In addition to osseous lesions, many articular lesions are commonly found on chest computed tomography (CT). Incidental articular findings have been reported in up to 3% of chest CT.1 Considering the wide spectrum of pathologies, it is not uncommon for radiologists to encounter a musculoskeletal finding with unknown clinical significance, which hampers proper recommendations and further steps. Familiarity of radiologists with these pathologies, their characteristic imaging features, and management could have a significant impact on patient care by preventing overutilization of medical imaging resources and avoiding unnecessary interventions. This review provides a comprehensive algorithmic approach to the articular lesions most commonly seen on chest CT.
APPROACH TO ARTICULAR LESIONS
Articular pathologies seen on chest CT can involve synovial (acromioclavicular [AC], glenohumeral, sternoclavicular, costovertebral, and costotransverse) and cartilaginous (manubriosternal and intervertebral discs) joints (Fig. 1). Figure 2 recommends an algorithmic approach to synovial and cartilaginous joint pathologies as seen on chest CT. For the sake of brevity, less diagnostically challenging pathologies such as dislocations, rare articular pathologies such as tenosynovial giant cell tumors, and other intra-articular tumors are not discussed in this article. Dedicated joint magnetic resonance imaging (MRI) with and without intravenous contrast should be recommended if there is diagnostic suspicion for intra-articular neoplasm on CT.
Synovial Joint Pathologies
Glenohumeral Joint Pathologies
A reasonable approach would be to initially exclude more common joint pathologies, such as osteoarthritis. If there is joint space narrowing, peripheral osteophytosis, subchondral sclerosis and cysts, and presence of intra-articular bodies, a definitive diagnosis of osteoarthritis could be made. No further imaging follow-up recommendation is generally needed based on finding of joint degeneration. However, osteoarthritis could be superimposed on underlying joint pathologies such as inflammatory, crystal-induced, neuropathic, or amyloid arthropathy.
When present, number and size of intra-articular bodies are important diagnostic features. When there are numerous intra-articular bodies, radiologists should be able to differentiate primary from secondary osteochondromatosis. Intra-articular bodies of different sizes are seen in secondary osteochondromatosis due to osteoarthritis. Primary synovial chondromatosis is an uncommon benign neoplastic process with nodules of hyaline cartilage in the subsynovial tissue of a joint, tendon sheath, or bursa. If calcified, the term “osteochondromatosis” should be used. In primary osteochondromatosis, intra-articular bodies are generally more numerous with almost similar sizes. These patients are younger without other signs of joint osteoarthritis.2 Treatment of primary osteochondromatosis is different from secondary osteochondromatosis and includes removal of the intra-articular bodies with or without synovectomy to prevent further formation of intra-articular bodies.2,3 Management of secondary osteochondromatosis includes anti-inflammatory medication and treatment of the inflammatory joint symptoms. When symptoms prohibit adequate function, surgical management is indicated to improve long-term function and prognosis.4 Magnetic resonance imaging without administration of intravenous or intra-articular contrast could be recommended in patients with relevant symptoms for more detailed evaluation of the intra-articular structures, such as cartilage and synovium.
One common masquerader of the intra-articular body is hydroxyapatite deposition disease, also known as calcific tendinosis. Differentiation of these 2 distinct pathologies is important because of different treatments. Intra-articular body demonstrates dense sclerotic margins with internal trabeculations, like trabecular bone covered with dense cortex, and is located within the joint capsule or displaced along the joint recesses. Calcific tendinosis occurs along the periarticular tendons such as rotator cuff tendons and appears as globular amorphous calcification. There is no internal trabeculation or dense peripheral cortex. Noncontrast MRI of the affected joint can be suggested for further evaluation of calcific tendinosis if there is relevant symptom. Magnetic resonance imaging shows the degree of inflammatory changes, consistency of the tendon, and presence of associated bursitis or synovitis. The affected tendon could also be assessed more precisely for ultrasound-guided barbotage.5
In the presence of joint effusion, the possibility of septic arthritis should always be considered. Definitive diagnosis of septic arthritis is through arthrocentesis; however, imaging plays crucial role in narrowing down the differential diagnoses. Imaging can confirm the presence of joint effusion, exclude soft tissue abscess and other extra-articular causes of regional inflammatory or infectious changes, and assess possible complications of septic arthritis, such as cartilage damage, osteomyelitis, and Brodie abscess. Computed tomography is not the preferred imaging modality for assessment of septic arthritis due to limited soft tissue contrast and poor visualization of bone marrow changes. Findings such as osseous erosions and pericapsular soft tissue stranding in the presence of joint effusion should raise concern for septic arthritis (Fig. 3). Magnetic resonance imaging with administration of intravenous contrast should be recommended if findings are concerning for septic arteritis and/or there is clinical concern for septic arthritis.
