Guiding the diagnosis of inflammatory arthritis

INTRODUCTION

Arthritis is a broad term encompassing over 100 disorders affecting joints and surrounding tissues, primarily causing joint pain, swelling, stiffness, and functional impairment. The most common type, osteoarthritis, is a degenerative condition caused by mechanical wear and tear of cartilage. In contrast, inflammatory arthritis comprises diseases where inflammation plays a central role, leading to synovitis, cartilage destruction, and bone erosion.^[1] This includes autoimmune conditions such as rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS), as well as inflammatory disorders such as polymyalgia rheumatica, which affects mainly older adults with proximal muscle pain and stiffness.^[2,3]

Not all inflammatory arthritis is autoimmune. Crystal-induced arthritis, such as pseudogout from calcium pyrophosphate deposition, provokes inflammation through crystal accumulation rather than immune dysregulation.^[4] Infectious arthritis arises from microbial invasion of the joint space – most commonly by bacteria – and can cause rapid cartilage destruction if untreated.^[5,6] Yet, infections can also act as triggers for persistent inflammation long after the pathogen has cleared. Chronic arthritis following viral or bacterial infections – such as chronic chikungunya arthritis and post-Lyme immune arthritis – illustrates this bridge between infection and autoimmunity. In these conditions, viral or bacterial antigens may persist within synovial tissues, sustaining immune activation and producing clinical patterns that mimic rheumatoid or spondyloarthropathy. Recognizing these infection-induced chronic arthritides is essential, as they challenge the classical division between infectious and autoimmune disease and carry unique therapeutic implications.^[7,8]

Early recognition and distinction between autoimmune, crystal-induced, and infectious types are crucial for guiding appropriate therapy and improving outcomes. This review provides a comprehensive overview of inflammatory arthritis by anatomic location, highlighting essential clinical and imaging features for differential diagnosis.

THE CLINICAL STORY IN INFLAMMATORY ARTHRITIS

The clinical journey of a patient with inflammatory arthritis often begins with gradually evolving joint pain, swelling, and stiffness over several weeks to months. A hallmark is morning stiffness lasting more than 30 min, usually improving with movement – helping distinguish it from mechanical or degenerative causes. Patients often report difficulty walking, rising from bed, or using their hands due to pain and limited mobility. The pattern of joint involvement – symmetric or asymmetric, and affected joints – guides clinical diagnosis. Additionally, associated systemic symptoms like fatigue, low-grade fever, or weight loss, and extra-articular features such as dry eyes, skin rashes, or oral ulcers may indicate diagnoses such as PsA, lupus, or Sjögren’s syndrome.^[9-11]

On examination, clinicians look for signs of true synovitis: Soft tissue swelling, warmth, tenderness, and reduced motion. Extra-articular signs – nail pitting, psoriatic plaques, or subcutaneous nodules – further support the diagnosis. Laboratory tests complement clinical findings: Elevated inflammatory markers (erythrocyte sedimentation rate, C-reactive protein [CRP]) indicate systemic activity, while serological tests like rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP), antinuclear antibody (ANA), and human leukocyte antigen B27 (HLA-B27) help confirm or exclude specific conditions. This clinical context is vital for radiologists in choosing imaging modalities, focusing on anatomy, and interpreting findings, ensuring imaging complements clinical evaluation.^[9-11]

WHY IMAGING IS NEEDED IN INFLAMMATORY ARTHRITIS

Despite thorough history, examination, and laboratory tests, imaging plays a unique, indispensable role in evaluating inflammatory arthritis. Early inflammation can be subtle, with signs missed or attributed to other causes. Imaging reveals hidden pathology – synovitis, bone marrow edema, early erosions – before swelling or deformity appear confirming diagnosis and enabling early treatment to prevent irreversible damage, as seen in Figure 1.^[12-14]

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Figure 1:

A 67-year-old female with longstanding rheumatoid arthritis with severe hand deformities.

