer: This report is for reference only and does not replace in-person consultation or the advice of a professional physician. If you have any questions or if your condition changes, please consult a specialist or visit a hospital promptly.
Calcium hydroxyapatite deposition disease (HADD) – intra-articular