Amyloidosis is extracellular deposition of the fibrous protein amyloid in one or more sites in the body. Amyloid arthropathy, a skeletal manifestation of amyloidosis, most commonly occurs in patients on long-term hemodialysis. It may involve either the axial skeleton (especially the cervical spine) or the appendicular skeleton. It is distinct from but could coexist with renal osteodystrophy.6 Imaging manifestations of amyloid arthropathy resembles inflammatory arthritis. There is joint effusion, periarticular soft tissue swelling, periarticular osteopenia, and subchondral cystic lesions, usually with sclerotic margins (Fig. 4). The joint space is preserved until late in the course of the disease. Presence of these features on CT should raise concern for amyloid arthropathy and MRI with and without administration of intravenous contrast should be recommended. Magnetic resonance imaging shows joint effusion and deposition of abnormal soft tissue covering the synovial membrane, filling the subchondral defects, and extending to periarticular soft tissue. The abnormal deposition has low to intermediate signal intensity on T1- and T2-weighted images (WIs).7–9
Acromioclavicular Joint Pathologies
The previously mentioned general approach for the GH joint applies to the AC joint with the caveat that specific pathologies, such as hydroxyapatite deposition disease, amyloidosis, or osteochondromatosis, are less common. Additional pathologies include distal clavicular osteolysis, AC joint separation, septic arthritis, and inflammatory conditions, such as rheumatoid arthritis, hyperparathyroidism, and scleroderma.10
Distal clavicular osteolysis, also known as weightlifter's shoulder, is more common in young males who frequently lift heavy objects overhead (such as construction or factory workers) or athletes who exert force on the shoulder by repetitive overhead movement (such as tennis or squash players and competitive swimmers). Computed tomography shows AC joint widening with resorption and erosion of the distal clavicle and regional demineralization. These features, other than joint space widening, are not seen in traumatic AC dissociation or distal clavicular resection. Magnetic resonance imaging can help differentiate distal clavicular osteolysis from infectious and inflammatory causes of arthritis and should be recommended if there is clinical suspicion. In inflammatory or infectious AC arthritis, there will be subarticular plate erosion or marrow signal changes of the acromion on T1WI, which is not seen in distal clavicular osteolysis.11
Another less common entity that could be diagnostically challenging on CT is AC joint cysts. Acromioclavicular joint cyst presents as a fluid filled cystic structure along the superior aspect of AC joint. It is an uncommon and unusual sequela of chronic full-thickness rotator cuff tear. In the absence of a rotator cuff, there is rotator muscle atrophy, and the deltoid pulls the humeral head superiorly and causes repeated strike of the humeral head onto the acromion and AC joint, which ultimately results in subacromial sclerosis and remodeling as well as tearing of the inferior AC ligament. Joint fluid escapes into the AC joint and finally accumulates into the subcutaneous tissues superior to the AC joint secondary to a tear of the superior AC ligament. This is called the “geyser” phenomenon or sign12,13 (Fig. 5).