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As the disease advances, imaging maps the full extent of joint involvement, uncovering subclinical inflammation undetected by symptoms alone. This is vital in complex cases with vague or overlapping symptoms. Imaging differentiates inflammatory arthritis from osteoarthritis, crystal arthropathy, or infection by highlighting specific tissue and structural changes.^[13,15]

Imaging objectively measures disease activity, tracks therapy response, and detects progression or remission early. Imaging also guides interventions like joint aspirations or injections for precision and safety.^[13,15]

Ultimately, imaging bridges the gap between surface signs and deeper joint processes, enhancing clinical judgment, clarifying uncertainty, and guiding management for patients with inflammatory arthritis.^[13,14,16]

IMAGING MODALITIES

The main imaging modalities used in the assessment of inflammatory arthritis include:

• Conventional radiography (X-ray): Conventionally, the first-line imaging tool, X-rays are useful for detecting established joint damage such as erosions, uniform joint space narrowing, and periarticular osteopenia. However, they are less sensitive in early disease and cannot visualize soft tissue inflammation.^[17]

• Ultrasound (USG): Musculoskeletal USG can detect synovitis, tenosynovitis, bursitis, and erosions with greater sensitivity than clinical examination or X-ray, especially in early disease. It also allows for dynamic assessment and can guide joint interventions. Newer techniques such as Superb Microvascular Imaging and Shear Wave Elastography further enhance its utility.^[13,16,17]

• Magnetic resonance imaging (MRI): MRI is highly sensitive for early inflammatory changes, including synovitis, bone marrow edema (an early marker of inflammation), and erosions. It provides a detailed assessment of both soft tissue and bone and is valuable in both peripheral and axial joints. Advanced MRI techniques such as quantitative MRI, T2- and T1ρ-mapping, and delayed gadolinium-enhanced magnetic resonance imaging of cartilage (dGEMRIC) are being developed to further improve diagnostic accuracy.^[13,18]

• Computed tomography (CT): CT is less commonly used but can be helpful in assessing complex bony anatomy, subtle erosions, or when MRI is contraindicated. Dual-energy CT (DECT) can detect urate crystals in gout and is an emerging tool in the evaluation of inflammatory arthritis.^[13,19]

• Emerging and metabolic imaging techniques: Techniques such as positron emission tomography (PET)/CT, multispectral optoacoustic tomography, and fluorescence optical imaging are being explored for their ability to detect metabolic and vascular changes associated with inflammation, potentially identifying disease before structural damage occurs.^[16]

IMAGING FINDINGS

The imaging findings in inflammatory arthritis follow a clear continuum, reflecting the progression of disease from early inflammation to advanced joint damage. Initially, conventional X-rays may appear normal as structural changes have not yet developed. However, imaging techniques like USG and MRI can detect early inflammatory signs such as synovial thickening, joint effusion, tenosynovitis, and bone marrow edema (on MRI) – an important marker of active inflammation and predictor of future erosions.

The European Alliance of Associations for Rheumatology-Outcome Measures in Rheumatology (EULAR-OMERACT) USG scoring system is a standardized, validated tool for assessing synovitis in patients with RA. Developed jointly by the EULAR and OMERACT, this system provides semiquantitative grades (0–3) based on two main USG features – B-mode (gray-scale, [GS]): Assesses synovial hypertrophy (thickening of the synovial membrane) and Power Doppler (PD): Evaluates synovial vascularity (blood flow/active inflammation) [Table 1 and Figure 2].^[20]

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Figure 2:

(a-b) European alliance of associations for rheumatology outcome measures in rheumatology ultrasound scoring system of: synovial hypertrophy on gray scale and synovial vascularity on power Doppler. Grade 0 to grade 3 as increasing grade of severity.

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As inflammation persists, imaging reveals synovial hypertrophy and the formation of early bone erosions, especially at joint margins. Radiographs may start to show periarticular osteopenia and joint space narrowing due to cartilage loss. With ongoing disease activity, these erosions enlarge, joint space narrowing becomes more uniform, and deformities may develop due to ligament and tendon damage.

In advanced stages, imaging demonstrates severe erosive changes, joint subluxations or dislocations, and sometimes ankylosis (joint fusion), leading to significant functional impairment.

ROLE OF IMAGING IN SUBCLASSIFYING INFLAMMATORY ARTHRITIS

Once inflammatory arthritis has been established on imaging, further subclassification relies on a careful analysis of specific radiologic features that distinguish between the major subtypes. The major subtypes have been mentioned in Table 2. The first clue often lies in the pattern of joint involvement. Symmetric involvement of the small joints of the hands and feet, particularly the metacarpophalangeal (MCP) and proximal interphalangeal (PIP) joints, is highly suggestive of RA. In contrast, an asymmetric distribution, especially if the distal interphalangeal (DIP) joints or the axial skeleton are affected, raises suspicion for the seronegative spondyloarthropathies (SpA), such as PsA or AS.

