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 Table of Contents  
Year : 2018  |  Volume : 13  |  Issue : 5  |  Page : 48-56

Sonography of common rheumatic diseases

1 Division of Rheumatology, University of Florida College of Medicine, Jacksonville, Florida, USA
2 Division of Rheumatology, University of California Los Angeles, Los Angeles, California, USA

Date of Web Publication1-Aug-2018

Correspondence Address:
Prof. Gurjit S Kaeley
Division of Rheumatology, University of Florida College of Medicine, Jacksonville 653-1 West Eight Street, LRC 2nd Floor L-14, Jacksonville, FL 32209-6561
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0973-3698.238202

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There has been a major sea change in the care of rheumatology patients with the advent of bedside ultrasound (US). US not only offers an ionizing free form of imaging but can also evaluate the vascularity of structures without using contrast. Sonography has generated much excitement with the depiction of disease processes affecting anatomical structures, and in some cases, has changed our views of the pathophysiology. It has also enabled establishing the diagnosis when the clinical picture is unclear. In this article, the role of US in major rheumatic syndromes will be outlined with high-quality sonographic images.

Keywords: Chondrocalcinosis, double contour, enthesitis, gout, osteoarthritis, Sonography, synovitis

How to cite this article:
Kaeley GS, Ramrattan LA, Ranganath VK. Sonography of common rheumatic diseases. Indian J Rheumatol 2018;13, Suppl S1:48-56

How to cite this URL:
Kaeley GS, Ramrattan LA, Ranganath VK. Sonography of common rheumatic diseases. Indian J Rheumatol [serial online] 2018 [cited 2022 Aug 14];13, Suppl S1:48-56. Available from:

  Introduction Top

Musculoskeletal ultrasound (US) use is rapidly gaining a place in routine rheumatology practice. Sonography is able to examine joints as well as surrounding tissues with great detail. In some cases, the resolution is better than magnetic resonance imaging (MRI). In the ensuing article, the use of sonography in spondyloarthropathies, crystalline arthropathies, rheumatoid arthritis (RA) as well as osteoarthritis (OA) will be summarized. Representative high-quality images have been provided to underline key findings. Finally, much of the excitement in use of musculoskeletal US is not only to be able to rapidly make the diagnosis at the bedside but also view the pathological changes in various diseases. As it will be seen in the section on spondyloarthropathies, our traditional views on pathophysiology have been challenged due to findings seen on US.

  Sonography of Spondyloarthropathies Top

Spondyloarthropathies are a group of inflammatory arthropathies characterized by the presence of enthesitis. Entheses play an important role in the dissipation of mechanical stress. Of note, enthesitis occurs at fibrocartilaginous entheses, whereas, metabolic enthesopathies tend to occur at membranous entheses.[1] The clinical evaluation of entheses is by palpation for tenderness of these areas. Validated indices incorporating a variety of entheses have been developed. Initially, these were extensive and developed for use in ankylosing spondylitis. Subsequent clinical entheseal indices have a smaller number of entheses and are more applicable to evaluation of spondyloarthropathies.[2] Of note is that all of these include the largest enthesis, the Achilles tendon, but vary over what other areas are included. Sonographic indices have followed a similar trend [Table 1]. Clinical evaluation is insensitive [3] and may be confounded by chronic pain syndrome/fibromyalgia,[4],[5] and also does not reflect underlying morphological changes.
Table 1: Commonly used clinical and sonographic entheseal indices