Sternoclavicular Joint Pathologies
The general approach to sternoclavicular joint pathology is similar to GH joint, as previously discussed. Sternoclavicular joint is a true synovial joint and is affected by a similar spectrum of pathologies that affect the rest of the synovial joints, including osteoarthritis, inflammatory, and crystalline-induced arthritides as well as traumatic pathologies including dislocation. Anterior dislocations are more common while posterior dislocations have the potential for mediastinal and vascular injury and need prompt stabilization. Septic arthritis of the sternoclavicular joint should be considered in the differential in patients with risk factors (such as history of intravenous drug use, alcoholism, diabetes, HIV, and other immunosuppressed states), localizing symptoms, and laboratory markers of infection. Computed tomography manifestation of septic arthritis includes erosion with osteolysis and widening of the joint with effusion as well as surrounding soft tissue changes, such as edema, enhancement, and soft tissue thickening (Fig. 6).
Chronic recurrent multifocal osteomyelitis (CRMO) and synovitis, acne, pustulosis, hyperostosis, osteitis (SAPHO) syndrome are closely related syndromes. Both are chronic idiopathic inflammatory disorders with cutaneous manifestations as well as nonpyogenic osteomyelitis involving joints, spine, and metaphyses of appendicular skeleton. The sternoclavicular joint and medial clavicle are unique sites with predilection to SAPHO and CRMO. Computed tomography manifestations of SAPHO/CRMO in the sternoclavicular joint include lytic as well as sclerotic changes of the medial clavicle, ligamentous ossification, and fusion of the joint.14
Cartilaginous Joint Pathologies
Intervertebral Disc Pathologies
Most intervertebral disc pathologies encountered on a chest CT are chronic and incidental. Magnetic resonance imaging is the study of choice for a suspected disc or spinal soft tissue pathology. Common disc pathologies include Schmorl nodes, diffuse idiopathic skeletal hyperostosis (DISH), ankylosing spondylitis (AS), pyogenic discitis osteomyelitis, and ossification of the posterior longitudinal ligament.
Schmorl nodes represent herniation of nucleus pulposus component of intervertebral disc through a disrupted and weakened endplate.15,16 They are often an incidental finding in the spine and discovered in the chronic phase on CT as low-density foci of disc material abutting the endplate with a sclerotic margin (Fig. 7). However, they can be symptomatic in the acute phase and occasionally require further evaluation with MRI when diagnosis is uncertain. During the acute phase, Schmorl nodes show edema and enhancement due to inflammation. Key differential diagnosis for Schmorl nodes includes compression fracture, focal metastatic lesion, and discitis. Lack of erosive changes in the adjacent endplate and contiguity to the adjacent parent disc are key distinguishing factors.
Pyogenic discitis osteomyelitis (also known as spondylodiscitis) is rarely encountered in a routine chest CT; however, it is important to be familiar with imaging findings of spinal infection. Computed tomography images may show endplate destruction with lysis and fragmentation, disc height loss, and paraspinous and epidural soft tissue infiltration (Fig. 8).17 There may be extension into the paraspinous pleural space as well as lung parenchyma. In case of a suspected spondylodiscitis, it is important to recommend MRI with contrast to further assess soft tissue and epidural involvement. Tuberculous spondylitis is very rare in the United States, and findings may include preferential involvement of the anterior vertebral body with associated short-segment kyphosis called a Gibbus deformity, subligamentous spread with sparing of the disc spaces, large paraspinous abscesses, and skip lesions involving noncontiguous vertebrae (Fig. 9).18
Diffuse idiopathic skeletal hyperostosis, as its name indicates, is an idiopathic condition characterized by ossification of ligaments and entheses. It typically affects elderly individuals and unlike its close mimic, AS, clinical manifestations are rare. On CT images, DISH is characterized by flowing ossification along the anterior longitudinal ligament and paravertebral connective tissues (Fig. 10). In addition, DISH can be associated with ossification of the posterior longitudinal ligament as well as ligamentum flavum, supraspinous, and interspinous ligaments (Fig. 11).19
Ankylosing spondylitis is an inflammatory spondyloarthropathy that affects younger individuals and is more commonly associated with symptoms, such as pain, decreased range of motion, and stiffness. Ankylosing spondylitis is characterized by syndesmophytes, which represent thin linear ossification of peripheral annulus fibrosus (Fig. 12). In contrast to AS, ossifications of anterior longitudinal ligament in DISH are bulky and are typically separated by a lucent line from vertebral bodies. In addition, AS is associated with enthesitis of the anterior corner of vertebral bodies (Romanus lesion) and associated chronic remodeling resulting in sclerosis (“shiny corner” sign) and squaring of anterior corners of vertebral bodies.