The nature and distribution of erosions provide further diagnostic clarity. Marginal erosions in small joints are a hallmark of RA, while erosions accompanied by adjacent new bone formation – such as periostitis or enthesophyte development – point toward PsA or other SpA. The presence of bone proliferation, including syndesmophytes or ankylosis, is particularly characteristic of AS and related conditions.

A key differentiating feature in SpA is enthesitis, or inflammation at tendon and ligament insertions, which is best visualized on MRI or USG. Similarly, the detection of sacroiliitis – manifested by bone marrow edema, erosions, sclerosis, or ankylosis of the sacroiliac joints – is a strong indicator of axial spondyloarthritis or AS.

Certain classic deformities also aid in subclassification. The presence of dactylitis (sausage digit) or the distinctive “pencil-in-cup” deformity is highly suggestive of PsA. Periarticular osteopenia, on the other hand, is an early and prominent feature of RA, while marked tenosynovitis and synovial hypertrophy are also more pronounced in this subtype.

By systematically evaluating these imaging features – distribution and symmetry of joint involvement, the pattern and type of erosions, bone proliferation, enthesitis, sacroiliitis, and classic deformities – radiologists and clinicians can accurately subclassify established inflammatory arthritis and guide targeted management strategies.

However, clear subclassification is not always possible. Imaging patterns often overlap, early disease may be subtle, and atypical or mixed presentations occur. In such cases, a combined approach using clinical, laboratory, and imaging data with longitudinal follow-up is essential. In addition, a variety of other systemic, autoimmune, infectious, and vasculitic disorders can also present with joint inflammation. These are outlined in Table 3, along with their typical imaging clues, to aid a broader differential diagnosis.

MEETING A FEW GIANTS

RA

RA is a chronic, systemic autoimmune disease that primarily targets the synovial joints, leading to persistent inflammation, progressive joint destruction, and significant disability if left untreated. Affecting about 0.5–1% of the adult population and presents two- to three-fold more frequently in women than in men.^[21] The hallmark of RA is symmetric inflammation of peripheral joints – most notably the radiocarpal, MCP, and PIP joints – often accompanied by systemic symptoms such as fatigue and low-grade fever.^[22]

The pathogenesis of RA involves a complex interplay between genetic susceptibility and environmental triggers, resulting in an aberrant immune response. The synovial membrane becomes infiltrated with immune cells, including T cells, B cells, macrophages, and plasma cells, which produce autoantibodies such as RF and anti-cyclic citrullinated peptide (anti-CCP) antibodies. This immune activation leads to the release of pro-inflammatory cytokines (e.g., tumor necrosis factor alpha, interleukin [IL]-6, IL-1) and destructive enzymes, driving synovial hyperplasia, pannus formation, and the eventual erosion of cartilage and bone. Over time, this process results in joint space narrowing, periarticular osteopenia, and characteristic marginal erosions visible on imaging [Figures 3 and 4].^[22,23]

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Figure 3:

Rheumatoid arthritis: (a) X-ray and (b-f) MRI images of wrist- (b and c) T1 and PDFS coronal, (d and e) T1 and PDFS axial images showing periarticular marginal erosions (white arrows in a to d) and synovitis(* in d and e) in radio-carpal and intercarpal joints and tenosynovitis of extensor tendons (arrowhead in f). MRI: Magnetic resonance imaging, PDFS: Proton density fat-saturated

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Figure 4:

Rheumatoid arthritis: USG images showing (a) synovitis in wrist joint (arrowhead), (b) marginal erosions with (c) power doppler signal suggesting neovascularization (white arrow in b and c) and (d) tenosynovitis (*) with (e) power doppler signal. USG: Ultrasonography

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In early RA, plain radiographs may appear normal or show subtle periarticular soft-tissue prominence and juxtaarticular osteopenia due to hyperemia and inflammation. The earliest specific sign is marginal erosion – a small cortical break at the “bare areas” of bone where synovium directly attaches, commonly seen at the radial aspect of the second and third metacarpal heads, base of proximal phalanges, and ulnar styloid process. Progressive inflammation causes uniform joint-space narrowing, in contrast to the asymmetric loss seen in osteoarthritis.