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Morphological changes may not only occur at the anchoring of the enthesis but also in the surrounding soft tissues. Preliminary definitions of elementary lesions that constitute enthesitis have been published.[6] These include, hypoechogenic change of the ligament or tendon at the enthesis, and may be defined as loss of fibrillar echotexture; increased thickening of the ligament or tendon at enthesis; calcifications at tendon insertion; enthesophyte formation, bone erosion at insertion of enthesis; and entheseal Doppler signal within 2 mm of the margin adjacent to the bone [Figure 1]. Of note, adjacent bursitis did not reach a sufficient level of consensus to be included. Furthermore, when examining entheses, bone erosions may be found adjacent to the enthesis and not at the insertion [Figure 2]. Benjamin and McGonagle have proposed an alternative view – proposing that the enthesis should be considered to be an enthesis organ.[7] The enthesis organ concept recognizes the role of the enthesis as a mechanical load dissipater and notes that fibrocartilaginous changes occur to the anchoring of the entheses as well as where it may rub on bone. Furthermore, bone areas such as the superior pole of the calcaneus also have fibrocartilage, allowing smooth gliding of the tendon. These areas are prone to mechanical loading and defects can be seen in normal individuals which may explain the location of erosions in spondyloarthropathy. The enthesis organ concept also recognizes the role of the adjacent bursa – not only for normal stress dissipation – but also as a source for inflammation since synovial hypertrophy (SH) can occur in this region and may help propagate adjacent erosions.
Figure 1: Examples of morphological changes seen in enthesitis. (a and b) Distal patellar ligament showing entheseal thickening, loss of fibrillar echotexture (arrows) as well as Power Doppler signal in the tendon body and enthesis. (c and d) Proximal patellar ligament showing entheseal thickening, loss of fibrillar echotexture, as well as intratendinous calcifications with posterior acoustic enhancement (arrowheads). Doppler signal is noted about the area of calcification.

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Figure 2: Achilles tendon enthesitis. (a and b) Enthesitis manifested by a thickened Achilles tendon with loss of fibrillar echotexture. Erosion is seen in the superior pole of the calcaneus (arrows), as well as evidence of retrocalcaneal bursal distension (arrowheads) next to the Kager's fat pad (K). In the Doppler image, increased vascularity is seen in the tendon, enthesis, as well as bursa and tissue, abutting the erosion

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In patient with early spondyloarthropathy or patients with psoriasis in whom the diagnosis of psoriatic arthritis (PsA) is not clear, sonography of the entheses may be helpful. The two most commonly used sonographic indices are the Glasgow US Enthesis Scoring System (GUESS) and Madrid sonography enthesitis index [Table 1].[3],[8] The GUESS system does not include Doppler. Both indices have been shown to be able to distinguish between normal populations and those with spondyloarthropathy. However, more recent studies have raised the question regarding confounding with high body mass index, since the majority of entheses are in the lower extremity.[9] This has led to some interest in incorporating more upper extremity entheses to decrease confounding with body mass index. Zabotti et al. compared patients with early RA compared to early PsA and reported increased prevalence of extensor tendon (ET) paratenonitis at the metacarpophalangeal (MCP) joint, central slip enthesitis at the proximal interphalangeal (PIP) joints in PsA patients. An example of extensor slip enthesitis at the distal IP joint can be seen in [Figure 3].
Figure 3: Features of Distal Phalangeal Joint Enthesitis. (a and b) Extended view of the distal interphalangeal joint including nail bed in a patient with PsA. Not the thickened extensor slip with an enthesophyte (arrows), osteophyte formation (arrowhead), synovial hypertrophy, as well as thickened nail bed. (b) Corresponding Doppler image displaying Doppler signal at the enthesis as well in the synovial recess

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In conclusion, sonography is eminently suited to the examination of peripheral entheses, many of which are readily accessible for imaging. US not only can provide high-resolution images of these areas, but also the degree of vascularity with use of color flow or power Doppler (PD) can be documented. These sonographic findings are useful in diagnosing early spondyloarthritis especially when the clinical examination may not be clear.

  Sonography of Crystalline Arthropathies Top

Sonography for crystalline arthropathies has increasingly become more prominent not only because features of gout can be demonstrated in soft tissues and joints, but also because it can differentiate chondrocalcinosis from urate deposition.