Costochondral Junction Pathologies
Although captured in many radiologic examinations, the costal cartilage has often been overlooked. Common incidental findings of costal margins include diffuse enlargement, focal masses, destruction, or premature calcification. Diffuse enlargement of the costal cartilages is seen in acromegaly and rickets. In acromegaly, induction of periosteal bone formation at existing cartilage-bone junctions results in expanded costochondral junctions.20 In rickets, failure of calcification and osteoid mineralization results in the classic rachitic rosary appearance. Focal masses at the costal cartilages may represent primary or secondary malignancies, traumatic sequelae, infectious, or inflammatory processes. Chondrosarcomas are one of the primary malignancies that occur in approximately 10% of cases at the thoracic cage with the characteristic imaging appearance of an expansile mass with coarse calcifications and associated soft-tissue masses. Direct invasion of the costal margin can occur in lung cancer or breast cancer. An exuberant callus can form in response to trauma or surgery. Physical deformity, focal discontinuity or displacement of the costal cartilage, partial calcification, and pattern of uptake on bone scintigraphy can help distinguish it from tumors of the costal margins.20,21 Posttraumatic uptake usually has a focal appearance and could involve more than one contiguous costal cartilage while neoplastic involvement is usually more linear and could be solitary or scattered.
Costochondritis may occur because of inflammation, infection, trauma, or as a postoperative complication. It can be defined as pain and tenderness without significant swelling on the costochondral or chondrosternal junctions that most commonly affect the second to fifth costal cartilages. It represents as chondral enlargement or destruction, low attenuation of the cartilage, and localized peripheral calcification.22 Tietz syndrome is a painful chest wall condition, which could have an inflammatory etiology. This can be distinguished from costochondritis by the presence of swelling in the region of pain and tenderness. It most commonly involves single costal cartilage, with the second and third costochondral junctions as the most common locations. Computed tomography findings include sclerosis at the manubriosternal junction, partial calcification of the costal cartilage, and soft tissue swelling. Premature costal cartilage calcification, which occurs before the age of 40 years, is another finding, which might be associated with malignancy, autoimmune disorders, chronic renal failure, or thyroid disease.20,23
Manubriosternal Junction Pathologies
Conditions that affect the manubriosternal junction include congenital anomalies, degenerative and inflammatory conditions, and traumatic dislocations and fractures. Partial manubriosternal fusion or nonfusion of sternal body segments that might mimic fractures are depicted by sclerotic margins and lack of adjacent soft tissue stranding. Dislocation at the manubriosternal joint is an uncommon condition that might occur because of direct or indirect trauma.23–25
Arthritis that may affect the manubriosternal joint includes septic arthritis, osteoarthritis, rheumatoid arthritis, AS, psoriasis, gout, and pyrophosphate deposition disease. Computed tomography helps accurately detect bone abnormalities and calcifications. Magnetic resonance imaging better depicts bone marrow, erosions, and extra-articular soft tissues. Osteoarthritis might affect manubriosternal joints presenting with joint space narrowing and marginal osteophytosis (Fig. 13). Erosion and indistinct cortical margins have been observed in rheumatoid arthritis of the manubriosternal joint. Erosions and partial or complete fusion of the manubriosternal are imaging features of AS, reactive arthritis, and psoriatic arthritis.24
Chest CTs are commonly encountered with various articular findings in daily practice. Familiarity with imaging characteristics, their clinical significance, and the proper next step imaging recommendation and management can improve patient care by preventing collateral patient anxiety, overutilization of medical imaging resources, and avoiding unnecessary interventions.
