Pellegrini-Stieda Disease

Etiology

The pathogenesis of Pellegrini-Stieda lesions is generally attributed to injury of the MCL, initiating acute inflammation followed by delayed dystrophic ossification at or near the ligament’s femoral origin. The inciting trauma is classically described as a macrotraumatic event, either direct or indirect, producing valgus stress and mechanical disruption of superficial or deep MCL fibers. This mechanism aligns with Köhler’s 1903 observations linking the characteristic ossification to athletic injuries involving valgus loading of the knee.

Although macrotrauma remains the predominant mechanism, microrepetitive damage may also contribute to Pellegrini-Stieda disease. Reports in the physiatric literature describe forceful manipulation of a stiff knee during postsurgical rehabilitation or therapeutic interventions provoking ossific changes in the MCL, particularly in patients presenting with new-onset medial knee pain, edema, or ROM limitation during recovery.[5][6] In such cases, the pathophysiology may reflect cumulative low-grade traction injury rather than a single traumatic insult.

Pellegrini-Stieda-like ossifications have also been documented in patients without direct knee trauma but with central neurological conditions, such as spinal cord or traumatic brain injury.[7] In these populations, periarticular calcifications require cautious interpretation, as the radiographic appearance may be confounded by heterotopic ossification or myositis ossificans, both of which occur more frequently in neurologically compromised individuals. Differentiation from true Pellegrini-Stieda lesions often requires clinical history, temporal evolution, and advanced imaging.

Epidemiology

Although the precise incidence of Pellegrini-Stieda lesions remains undefined, a 7-year retrospective review of a clinical radiology database from the University of Colorado and the University of Alabama at Birmingham identified 332 knee radiograph reports containing the term “Pellegrini-Stieda,” suggesting the lesion is not uncommon in clinical practice.[8] Epidemiologic data indicate a male predominance, most often affecting adults aged 25 to 40. This distribution may reflect the higher risk of ligamentous injury in physically active men during peak musculoskeletal activity years.[9]

Pathophysiology

Whether triggered by a single macrotraumatic event or repetitive microtrauma, the initiating insult in Pellegrini-Stieda lesions leads to calcific ossification of soft tissue structures adjacent to the medial femoral condyle. In patients with spinal cord or traumatic brain injury, heterotopic ossification in this region may arise through neurogenic mechanisms involving a complex interplay of humoral, neural, and local factors. Proposed contributors include tissue hypoxia, altered calcium metabolism (such as hypercalcemia), dysregulated sympathetic activity, prolonged immobilization, and subsequent mechanical mobilization.[10]

Traditionally, Pellegrini-Stieda lesions have been attributed to ossification within the proximal portion of the MCL at its femoral origin. However, this stereotypical localization has been increasingly questioned.[11] Studies incorporating magnetic resonance imaging (MRI) and cadaveric dissection have revealed more heterogeneous distribution patterns, often with ossific foci located inferior to the classical site of the MCL origin.[12] Mendes et al proposed a 4-type imaging-based classification according to the anatomical distribution of the ossified lesion, as follows:

• Type 1: Beak-like ossification arising from the medial femoral condyle and extending inferiorly into the MCL
• Type 2: Teardrop-shaped ossification confined within the MCL with no attachment to the femur
• Type 3: Elongated ossification located superior to the femoral condyle within the distal adductor magnus tendon
• Type 4: Beak-like ossification resembling type 1, but extending into both the MCL and the adductor magnus tendon

This classification reflects a growing consensus that ossification in Pellegrini-Stieda lesions is not necessarily confined to the MCL. Increasing evidence demonstrates frequent involvement of adjacent structures, including the adductor magnus tendon, medial head of the gastrocnemius, and medial patellofemoral ligament, suggesting that exclusive attribution to the MCL is anatomically oversimplified.

Although many Pellegrini-Stieda lesions are asymptomatic and discovered incidentally on imaging, some patients develop localized medial knee pain, often with ROM restriction and joint effusion. When these symptoms accompany radiographic evidence of ossification, the condition is termed "Pellegrini-Stieda syndrome."

History and Physical

A representative clinical scenario of Pellegrini-Stieda disease involves a young man in his late 20s to early 30s presenting with right medial knee pain and ROM limitation. He reports a direct knee-to-knee collision to the medial aspect of the right knee, sustained a few weeks (usually 3) earlier during a recreational soccer match. The initial trauma caused acute pain that improved with rest and cryotherapy, but he now notes localized medial knee discomfort, stiffness, and reduced joint mobility. This delayed symptom onset after a valgus injury is characteristic of Pellegrini-Stieda disease, corresponding to the expected timeline of posttraumatic MCL ossification.

