PsO is a chronic skin disease affecting approximately 3% of the global population, and PsA develops in roughly 20–30% of patients with PsO over time [14]. Numerous studies have investigated the transition from PsO to PsA, leading to the introduction of the concept of the ‘PsD continuum’—a progressive model of disease development that mirrors the paradigm established for RA [15, 16].

In this framework, PsA is not typically viewed as the sudden onset of inflammatory arthritis but rather as a dynamic continuum that begins with a preclinical phase characterized by immune dysregulation and subclinical inflammation. This may progress through a symptomatic subclinical stage, where symptoms, such as arthralgia, fatigue, or stiffness, emerge before evolving into clinically apparent PsA.

International rheumatology organizations, including the European Alliance of Associations for Rheumatology (EULAR), have outlined three distinct phases in the transition from PsO to PsA [17, 18]:

1.

The increased risk phase: This phase involves individuals with PsO who have additional risk factors, such as genetic predispositions (e.g., familiarity and specific HLA alleles) as well as obesity, nail PsO, and extensive skin involvement. These factors contribute to a long-term risk of developing PsA, which typically manifests 7–12 years after the onset of PsO.

2.

The subclinical phase: Characterized by imaging-detected musculoskeletal inflammation and/or arthralgia, this phase represents a short-term risk of PsA, generally up to 1–3 years.

3.

The clinical phase: Involves individuals with PsO and clinically evident synovitis. They should be considered to have PsA, when alternative diagnoses are excluded.

While progression generally increases through these stages, it is not always linear. For instance, some individuals with PsO and arthralgia may experience symptom regression, while others may develop symptoms even as imaging abnormalities resolve.

A deep understanding of this continuum is essential not only for unravelling the pathogenesis of PsA but also for identifying individuals at high risk [19]. Early identification of these subjects is paramount, as it opens the door to preventive strategies, ranging from lifestyle modifications to pharmacological interventions, that could potentially delay or even prevent the onset of PsA in at-risk populations [20, 21].

Within the pre-clinical context, ultrasound plays a crucial role in detecting subtle signs of musculoskeletal inflammation in areas that are difficult to assess clinically, including the distal interphalangeal (DIP) joints of the hands and toes, pulleys, and small tendons (Fig. 1).

Fig. 1

Ultrasound detection of subclinical inflammation in patients with psoriasis at risk of psoriatic arthritis. Legend. (a) Synovitis in the distal interphalangeal joint (DIP) joint of the finger with synovial hypertrophy and power Doppler signal (dorsal longitudinal scan); the image also shows enthesitis of the tendon insertion into the distal phalanx with entheseal power Doppler signal. (b) Grey-scale transverse volar scan of the A1 pulley demonstrates severe thickening with hypoechoic appearance, accompanied by Power Doppler (b’) signal. (c) Grey-scale image of tenosynovitis in the flexor tendons of the 2nd toe with synovial hypertrophy and active inflammation (the latter demonstrated by the presence of power Doppler signal) (c’) (volar transverse scan). Acronyms: dip: distal interphalangeal; et: extensor tendon; fft: finger flexor tendons; tft: toe flexor tendons

Several studies have highlighted the utility of ultrasound for detecting subclinical inflammation in PsO patients [22]. A seminal study by Gisondi and colleagues demonstrated subclinical enthesopathy in patients with PsO, reporting significantly higher Glasgow Ultrasound Enthesitis Scoring System (GUESS) scores— an ultrasound based validated tool for assessing enthesitis—in asymptomatic PsO patients compared with healthy controls (HCs) (p < 0.001) [23]. Subsequently, another study found that 85% of PsO patients showed signs of synovitis versus 55% of HCs, with active synovitis observed exclusively in the PsO group (27.5% vs. 0%, p = 0.01) [24]. A further study comparing PsO with arthralgia (PsOAr), asymptomatic PsO, and HCs reported higher rates of ultrasound-detected tenosynovitis in PsOAr patients (29.5%) than in asymptomatic PsO (5.3%) or HCs (3.5%) (p < 0.01) [25].

Longitudinal studies suggest that ultrasound-detected inflammation may predict PsA development. In a two-year prospective study of 109 PsO patients and 90 HCs, ultrasound-detected synovitis and enthesitis were significant predictors of PsA (p < 0.001) [26]. Similarly, higher baseline GUESS scores were associated with concomitant synovitis and an increased risk of progression to PsA [27]. In a study of 102 patients (54 with PsOAr and 48 with PsO), those with active enthesitis detected by ultrasound at baseline were significantly more likely to develop PsA over an average follow-up of 309 days (p = 0.03) [25]. Baseline synovitis or tenosynovitis scores, however, did not correlate significantly with PsA progression. Alongside imaging findings, clinical features also showed strong predictive value, particularly when combined with ultrasound data. In a longitudinal study of 384 PsO patients followed for a mean of 33.0 ± 20.9 months, subclinical PsA, as defined by arthralgia, conferred a markedly higher risk of progression compared with PsO alone (hazard ratio [HR] = 11.7; 95% confidence interval [CI]: 1.57–86.7; p = 0.016), highlighting the importance of emerging musculoskeletal symptoms in PsA prevention [28].