With chronicity, radiographs demonstrate extensive erosions, joint subluxations, and ulnar deviation of the fingers at the MCP joints. Boutonnière deformity, characterized by flexion of the PIP joint with hyperextension of the DIP joint due to central slip extensor tendon disruption, and swan-neck deformity, defined by PIP hyperextension with DIP flexion resulting from volar plate attenuation and extensor tendon imbalance, reflect advanced tendon and ligament destruction. Ligamentous laxity and carpal collapse result from progressive structural damage and altered biomechanics. Ankylosis may occur in late stages, particularly within the carpal bones, while periarticular osteopenia persists as a key distinguishing feature.

While radiography remains the cornerstone for assessing structural progression, USG and MRI enable early detection of synovitis, tenosynovitis, bone marrow edema, and small erosions before they are visible on X-rays. PD USG provides a dynamic assessment of synovial vascularity and response to therapy. Serial imaging thus plays a crucial role in disease activity scoring and monitoring therapeutic response, helping achieve treat-to-target goals.

The EULAR-OMERACT USG synovitis scoring grades GS synovitis (0–3 based on synovial hypertrophy thickness) and PD signal (0–3 for vascularity), offering bedside quantification of inflammation for treat-to-target monitoring and predicting erosive progression in daily practice, though limited by operator-dependence and restricted field-of-view for deep structures.^[24] RA MRI scoring system scores synovitis (0–3), bone marrow edema (0–10 per bone), and erosions (0–10), excelling in early structural damage detection and clinical trial endpoints but hindered by high cost, time demands, and contraindications like pacemakers.^[25,26] Quantitative MRI techniques, such as diffusion-weighted imaging for cellularity, T2 mapping for edema, and magnetization transfer for synovial proliferation, aid therapy response prediction yet face challenges from technical complexity and limited availability.^[27]

Contrast-enhanced MRI highlights synovial enhancement post-gadolinium to quantify synovitis.^[28] Dynamic contrast-enhanced (DCE)-MRI measures perfusion kinetics (e.g., K^trans for vessel permeability), helping distinguish active inflammation from fibrosis and assess early disease-modifying antirheumatic drugs (DMARD) response, though limited by contrast risks like nephrogenic systemic fibrosis and specialized software needs.^[29]

RA generally involves the small peripheral joints of the hands and feet, but axial involvement is unusual. When the spine is affected, it is almost exclusively limited to the cervical spine, particularly the atlantoaxial (C1–C2) and craniovertebral junction. Here, chronic synovitis can cause pannus formation and erosions of the odontoid process, leading to atlantoaxial instability or subluxation. Lower spine or lumbar involvement is not typical in RA and helps distinguish it from the SpA [Figure 5].^[30,31]

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Figure 5:

Rheumatoid arthritis in cranio-vertebral junction: (a and b) MRI sagittal contrast enhanced T1 fat saturated images and T1 images respectively show heterogeneously enhancing retrodental soft tissue causing adjacent bone erosions (white arrow in a and b). (c) CT axial images show erosions in the posterior aspect of anterior arch of Atlas (arrow). MRI: Magnetic resonance imaging, CT: Computed tomograpgy

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Diagnosis of RA is based on a combination of clinical features, serologic markers, and imaging findings. Early and aggressive treatment with DMARDs is crucial to control inflammation, prevent irreversible joint damage, and improve long-term outcomes. Advances in targeted therapies have significantly improved the prognosis for many patients, but RA remains a leading cause of disability and work loss worldwide.^[23]

Key classification criteria

Modified New York Criteria (1984) for AS: Radiographic sacroiliitis (bilateral grade 2–4 or unilateral grade 3–4) PLUS ≥1 clinical criterion: Inflammatory back pain ≥3 months before age 40, limited lumbar flexion, or chest expansion <2.5 cm.^[34]

Assessment of spondyloarthritis international society (ASAS) Criteria (2009) for axial SpA: Back pain ≥3 months, onset <45 years PLUS:

• Imaging arm: Sacroiliitis on X-ray/MRI short tau inversion recovery (STIR sagittal spine from C7-S1 including costovertebral/costotransverse joints + coronal oblique SI joints) + ≥1 SpA feature,^[35] OR