The inclusion of US features of gout in the EULAR/ACR 2015 gout classification criteria underscores the importance of imaging in the detection of gout.[10] The classification criteria specified US detected double contour and urate deposition detected by dual-energy computed tomography. “Double contour” refers to gout deposition on the superficial surface of cartilage. Consensus definition of the double contour sign includes the hyperechoic band over the anechoic superficial margin of articular hyaline cartilage which can range from focal to homogeneous thickening and whose reflectivity is independent of the angle of insonation [11] [Figure 4]. Of note, it must not be mistaken for the interface sign, which is well defined, sharp, and disappears when angle of insonation is changed. Recent meta-analysis has suggested double contour pooled sensitivity of between 0.65 and 0.83 and pooled specificity of 0.76–0.89.[12],[13]
Figure 4: Double contour sign. (a) Double contour sign at the femoral condyle – note the irregular chondrosynovial deposition (arrowheads). (b) Double contour sign (arrowheads) at the metacarpophalangeal joint ostensibly seen despite probe not being perpendicular to the superficial aspect of the cartilage

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Tophaceous deposits range from loose aggregates to well-defined tophaceous deposits. These may be seen as heterogeneous collection of material with hyperechoic foci (“snow storm” appearance) [Figure 5]a. A smaller collection of tophi may have an anechoic rim. These deposits may be found in joints as well as soft tissues.[11] Long-standing tophi may appear as dense structures with poor posterior acoustic reflection. Pooled sensitivity for tophus detection ranges from 0.54 to 0.65 and pooled specificity from 0.75 to 0.93.[12],[13] The tendons that have most frequently been reported as showing tophaceous deposits include the patellar ligament, Achilles tendon, quadriceps tendon and triceps tendons.[14],[15],[16] Tophaceous deposits may appear as heterogeneous collection of material to hyperechoic linear areas [Figure 5]b.
Figure 5: Tophaceous deposits. (a) Heterogeneous material (arrows) with hyperechoic dots seen on the dorsal aspect of the first metatarsophalangeal joint. (b) Tophaceous deposits (arrowheads) seen in the distal patellar ligament (P)

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Since US findings of gout have been included in classification criteria, the next question is what combination of sites has the best yield and feasibility for detection of urate deposition. Naredo et al. have suggested examining the radiocarpal joint as well as patellar tendon and triceps tendon for hyperechoic aggregates, and first metatarsal phalangeal joint (MTP), talar dome, second metacarpal or femoral cartilage for double contour.[14] Bhadu et al.[17] in a case–control study suggested that the knee and first MTP may be of sufficient sensitivity and more feasible than the six sites suggested by Naredo et al.[14] However, it seems that examination of the sentinel or most symptomatic joint as well as the knee cartilage and patellar ligament as well as MTP 1 may offer a comprehensive and feasible approach.

Calcium pyrophosphate deposition

CPPD is a predominantly articular finding, and its presentation can vary from asymptomatic chondrocalcinosis to chronic synovitis. The most common areas for deposition are fibrocartilage and hyaline cartilage where CPPD crystals deposit in the middle of the cartilage. The deposition may also occur within the synovial cavity as well as tendons and ligaments. A recent literature review summarized the target tissues being studied for CPPD disease as well as detailed diagnostic probabilities based on a variety of gold standards.[18] The review also highlighted that majority of the literature was from two centers in Italy. Consensus definitions of sonographic findings of CPPD in various tissues have been developed and tested in a web exercise as well as patient exercise. At fibrocartilage and hyaline cartilage hyperechoic deposits with similar echogenicity to bone and that move together with the structure are defined as representing CPPD [Figure 6]a and [Figure 6]b. At the tendons, CPPD deposition was defined as linear hyperechoic areas and in the synovial cavity as hyperechoic dots of variable size [Figure 6]c. Reliability was high in the triangular fibrocartilage and acromioclavicular joints, but patient based reliability was poor in other sites.[19] Although US is felt to be likely superior to plain radiography for diagnosis of CPPD at superficial sites such as the wrist, further work is needed to validate these definitions.
Figure 6: Sonographic features of chondrocalcinosis. (a) Punctate calcification in the femoral condyle (arrow), (b) Chondrocalcinosis seen in the triangular fibrocartilage complex (arrow), (c) Dorsal proximal interphalangeal joint showing punctate deposits (arrowheads) as well as osteophyte (O)

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  Principles of Sonography in Rheumatoid Arthritis Top

RA is the most common autoimmune inflammatory destructive arthritis with a prevalence of about 1%. The salient feature of RA is the symmetrical polyarthritic involvement of diarthrodial or synovial joints, which if left untreated, leads to synovial tissue proliferation that destroys the joint. Of the publications investigating arthritis and musculoskeletal US (MSK US), RA is likely the most researched.

