A woman in her 40s presented with left knee pain for 4 months that had been progressively getting worse. She had a history of idiopathic chronic thromboembolic disease on 3 L of oxygen, poor dental hygiene with brittle teeth, and Crohn disease, for which she had undergone colectomy with ileostomy.
The pain was located over her patella, and she said the pain felt like “someone shattered my knee cap.” She was unable to fully bear weight due to the pain. The pain worsened with any movement and improved with rest but not with ibuprofen and acetaminophen. She denied any history of trauma or injury. She had previously been on long-term prednisone for her Crohn disease. Her past medical history was also significant for bilateral humeral head and femoral head epiphyseal osteonecrosis, for which she underwent bilateral glenohumeral hemiarthroplasty several years earlier.
Physical examination was normal with no effusion or ecchymosis. She had pain with flexion and extension and tenderness to palpation of the knee over the patella, with no joint line tenderness.
Plain radiography showed multifocal, patchy serpiginous sclerotic areas in the distal femoral metadiaphysis and proximal tibial metadiaphysis (Figure 1). Based on the plain radiography, the diagnosis of bone infarct (osteonecrosis) was made. Nevertheless, based on the patient’s pain pattern and physical examination, it was not clear that the extra-articular bone infarct was the source of her pain. She was treated conservatively with physical therapy and oral pain medication (acetaminophen as needed was advised given her complex medical history).
![Plain radiography of the left knee (anteroposterior [left], lateral [middle], and sunrise [right] views) showed multifocal, patchy serpiginous sclerotic areas in the distal femoral metadiaphysis and proximal tibial metadiaphysis. Normal alignment was maintained. There was no fracture, dislocation, or effusion. Bone mineralization was normal, and there were no degenerative or productive changes. Joint spaces were preserved, and there was no collapse of the articular surfaces.](https://www.ccjm.org/content/ccjom/93/7/383/F1.large.jpg?width=800&height=600&carousel=1)
Plain radiography of the left knee (anteroposterior [left], lateral [middle], and sunrise [right] views) showed multifocal, patchy serpiginous sclerotic areas in the distal femoral metadiaphysis and proximal tibial metadiaphysis. Normal alignment was maintained. There was no fracture, dislocation, or effusion. Bone mineralization was normal, and there were no degenerative or productive changes. Joint spaces were preserved, and there was no collapse of the articular surfaces.
OSTEONECROSIS
Osteonecrosis is the death of bone as a result of insufficient vascular supply.1,2 When the epiphysis is involved, the condition is typically referred to as epiphyseal osteonecrosis, avascular necrosis, or aseptic necrosis; when the metadiaphysis is involved, it is termed a bone infarct.1,2 Epiphyseal osteonecrosis is the most common form, typically affecting the femoral head and knee.1–3 Bone infarcts are less common, and their exact prevalence remains unknown. When they do occur, the distal femur and proximal tibia are the most frequently involved sites.1–4 Pain is the most common symptom of epiphyseal osteonecrosis, whereas bone infarcts are usually asymptomatic.
Types, epidemiology, risk factors
Osteonecrosis is classified as spontaneous, secondary, or postarthroscopic.3,5 Historically, spontaneous osteonecrosis of the knee (SONK) is the most common type and often affects patients in their sixth decade of life or later.3,5–7 However, this concept is not universally accepted. Increasing evidence suggests that SONK represents a fracture occurring in osteopenic bone rather than true osteonecrosis. Histologic studies consistently show the absence of bone necrosis, and instead reveal microfractures and active bone remodeling as the defining pathologic features.8 Consequently, the validity of the term osteonecrosis in this context has been challenged, and the condition is now more accurately described as a subchondral insufficiency fracture of the knee.1,8
The exact incidence of SONK is not well established, but studies suggest it may be as high as 3.4% in patients over age 50 and 9.4% in those over 65.3,5,9 However, the true prevalence is likely underestimated, as many cases go undiagnosed and present only at end-stage osteoarthritis.3,5,7
Risk factors for all types of osteonecrosis include trauma (except in the case of bone infarcts), glucocorticoid use, alcohol consumption, hemoglobinopathies, dyslipidemia, human immunodeficiency virus infection, Gaucher disease, dysbaric conditions, and idiopathic causes, as seen in spontaneous osteonecrosis.1–3,9 Corticosteroids remain the most common cause of non-traumatic osteonecrosis. The multifactorial pathogenesis of corticosteroid-induced osteonecrosis makes its occurrence difficult to predict.2,3,7,10 However, it is well established that risk increases with higher doses, longer duration of therapy, and use of long-acting corticosteroids.1–3,10 Risk is also elevated when corticosteroids are administered via the parenteral route.11,12
Imaging studies
Plain radiographs may remain unremarkable for years in cases of bone infarct. Early radiographic signs include periosteal reaction and medullary lesions characterized by sheet-like central lucency surrounded by sclerosis with a serpiginous border—commonly referred to as a “smoke up the chimney” appearance.2,4,13 Periostitis in the metaphyseal region may be present in cases of bone infarct; however, it is uncommon and typically occurs only when the infarct is large and extends to the endosteum.13,14
Magnetic resonance imaging (MRI) can detect bone infarcts, often incidentally, as patients are typically asymptomatic.2,4,6,13 Typical MRI findings include medullary lesions with scalloped, serpiginous, tortuous borders.2,11 MRI is also useful for detecting and evaluating avascular necrosis in the adjacent epiphysis.
Differential diagnosis
The differential diagnosis of bone infarcts includes bone marrow edema syndrome, chronic osteomyelitis, tumors, and, less commonly, enchondroma.2,4,13 MRI is an essential diagnostic modality not only for identifying bone infarction but also for evaluating other potential pathologies, including metabolic bone marrow disorders, infection, and malignancy.4,6,13,14
PATIENT’S OUTCOME AND FOLLOW-UP
Because the patient’s other health issues and sources of pain were more concerning, she did not report left knee pain during subsequent visits. Three years later, unrelated biplanar whole-spine radiography incidentally revealed a similar lesion in the right distal femoral metadiaphysis (Figure 2). Based on her pain history, physical examination, and plain radiography, the etiology of her knee pain could not be accurately determined; however, the bone infarct was not felt to be the primary pain source. Owing to multiple hospitalizations and medical complexity, knee MRI was never obtained, despite being critical for further evaluation. The differential diagnosis for her knee pain remained broad, including osteochondral lesions, early degenerative joint disease, meniscal pathology, and tendinopathy.
Anteroposterior plain radiographs of both knees, taken 3 years later, showed multifocal, patchy serpiginous sclerotic areas in the distal femoral metadiaphyses bilaterally and the proximal left tibial metadiaphysis.
TAKE-HOME POINTS
This case highlights the importance of recognizing findings of osteonecrosis (bone infarct) on plain radiographs. Although often incidental, such findings should prompt consideration of underlying pathology and, when patients are symptomatic, further evaluation—most notably with MRI—to determine the etiology of symptoms.
DISCLOSURES
The authors report no relevant financial relationships which, in the context of their contribution, could be perceived as a potential conflict of interest.
- Copyright © 2026 The Cleveland Clinic Foundation. All Rights Reserved.