• Clinical arm: HLA-B27 + ≥2 SpA features (arthritis, enthesitis, uveitis, dactylitis, psoriasis, IBD, good nonsteroidal anti-inflammatory drugs response, family history, elevated CRP).^[34,36]

ASAS peripheral SpA criteria: Arthritis, enthesitis, or dactylitis PLUS ≥1 SpA feature (uveitis, psoriasis, IBD, preceding infection, HLA-B27, sacroiliitis).^[37]

AS is the prototype of axial spondyloarthritis, characterized by chronic inflammation of the sacroiliac joints and spine, resulting in pain, stiffness, and progressive ankylosis. Radiographically, the earliest finding is sacroiliitis, initially appearing as blurred joint margins, subchondral sclerosis, and small erosions, progressing to pseudo-widening and ultimately complete ankylosis. In the spine, inflammation at the vertebral corners (Romanus lesions) produces squaring of vertebral bodies and the shiny corner sign due to reactive sclerosis. With chronicity, syndesmophytes – thin, vertical, marginal ossifications bridging adjacent vertebrae – form the classic “bamboo spine” appearance. Additional features include facet joint ankylosis, costovertebral and costotransverse joint fusion, and ossification of spinal ligaments, contributing to rigidity.

In advanced AS, the combination of spinal rigidity and osteopenia predisposes to unstable fractures, particularly through the vertebral body or intervertebral disc space (carrot-stick fractures), even after minor trauma. These fractures most often occur at the lower cervical or thoracolumbar junction and may extend transversely through all three spinal columns, making them highly unstable and often associated with neurological compromise. Andersson lesions, representing discovertebral erosions or pseudoarthrosis, can also be seen in chronic cases, mimicking infection [Figure 6].^[37]

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Figure 6:

Ankylosing spondylitis: (a) Bilateral sacroiliitis in STIR coronal images with subarticular patchy bone marrow edema (white arrows). (b) Enthesitis seen in paraspinal region in STIR axial images (white arrows). (c) Bone marrow edema seen at the anterior corners of the vertebrae on T2 sagittal image (white arrows) - shiny corner sign- Romanus lesion, that is active inflammation of the entheses where annulus fibrosus attaches to the vertebral body.

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It is important to distinguish AS from diffuse idiopathic skeletal hyperostosis (DISH), which also involves spinal changes but is characterized by flowing calcification of the anterior longitudinal ligament without sacroiliac joint involvement, lacks significant inflammation, and usually occurs in older individuals with metabolic conditions like diabetes. DISH does not usually cause the inflammatory symptoms typical of AS [Figure 7].^[38]

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Figure 7:

(a) Diffuse idiopathic skeletal hyperostosis: CT sagittal reformatted image showing flowing ossification of the anterior longitudinal ligament in thoracic spine for more than four vertebral levels (white arrows). (b) Ankylosing spondylitis: X-ray lateral spine image showing ankylosis/fusion of vertebral bodies (white arrows), fusion of facet joints (—) and fusion of posterior elements of cervical spine (arrowheads).

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PsA is a seronegative spondyloarthropathy associated with psoriasis, presenting with nail changes (pitting, onycholysis), dactylitis, and erythematous scaly plaques. It may involve both peripheral joints and the axial skeleton.

Radiographically, PsA shows a characteristic mix of erosive and proliferative changes. Early disease manifests as periarticular prominence from synovial hypertrophy, periostitis, and marginal erosions near entheses. With progression, classic “pencil-in-cup” deformities, acroosteolysis, and ankylosis of small joints develop, often with asymmetric DIP involvement. Enthesitis-related periosteal new bone formation produces syndesmophyte-like spurs, while axial disease demonstrates asymmetric sacroiliitis and coarse, non-marginal parasyndesmophytes, distinct from the thin, marginal lesions of AS.