Anatomical structures of interest in rheumatoid arthritis

While RA causes synovitis of the upper and lower extremities [Figure 7], [Figure 8], [Figure 9], [Figure 10], RA can also affect the tendons throughout the disease [Figure 11], [Figure 12], [Figure 13], and anecdotally tendon involvement can occur as the first US clue to early RA diagnosis. Pathology seen by MSK US can include the ETs of the wrists, extensor carpi ulnaris, and flexor/ETs of the fingers. MSK US can detect erosions earlier than with plain radiographs. The presence of “large” erosions in the joints of MCP 2/5, metatarsophalangeal (MTP) 5, and the distal ulna were specific and predictive of RA.[20] MRI may be better suited to give a comprehensive evaluation of the burden of erosive disease in the hands since US is limited by its inability to visualize all aspects of the joint. Joint space narrowing and cartilage damage by US of the small and medium joints are not yet well characterized in RA.
Figure 7: Features of MCP synovitis. (a and b) Dorsal long and short scans of the metacarpophalangeal joint revealing synovial hypertrophy (arrowheads) below extensor tendon. (c and d) Corresponding Doppler imaging revealing Power Doppler signal over synovial hypertrophy

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Figure 8: Dorsal proximal interphalangeal synovitis. (a) Synovial hypertrophy and effusion seen at dorsal recess of the proximal interphalangeal joint (starred). (b) Corresponding Doppler image revealing vascularity in the synovium and extensor tendon

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Figure 9: Radiocarpal and midcarpal synovitis. (a) Midline long scan of the wrist revealing radiocarpal synovial hypertropy (two stars) manifested as distension of the recess between radius (R) and lunate (L), as well as midcarpal synovial hypertrophy between lunate and capitate (C). Note the septum in between radiocarpal joint (arrowheads) and midcarpal joint that carries normal feeding blood vessels (b) Corresponding Doppler image showing vascularity in the feeding blood vessels as well as over the midcarpal recess

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Figure 10: Distal radioulnar joint synovitis. (a and b) Longitudinal B-mode and Doppler scans of the distal radioulnar joint revealing marked distension of the recess (starred) as well as vascularity indicating active synovitis

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Figure 11: Extensor Carpi Ulnaris Tenosynovitis. (a) Synovial hypertrophy (arrowheads) of the extensor carpi ulnaris tendon sheath seen from ulna, overlying the triquetrum until its insertion at the base of the 5th metacarpal. (b) Corresponding Doppler image revealing marked vascularity. (c and d) Short-axis images revealing synovial hypertrophy as well as tendon split (arrow) and corresponding marked vascularity

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Figure 12: Volar tenosynovitis about the proximal interphalangeal joint. (a) Synovial hypertrophy (arrowheads) seen in the sheath of the flexor tendons as well as synovial hypertrophy in volar recess of proximal interphalangeal joint (starred). (b) Corresponding vascularity seen in the tenosynovium

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Figure 13: Dorsal metacarpophalangeal joint tendinitis/paratenonitis. (a and b) Long and short-axis views of the metacarpophalangeal joint revealing vascularity of and about the extensor tendon (arrowhead). The extensor tendon at this level does not have a synovial sheath suggesting inflammation of the paratenon and hence the term paratenonitis. Mild amount of synovitis is seen closer to the bone

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General concepts of MSK ultrasound in rheumatoid arthritis

