POSTGRADUATE ORTHOPEDIC INSTRUCTION -
IMAGING
Case Resolution
Juan Pablo Ghisi,* Joaquín Escotorín**
*Magnetic Resonance Imaging Department, Hospital General de Agudos “Dr. Juan A.
Fernández”, Autonomous City of Buenos Aires,
Argentina
**Diagnostic Imaging Department, Sanatorio San
Lucas, San Isidro, Buenos Aires, Argentina
Case Presentation on page 79.
ABSTRACT
The disease is
described, along with its imaging findings as observed with each
diagnostic modality.
Keywords: Knee;
calcifications; pain.
Level of Evidence: IV
Enfermedad por depósito de cristales de hidroxiapatita
RESUMEN
Se desarrolla la
enfermedad y cómo se visualiza las imágenes, en cada caso, según el estudio.
Palabras clave: Rodilla; calcificaciones; dolor.
Nivel de Evidencia: IV
Hydroxyapatite crystal deposition disease.
Crystal
deposition diseases comprise a group of conditions in which the accumulation of
crystals within the joint space or periarticular tissues leads to acute or
chronic inflammatory manifestations. From a practical standpoint, they can be classified into three main categories: those due to
monosodium urate deposition (gout), those related to calcium pyrophosphate
deposition, and those secondary to basic calcium phosphate deposition.1-3
Hydroxyapatite
deposition disease belongs to the latter group. In the literature, it is referred to by various terms that partly reflect the
anatomical structure involved and partly the clinical presentation: hydroxyapatite
deposition disease, hydroxyapatite crystal deposition disease, basic calcium
phosphate deposition, calcific tendinitis, calcific periarthritis,
calcific bursitis, and, in intra-articular locations or more destructive forms,
hydroxyapatite arthropathy. Within this spectrum, the
so-called Milwaukee syndrome represents an advanced form of arthropathy
associated with basic calcium phosphate crystals, most commonly described in
the shoulder, although knee involvement has been reported
in some series.1-5
Unlike
calcium pyrophosphate deposition disease, which typically presents as chondrocalcinosis with linear or lamellar calcifications in
cartilage and fibrocartilage, and urate deposition, which tends to produce bone
erosions and tophi, hydroxyapatite deposition disease is characterized by
amorphous, periarticular calcifications most commonly located in tendons,
bursae, and the joint capsule, and less frequently in ligamentous structures.
This distinction is important in imaging assessment, as it helps guide the
differential diagnosis based on the pattern of distribution and the morphology
of the calcifications.1-4,6
From a
pathophysiological perspective, three phases are described:
precalcific, calcific, and postcalcific,
a classification originally established for calcific tendinitis of the shoulder
and applicable, by extension, to other periarticular locations. The calcific
phase, in turn, includes formative, resting, and resorptive
stages. The resorptive stage usually corresponds to
the period of greatest clinical expression, as the deposit may fragment or
liquefy and trigger a marked inflammatory response in the surrounding tissues.
This evolutionary behavior explains the variability of imaging findings and the
fact that the same lesion may appear as a well-defined calcification at one
time and as a poorly defined lesion with perilesional edema at another.1,3,6
Although
the shoulder is the most common site of involvement, the knee is also a
recognized location. In this joint, the quadriceps tendon, patellar tendon,
periarticular bursae, capsule, and ligamentous structures may be affected.
Involvement of the medial collateral ligament is uncommon but of particular
interest, as it may mimic enthesopathy,
post-traumatic sequelae, or avulsion injuries.1-4,6
On
radiographs, the condition typically appears as an amorphous, rounded, or oval
calcification with variable density. During resting phases, it tends to be more
homogeneous and well defined, whereas in symptomatic or resorptive
phases, it may appear faint, cloud-like, or poorly defined. Radiography
therefore remains the most useful initial modality for detecting calcifications
and guiding diagnostic suspicion.1,3,4,6
Computed
tomography allows more precise confirmation of the calcific
nature of the deposit, accurate assessment of its size and location, and
evaluation of possible cortical erosions or extension into adjacent tissues.