USG reveals synovial hypertrophy with PD hypervascularity, enthesitis, and paratenonitis, particularly along the extensor tendons. Erosions, enthesophytes, and peritendinous edema are commonly seen, reflecting both structural and inflammatory activity [Figure 8].^[39]

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Figure 8:

Seronegative spondyloarthitis (USG images): (a,b) Enthesitis at the insertion site of Achilles tendon with power doppler signal seen within (white arrows in a and b). (c) Paratenonitis of the extensor digitorum tendon of 4th finger (white arrow). (d,e) Synovitis in radiocarpal joint (white arrow in d) and interphalangeal joints respectively with periarticular erosions and power doppler signal (* in e). (f) X-ray hand showing new bone formation- periostitis- syndesmophyte like bony growth at enthesis (white arrows). USG: Ultrasonography

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Reactive arthritis (ReA) develops typically 1–4 weeks after a triggering bacterial infection, usually of the genitourinary or gastrointestinal tract. It classically presents as an asymmetric oligoarthritis of the lower limbs, enthesitis, conjunctivitis or uveitis, and genitourinary symptoms like urethritis. Unlike AS, ReA is often self-limited, though some cases can become chronic. ReA belongs to the SpA family due to shared HLA-B27 association and clinical manifestations despite having a post-infectious trigger [Figure 8].^[40]

Enteropathic Arthritis occurs in association with IBD (Crohn’s disease and ulcerative colitis), manifesting as peripheral or axial arthritis linked to bowel disease activity. It shares many features with AS and other SpAs but is differentiated by its gastrointestinal association and often milder spinal involvement.^[41]

SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis) is a rare autoinflammatory disorder considered within the spondyloarthritis spectrum. It typically combines musculoskeletal involvement – most often anterior chest wall pain with hyperostosis or osteitis – with dermatologic findings such as severe acne or palmoplantar pustulosis. Imaging plays a central role, as radiographs and CT reveal hyperostosis and sclerosis at the sternoclavicular region and spine, while MRI shows bone marrow edema and osteitis, often mimicking infection or metastasis. Recognition is crucial because, although it shares features with other SpA subtypes, it has a distinctive association with skin disease and a variable, relapsing course.^[42,43]

The umbrella term seronegative spondyloarthritis emphasizes that these diseases typically test negative for RF and other autoantibodies, distinguishing them from seropositive conditions such as RA. This group is subdivided into axial SpA (primarily axial skeleton involvement, including radiographic AS and non-radiographic axial SpA) and peripheral SpA (joint involvement outside the spine). Imaging, clinical features, laboratory markers, and genetic testing guide diagnosis and differentiation within this spectrum.^[41]

COMMON FEATURES AND DIFFERENTIATING POINTS

CRYSTAL DEPOSITION INDUCED ARTHRITIS

Crystal deposition-induced arthritis encompasses a group of inflammatory joint diseases triggered by the accumulation of crystals within articular and periarticular tissues. The most prevalent forms are gout, caused by monosodium urate crystals, and pseudogout, calcium pyrophosphate deposition disease (CPPD), resulting from calcium pyrophosphate dihydrate crystals. A third, less common group involves basic calcium phosphate (BCP) crystals – comprising hydroxyapatite, octacalcium phosphate, and tricalcium phosphate – which are implicated in a spectrum of disorders including hydroxyapatite deposition disease, calcific periarthritis, and destructive arthropathies such as Milwaukee shoulder syndrome. BCP crystals are also associated with calcific tendinitis and may contribute to cartilage degeneration in osteoarthritis, highlighting their dual role in both acute and chronic joint pathology.^[44,45]

Imaging is pivotal in diagnosing and managing these conditions, each showing distinct features across modalities, summarized in Table 4. In gout, conventional radiographs may initially be normal but eventually reveal classic “punched-out” erosions with overhanging edges, particularly in the first metatarsophalangeal joint and other peripheral sites. Soft tissue tophi may be visible as masses, sometimes calcified. USG is highly sensitive, demonstrating the specific “double contour sign” (urate crystal deposition on cartilage surfaces), tophi as heterogeneous hyperechoic masses, and associated synovitis or erosions. DECT uniquely identifies and quantifies urate crystals, distinguishing them from calcium deposits, making it invaluable for early diagnosis and monitoring therapy.^[46,47] MRI, while less specific, helps assess soft tissue involvement and complications such as bone marrow edema [Figure 9].^[48]

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Figure 9:

Gout USG images: (a) Synovitis with periarticular rat-bite erosions (white arrow) in first metatarso-phalangeal joint. (b) Echogenic intra-articular tophi (white arrow). (c) Intra-tendinous large tophus (white arrow) with tenosynovitis and power doppler signal (*). (d) Double contour sign of the articular cartilage (white arrows). (e) DECT image showing green coloured monosodium urate crystal depositions. USG: Ultrasonography, DECT: dual-energy computed tomography