MSK US is evaluated by PD and grayscale (GS) assessment of the synovium and tendons. When evaluating erosions, it is important to confirm its presence in both longitudinal and transverse views.[21] Synovitis is inferred by Doppler activity which has been associated with progression of erosions especially when persistent. It is important to consider several important factors that may affect interpretation and comparisons of images from one visit to another. Different US machines have varying sensitivity for detecting PD signal.[22],[23] Standardization of the room accommodations is needed to ensure appropriate lighting, comfort of the sonographer and patient, and temperature (too cold/hot room can lead to contraction/dilation of blood vessels resulting in variable PD signal). Nonsteroidal anti-inflammatory drugs are known to significantly decrease PD and GS;[24] thus, it may be advised to document of the timing of its administration. As expected, prednisone significantly decreases PD and GS as early as 2–8 days at low doses of 7.5–15 mg.[25] Positioning of the patient can also impact the amount of PD and GS visualized.[26],[27],[28] It is recommended that the joints of the hands and wrists be evaluated in the 0° position, and knees in the 30° position. This can be difficult in patients with swan neck and/or boutonniere deformities, and fused joints. Positioning for the MTP joints is a little more complicated due to the frequently seen clinical deformities, i.e., hammer toes/cock-up toes, overlapping toes, hallux valgus, and subluxed MTPs. In our experience, it may be necessary to have the patient flex their toes or manually flex the patients' toes to get the correct anatomic views and “open-up” the joint space for better visualization. The literature has yet to systematically provide guidance on these issues.

Selection of joints and current protocols in rheumatoid arthritis

Classic RA is manifested by the symmetric swelling and tenderness of the small joints-MCP, PIP, IP, and MTP joints. RA involvement of the wrist occurs approximately 75%–80% of the time during the disease. These are the joints most commonly evaluated in RA US protocols. Other joints that can be assessed by US include the knees, elbows, shoulders, hips, and ankles. These joints can be challenging due to a lower frequency of involvement, lack of standardization of the optimal views in RA, and increases in depth can decrease sensitivity of PD detection.

At present, there is no clear consensus of the ideal combination of joints or areas that can be optimally assessed. While in research trials, extensive number of joint areas may be examined, this is rarely feasible in clinical practice. The indications for scanning patients in routine practice include establishing the diagnosis by detecting subclinical synovitis, usually in patient in whom the clinical evaluation is unclear. The presence of erosions would indicate a poorer prognosis.[20] In addition US may detect ongoing synovitis abutting the erosion that would require escalation of therapy [Figure 14]. The second main indication of using US is to aid in evaluating regional pain, for example, shoulder or ankle pain or swelling. Another reason for using US is in the seronegative obese RA patient, where clinical examination of the joint for swelling may be unclear due to periarticular adiposity.[29] Clinical evaluation of the MTPs can be confounded by lower extremity edema, and utilization of US can be advantageous in distinguishing if there is true synovitis. Static and dynamic US can help in elucidating the anatomic source of pain as well as whether it is due to ongoing RA. Sonography is also useful when there is patient-physician discordance.[30],[31] US may also be useful in decision making for treatment escalation as well as de-escalation on a case by case basis. The validity of protocol routine scanning of patients at every visit is unclear. Two large randomized clinical trials in early RA evaluating a treat-to-target approach either by DAS or by US to achieving remission demonstrated equivalence across the arms.[32],[33]
Figure 14: Erosions of Metacarpophalangeal Joint. (a and c) Large erosion (arrow) seen at the metacarpal head in two planes. (b and d) Demonstrate ongoing vascularity of the pannus abutting the erosion

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In summary, US in RA is primarily tailored to the assessment of synovitis, which is easily visualized. Detection of erosions or PD synovitis by US early in the course of RA can aid in the recognition for more aggressive treatment.