The authors thank Nastaran Hosseini, MD.
1. Hall WB, Truitt SG, Scheunemann LP, et al. The prevalence of clinically relevant incidental findings on chest computed tomographic angiograms ordered to diagnose pulmonary embolism. Arch Intern Med
2. Murphey MD, Vidal JA, Fanburg-Smith JC, et al. Imaging of synovial chondromatosis with radiologic-pathologic correlation. Radiographics
3. Davis RI, Hamilton A, Biggart JD. Primary synovial chondromatosis: a clinicopathologic review and assessment of malignant potential. Hum Pathol
4. Habusta SF, Tuck JA. Synovial chondromatosis. StatPearls
. 2022. Available at: https://www.ncbi.nlm.nih.gov/books/NBK470463/
. Accessed April 24, 2022.
5. Gatt DL, Charalambous CP. Ultrasound-guided barbotage for calcific tendonitis of the shoulder: a systematic review including 908 patients. Arthroscopy
6. Llauger J, Palmer J, Rosón N, et al. Nonseptic monoarthritis: imaging features with clinical and histopathologic correlation. Radiographics
. 2000;20 Spec No:S263–S278.
7. Camacho CR, Meléndez AT, Valenzuela A, et al. Radiology findings of amyloid arthropathy in long-term haemodialysis. Eur Radiol
8. Ross LV, Ross GJ, Mesgarzadeh M, et al. Hemodialysis-related amyloidomas of bone. Radiology
9. Kiss E, Keusch G, Zanetti M, et al. Dialysis-related amyloidosis revisited. AJR Am J Roentgenol
10. Gordon BH, Chew FS. Isolated acromioclavicular joint pathology in the symptomatic shoulder on magnetic resonance imaging: a pictorial essay. J Comput Assist Tomogr
11. Ha AS, Petscavage-Thomas JM, Tagoylo GH. Acromioclavicular joint: the other joint in the shoulder. AJR Am J Roentgenol
12. Cooper HJ, Milillo R, Klein DA, et al. The MRI geyser sign: acromioclavicular joint cysts in the setting of a chronic rotator cuff tear. Am J Orthop (Belle Mead NJ)
13. Hiller AD, Miller JD, Zeller JL. Acromioclavicular joint cyst formation. Clin Anat
14. Jurik AG, Klicman RF, Simoni P, et al. SAPHO and CRMO: the value of imaging. Semin Musculoskelet Radiol
15. Mattei TA, Rehman AA. Schmorl's nodes: current pathophysiological, diagnostic, and therapeutic paradigms. Neurosurg Rev
16. Diehn FE, Maus TP, Morris JM, et al. Uncommon manifestations of intervertebral disk pathologic conditions. Radiographics
17. Tali ET, Oner AY, Koc AM. Pyogenic spinal infections. Neuroimaging Clin N Am
18. Torres C, Zakhari N. Imaging of spine infection. Semin Roentgenol
19. Olivieri I, D'Angelo S, Palazzi C, et al. Diffuse idiopathic skeletal hyperostosis: differentiation from ankylosing spondylitis. Curr Rheumatol Rep
20. Ontell FK, Moore EH, Shepard J-A, et al. The costal cartilages in health and disease. Radiographics
21. Malghem J, Vande Berg BC, Lecouvet FE, et al. Costal cartilage fractures as revealed on CT and sonography. Am J Roentgenol
22. Meyer CA, White CS. Cartilaginous disorders of the chest. Radiographics
23. Gregory PL, Biswas AC, Batt ME. Musculoskeletal problems of the chest wall in athletes. Sports Med
24. Restrepo CS, Martinez S, Lemos DF, et al. Imaging appearances of the sternum and sternoclavicular joints. Radiographics
25. Levine BD, Motamedi K, Chow K, et al. CT of rib lesions. AJR Am J Roentgenol