Evaluation

The diagnosis of Pellegrini-Stieda lesions is primarily radiographic, typically confirmed by the characteristic Pellegrini-Stieda sign on anteroposterior or oblique knee radiographs in conjunction with medial knee pain or ROM restriction. Radiographically, this sign appears as a linear or curvilinear calcification within the soft tissues medial to the femoral condyle, reflecting ossification at the MCL origin (see Image. Medial Collateral Ligament Calcification). Calcific ossification generally does not appear until about 3 weeks after the initial injury, consistent with the timeline of dystrophic mineralization.[13]

Differentiation from a medial femoral condyle avulsion fracture is important, as the latter results from traction injury with a bony fragment avulsed from its site of ligamentous or tendinous attachment. Although both entities may share overlapping locations and symptoms, their management and prognostic implications differ significantly.

MRI is a valuable adjunct in ambiguous or early cases. The images may demonstrate bone marrow edema at the medial femoral condyle with ossified or enthesopathic changes of the MCL, which often appear thickened and hypointense on T1-weighted sequences due to calcific infiltration. MRI also helps exclude intraarticular pathology or avulsion fractures.

Musculoskeletal ultrasonography has also gained attention as a noninvasive, dynamic modality for detecting Pellegrini-Stieda lesions. This modality provides real-time visualization of soft tissue calcifications and may demonstrate associated perilesional edema or hyperemia, supporting diagnosis in symptomatic individuals.

Treatment / Management

Conservative Management

The natural course of Pellegrini-Stieda lesions typically spans 5 to 6 months, during which the ossified lesion undergoes progressive maturation. Management is largely dictated by symptom severity and degree of functional impairment. In cases presenting with mild-to-moderate symptoms, initial treatment is conservative and focuses on symptom relief and functional restoration. The regimen includes activity modification to avoid exacerbating movements, physiotherapy aimed at maintaining and improving ROM and muscular strength, and administration of NSAIDs to alleviate pain and reduce inflammation.

Intraarticular corticosteroid injections may be considered as adjuncts to conservative therapy, particularly for patients with persistent pain and localized inflammation. Ultrasound-guided percutaneous calcific lavage, augmented by autologous platelet-rich plasma injection, has shown promise in cases refractory to standard conservative modalities.[14] This minimally invasive technique has been reported in isolated case literature to provide both clinical and radiographic improvement, though further studies are needed to establish broader efficacy.[15](B3)

Surgical Management

Patients with severe or function-limiting symptoms unresponsive to conservative measures may require surgical intervention. Operative treatment typically involves excision of the ossified or calcified lesion, with or without concurrent MCL repair or reconstruction, depending on the size and anatomical integration of the lesion. Arthroscopic techniques have also been described in the literature, including minimally invasive debridement and adhesiolysis, offering potential benefits of reduced morbidity and faster postoperative recovery.[16](B3)

However, surgical outcomes remain variable. In their earlier investigation, Kulowski and Riebel reported inconsistent results with a notable recurrence rate, raising concerns about the long-term durability of surgical excision. In contrast, Pellegrini’s original series and a subsequent update by Kulowski reported more favorable outcomes. Importantly, excision of large ossified masses may compromise MCL integrity, often requiring reconstruction to restore medial stability.

A case report documented the resolution of a Pellegrini-Stieda lesion following unicompartmental knee arthroplasty. Notably, the lesion, present preoperatively, disappeared during the postoperative course. This regression was hypothesized to result from biomechanical correction achieved by the procedure, which restored normal joint loading in a previously varus-aligned osteoarthritic knee.[17](B3)

Another case report described a combined therapeutic approach using extracorporeal shock wave therapy and iontophoresis. This intervention was effective in reducing both pain and calcific deposition associated with Pellegrini-Stieda disease.[18](B3)

Differential Diagnosis

Several radiological and clinical entities can mimic Pellegrini-Stieda disease and should be considered to avoid misdiagnosis. Radiologically, differentials include MCL calcification, which is typically benign and associated with metabolic disorders without prior trauma, as well as calcification of the distal adductor magnus tendon, myositis ossificans, heterotopic ossification, and medial femoral condyle avulsion fracture. Clinically, conditions that may present with overlapping symptoms include MCL sprain, medial meniscal tear, medial patellofemoral injuries, knee osteoarthritis, and tendinitis involving the semimembranosus, semitendinosus, or gastrocnemius. Careful correlation of patient history, physical examination findings, and imaging characteristics enables the clinician to distinguish Pellegrini-Stieda disease from these mimicking conditions.

Prognosis

Most cases of Pellegrini-Stieda disease resolve within 5 to 6 months with conservative management, including NSAIDs, corticosteroid injections, and ROM exercises. However, severe refractory cases may require surgical intervention.

Complications

Untreated Pellegrini-Stieda disease may result in restricted knee joint ROM and contracture, leading to gait abnormalities, impaired activities of daily living, and chronic pain. Some studies have reported poor surgical outcomes, with high recurrence rates or ligamentous defects after large lesion excisions requiring further reconstruction.