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CPPD is characterized radiographically by chondrocalcinosis – linear or punctate calcifications in cartilage, most commonly in knees and wrists. USG enhances the detection of hyperechoic deposits within cartilage and soft tissues, often before radiographic changes appear. CT further improves sensitivity for subtle or deep calcifications. MRI mainly reveals secondary inflammatory changes rather than crystal deposits directly [Figure 10].^[45,49]

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Figure 10:

Hydroaxapatite deposition disease (HADD)- subtype of basic calcium phosphate deposition disease (BCP): (a,b) USG shoulder image showing calcific tendinitis of supraspinatus tendon seen in long axis and short axis views respectively. (c-e) MRI shoulder images - T2 and PDFS coronal respectively showing supraspinatus calcific tendinitis with a large T2/PDFS hypointense deposit (white arrows in a-e) in the supraspinatus tendon and subacromial-subdeltoid bursa with (e) associated bursitis. USG: Ultrasonography; PDFS: Proton density fat-suppressed

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BCP crystal deposition commonly affects periarticular tendons and entheses, causing calcific periarthritis and tendinitis, especially around the shoulder and less commonly around the hip joint. Radiographs show amorphous, cloud-like periarticular calcifications, while USG and CT detect hyperechoic or dense deposits in tendons and soft tissues. MRI may reveal low-signal foci corresponding to calcifications with surrounding edema. [Figure 11] Notably, enthesitis is a hallmark of BCP crystal disease and can also occur, though less commonly, in CPPD and gout, reflecting crystal deposition at tendon or ligament insertions.^[49,50]

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Figure 11:

Calcium pyrophosphate dihydrate deposition disease (CPPD): (a) Xray shoulder showing linear cloud like calcification along the rotator cuff tendons (white arrows). (b) Xray wrist showing cloud like linear calcification at the site of triangular fibro-cartilage complex (white arrow). (c) USG wrist image showing synovitis in the radio-carpal joint with echogenic deposits (white arrows) and power doppler signal. (d) CT image of wrist showing hyperdense intra-articular deposits (white arrows). (e) DECT image showing no evidence of any green monosodium urate crystals. USG: Ultrasonography, CT: Computed tomography, DECT: Dual-energy computed tomography

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ROLE OF IMAGING IN DISEASE MONITORING AND REMISSION

In addition to diagnosis, imaging plays a central role in the longitudinal monitoring of inflammatory arthritis by providing an objective assessment of disease activity, treatment response, and remission. USG and MRI allow detection of residual or subclinical synovitis, tenosynovitis, enthesitis, and bone marrow edema, often preceding clinical or serologic relapse, while serial radiographs document structural progression or stability over time.^[16,18,24] DCEMRI enables quantitative assessment of synovial perfusion and vascular permeability, helping differentiate active inflammation from fibrotic or inactive tissue and facilitating early evaluation of therapeutic response.^[29] PET/CT, by detecting increased metabolic activity, provides whole-body assessment of inflammatory burden and may be useful in complex, multisite, or research settings.^[16,17] Although these advanced techniques are currently confined to specialized centers and clinical trials, their integration with conventional imaging supports treat-to-target strategies and improves the objective definition of true imaging remission beyond clinical assessment alone.^[17,24]

CONCLUSION

Inflammatory arthritis comprises a heterogeneous group of disorders with overlapping clinical features, in which imaging plays a pivotal role in early diagnosis, accurate subclassification, and longitudinal disease assessment. Key imaging principles include the use of USG and MRI for early inflammatory changes, radiographs for documenting structural damage, and recognition of pattern-based imaging features such as joint distribution, symmetry, erosions, bone proliferation, and enthesitis. A practical stepwise approach – beginning with radiographs, followed by USG or MRI in early or equivocal disease, and problem-solving tools such as MRI or DECT when indicated – enhances diagnostic confidence. Imaging further supports disease monitoring and treat-to-target strategies by detecting subclinical inflammation and structural progression. Advanced techniques, including quantitative MRI, DCE MRI, and PET/CT, extend imaging beyond morphology to functional and metabolic assessment, particularly in selected and research settings.