It is also particularly useful in the differential diagnosis with mature
ossification processes, such as Pellegrini-Stieda lesion,
in which imaging typically shows trabecular or cortical organization, unlike
the amorphous appearance characteristic of hydroxyapatite deposits.1,3,6
Ultrasound
demonstrates the deposits as hyperechoic foci, with or without posterior
acoustic shadowing, and allows real-time assessment of the inflammatory changes
in adjacent soft tissues. In more active phases,
Doppler imaging may show associated hyperemia. In addition, ultrasound has
therapeutic value, as it enables image-guided procedures such as aspiration or
lavage in selected cases.1,3,6
Magnetic
resonance imaging is not the most
sensitive modality for detecting calcifications but is highly useful for
assessing the inflammatory context. Deposits typically appear as foci of signal
void or hypointensity on all sequences, associated
with perilesional edema, bursitis, or reactive synovitis. MRI may pose
diagnostic challenges when interpreted in isolation, as the inflammatory
changes may predominate over visualization of the deposit and mimic traumatic,
infectious, or even neoplastic conditions. For this reason, correlation with
radiography, CT, or ultrasound is essential.1,3,6
In the
cases presented, the findings were located along the medial aspect of the knee,
anterior to the femoral insertion of the medial collateral ligament, with
calcific morphology and associated perilesional inflammatory
changes. The anatomical distribution, the appearance of the deposits, and the
adjacent soft-tissue reaction constitute a pattern consistent with
hydroxyapatite deposition in the medial capsuloligamentous
region. In one case, ultrasound confirmed the calcific nature of the finding,
whereas in the other, radiography demonstrated faint calcifications in the same
location, supporting this interpretation.6
In the
differential diagnosis of medial knee calcifications around the insertion area,
the following entities should be considered: enthesopathy, remote avulsion injury, post-traumatic
ossification (Pellegrini-Stieda lesion), medial
bursitis, and other crystal-induced arthropathies,
particularly calcium pyrophosphate deposition disease. Recognition of the
morphological pattern of the deposits and their multimodality correlation helps
avoid misinterpretation and guides appropriate diagnostic and therapeutic
management.1-3,6
From a
therapeutic standpoint, this is generally a self-limiting condition initially
managed conservatively with relative rest, physical therapy, and nonsteroidal
anti-inflammatory drugs. In cases of persistent symptoms, interventional
options may be considered, such as extracorporeal
shock wave therapy and image-guided percutaneous aspiration or lavage.
Arthroscopic or open surgery is reserved for severe or
refractory cases. In this context, imaging plays a role not only in diagnosis
but also in the planning and guidance of therapeutic procedures.1,3
These
two cases illustrate a rare and likely underdiagnosed cause of medial knee
pain: perinsertional calcific deposits of the medial capsuloligamentous complex, which, in their symptomatic phase,
may be associated with marked inflammatory changes and mimic trauma, infection,
or other arthropathies.
The
diagnostic approach should be based on multimodality
imaging correlation. Radiography is essential for identifying calcifications,
even when subtle. Computed tomography confirms the deposit, precisely defines
its location and extent, and helps differentiate calcification from
ossification. Ultrasound confirms its calcific nature, may provide information
about the stage of the process, and enables image-guided therapy. Finally,
magnetic resonance imaging delineates the extent of edema and reactive changes,
although it requires correlation with calcium-sensitive modalities to avoid
misinterpretation.
In the
medial knee, including this entity in the differential diagnosis when
evaluating enthesopathy or Pellegrini-Stieda lesion helps prevent overdiagnosis
of chronic ligament injury or post-traumatic sequelae and reduces unnecessary
additional studies or interventions.
REFERENCES
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Hayes CW, Conway WF. Calcium hydroxyapatite
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https://doi.org/10.1148/radiographics.10.6.2175444
2.
Garcia GM, McCord GC, Kumar R. Hydroxyapatite crystal deposition
disease. Semin Musculoskelet Radiol 2003;7(3):187-94. https://doi.org/10.1055/s-2003-43229
3.
Hegazi T. Hydroxyapatite deposition disease: a comprehensive
review of pathogenesis, radiological findings, and treatment strategies. Diagnostics (Basel) 2023;13:2678. https://doi.org/10.3390/diagnostics13162678
4.
Bonavita JA, Dalinka
MK, Schumacher HR Jr. Hydroxyapatite deposition disease. Radiology 1980;134:621-5. https://doi.org/10.1148/radiology.134.3.6243783
5.
Halverson PB, McCarty DJ, Cheung HS, Ryan LM. Milwaukee shoulder
syndrome: eleven additional cases with involvement of the knee in seven (basic
calcium phosphate crystal deposition disease). Semin Arthritis Rheum 1984;14(1):36-44. https://doi.org/10.1016/0049-0172(84)90007-6
6.
Hongsmatipa P, Cheng KY, Kim C,
Lawrence DA, Rivera R, Smitaman
E. Calcium hydroxyapatite deposition disease: imaging features and
presentations mimicking other pathologies. Eur J Radiol 2019;120:108653.
https://doi.org/10.1016/j.ejrad.2019.108653
J. Escotorín ORCID ID: https://orcid.org/0009-0006-4115-1034
Received on March 13th,
2026. Accepted after evaluation on March 19th, 2026 • Dr. JUAN PABLO GHISI • jpghisi@gmail.com • https://orcid.org/0000-0001-7991-9228
How to cite this article:
Ghisi JP, Escotorín J. Postgraduate
Orthopedic Instruction – Imaging. Case Resolution. Rev Asoc Argent Ortop
Traumatol 2026;91(2):184-186.
https://doi.org/10.15417/issn.1852-7434.2026.91.2.2324
Article Info
Identification: https://doi.org/10.15417/issn.1852-7434.2026.91.2.2324
Published: April, 2026
Conflict of interests:
The authors declare no conflicts of interest.
Copyright: © 2026, Revista de la Asociación Argentina de Ortopedia y Traumatología.