  Sonographic Features of Osteoarthritis Top

OA is one of the most common joint disorders worldwide causing significant pain and disability. In the third National Health and Nutrition Examination Survey III, approximately 37% of participants age >60 years or older had radiographic knee OA.[34] Radiological imaging has been used to diagnose and classify the severity of knee OA such as the Kellgren and Lawrence system. However, limitations include the inability to evaluate soft-tissue structures and the related inflammation.[35] It is important to note that there is discordance between radiological changes and symptoms. This, in part, may be because the soft-tissue pain generators are not imaged by plain radiographs.

US is a promising technique for assessing decrease in cartilage thickness, meniscus bulging, and formation of osteophyte as well as joint effusion, SH, and Baker's cyst.[36] Accurate and standardized measurements of these parameters are not only important for OA diagnosis/disease severity but also can be used in investigational studies. US has also been shown to be more sensitive than clinical examination in detecting fluid [37] and correlates well with MRI and arthroscopic findings. Musculoskeletal US can help to determine the source of knee pains. Geannette et al. showed that identifying and injecting osteophytes impinging on the adjacent tendon in the popliteus sulcus by US resolved the majority of symptoms in knee replacement patients.[38]

Structural changes

Cartilage can be demonstrated as anechoic tissue next to bone. Ultrasonographic grading (in vitro) of femoral cartilage correlated well with the histologic grading [39] of the femoral articular cartilage.[40] However, the limitations are that not all the surface of the cartilage can be examined due to lack of acoustic windows. Osteophytes are seen on US at the joint margins [Figure 15]. US Scoring systems have been developed,[36] but it is unclear whether these will have a role in defining OA by US compared to more advanced 3D reconstruction imaging which can better define bone remodeling. Sonography can demonstrate the medial collateral ligament and adjoining meniscus at the medial knee. Meniscal extrusion defined as meniscal margin extending beyond the tibial margin at the knee joint as well as meniscal cysts may be seen in [Figure 15]. Meniscal extrusion has been described as an important risk factor in the progression of knee OA.[41] Ultrasonographic evaluation in 270 subjects showed that medial meniscal extrusion was associated with radiographic knee OA progression over 3 years' follow-up period.[42]
Figure 15: Meniscal pathology. (a) Medial meniscus knee showing meniscal extrusion (arrowheads) and osteophyte (O). (b) Illustrating a parameniscal cyst (asterisk). Bifascicular medial collateral ligament (Arrows) is thickened and anechoic in (a) while in (b), the deep fibers have been dissected away from the meniscus by the cyst. Ultrasound cannot visualize the deep meniscus, but the presence of a meniscal cyst is highly suspicious of a meniscal tear

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Synovitis/joint effusion and popliteal cysts

A large European League Against Rheumatism study of 600 people with knee OA demonstrated SH or effusion in 46% of patients. SH [Figure 16] was defined as synovial thickening of ≥4 mm and effusion [Figure 16] recorded as present if the depth of fluid was >4 mm in the suprapatellar recess.[43] In a review study that included 24 studies in which US was used to detect changes in knee OA, the pooled prevalence from these studies found that effusion was present in 51.5% of patients, SH in 41.5%, and Doppler signal in 32.7%.[44] Popliteal cysts are readily identified at the semimembranosus/medial head of gastrocnemius junction [Figure 17]. Popliteal cysts have been associated with worse pain and poorer function in patients with knee OA.[45]
Figure 16: Effusion and Synovitis. (a) Showing effusions (asterisk) in the suprapatellar recess (a) between AFP: Anterior fat pad, PFP: Posterior fat pad. Synovial hypertrophy (arrowheads) and Power Doppler signal noted in the lateral parapetellar recess (b and c)

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Figure 17: Popliteal cyst. Extended view of a loculated (arrow indicates septa) popliteal cyst with posterior acoustic enhancement of the tendon of the medial head of gastrocnemius tendon. Arrowhead indicates a cartilaginous body with partial calcification within the popliteal cyst

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In summary, sonographic findings offer more insights about the pathology of OA than conventional radiography and correlates well with MRI and arthroscopic findings. Hence, it is a valuable tool in the quest for the treatment of this currently poorly treated debilitating disease.

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15], [Figure 16], [Figure 17]

  [Table 1]


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