Despite evidence of increased subclinical inflammation in PsO patients compared to HCs, its implications for disease progression and management are still unclear. More robust prospective studies are needed to determine whether ultrasound-detected abnormalities can reliably predict PsA progression. The recent EULAR points to consider highlight the critical role of imaging, particularly ultrasound, in detecting early musculoskeletal changes, such as synovio-entheseal abnormalities, which are hallmark indicators of PsA [17]. However, the task force cautions against using imaging alone to guide treatment in asymptomatic individuals, as such abnormalities are also common in healthy subjects. The 2023 guidance further recommends regular imaging surveillance in PsO patients with additional risk factors, such as nail involvement, obesity, or extensive skin disease, to support proactive risk management [17].

An emerging area of research investigates the role of ultrasound in identifying PsO patients who should be referred to rheumatology (e.g., primary care, dermatology clinic), often the first point of care for patients transitioning from PsO to PsA. One study compared three triage methods for PsO patients with arthralgia: physiotherapist evaluation, targeted musculoskeletal ultrasound of symptomatic joints and entheses, and PsA screening questionnaires. Combining targeted ultrasound with one of the other modalities yielded the best discriminative performance (AUC > 0.75) [29]. Similar positive results were observed when ultrasound was used in a dermatology setting [30, 31]. Overall, these findings suggest that integrating targeted ultrasound into triage strategies can enhance referral accuracy, optimizing early detection while minimizing unnecessary rheumatology consultations.

Ultrasound in the Diagnosis of PsA

In clinical practice, ultrasound is valuable in the early diagnostic assessment of PsA, particularly in patients with suspected or subclinical disease, especially since delayed diagnosis is linked to radiographic progression and poorer outcomes [5, 32]. At PsA onset, the most common presentation pattern is peripheral arthritis, predominantly oligo-arthritis (mean number of clinically swollen joints ranging from 1.5 to 3.2) [3, 4, 18].

Various studies on early PsA (disease duration < 1–2 years) have demonstrated the higher sensitivity of ultrasound compared to clinical examination in detecting synovitis and enthesitis: subclinical synovitis was reported in up to 76% of patients with early PsA, while entheseal abnormalities with PD signal were found in 5%–14% of cases [33,34,35]. These findings highlight the crucial role of ultrasound in detecting subclinical inflammation and in the comprehensive assessment of early PsA.

Joint erosions are common even in the early stages of PsA, indeed they are detected via ultrasound in 23%–33% of patients, especially in the wrist, second metacarpophalangeal joint, and fifth metatarsophalangeal joint [36]. High-resolution ultrasound allows visualization of millimetric cortical breaks, providing sensitive detection of early structural damage and informing timely management decisions (Fig. 2). Several studies have demonstrated the higher sensitivity of ultrasound compared to X-rays in detecting erosions, although most of this evidence comes from RA patients. X-rays may remain advantageous in certain areas where the ultrasound acoustic window is limited, such as the midfoot or posterior joints [37], highlighting the complementary roles of ultrasound and X-rays in early structural damage assessment in PsA.

Fig. 2

Ultrasound detection of early erosive changes in psoriatic arthritis. Legend.(a) Image showing multiple millimetric bone erosions (callipers) at the lateral aspect of the second metacarpophalangeal joint (longitudinal lateral view). (b) A “hot” bone erosion with a cortical break filled with synovial pannus (longitudinal lateral view). (c) Grey scale and (c’) power Doppler images showing close contact between synovial pannus and cortical bone with evident irregularities of the cortical bone (longitudinal dorsal view). (d) Grey scale and (d’) power Doppler images of the third proximal interphalangeal joint showing a “hot” bone erosion and active synovitis (longitudinal dorsal view). Acronyms: et: extensor tendon; it: interosseous tendon; mcp: metacarpophalangeal; pip: proximal interphalangeal

One study examined the benefit of incorporating ultrasound into the Classification Criteria for Psoriatic Arthritis (CASPAR). It involved 126 patients with PsO from a Danish nationwide cohort, assessing 48 joints and 12 entheses per patient using ultrasound. Results showed that integrating sonographic findings into the CASPAR criteria significantly improved PsA classification: 66% of patients were classified as PsA when combining CASPAR and ultrasound, compared to only 35% using clinical CASPAR criteria alone and 52% of cases using ultrasound alone [38]. These data highlight both the sensitivity of ultrasound and the importance of combining clinical and sonographic assessments for early diagnosis.

Differential diagnoses of PsA can be complex, particularly when distinguishing PsA from conditions such as fibromyalgia and osteoarthritis (OA). A cross-sectional study of 848 PsO patients referred for rheumatological evaluation revealed that only 14% were diagnosed with PsA, while 37% had nonspecific arthralgia, and 49% received alternative diagnoses, predominantly OA (44%) and fibromyalgia (41%) [39]. A prospective study of 156 PsA patients, including 42 with coexisting fibromyalgia, evaluated disease activity using both clinical composite scores, such as Composite Psoriatic Disease Activity Index (CPDAI), Disease Activity index for Psoriatic Arthritis (DAPSA), and Psoriatic Arthritis Disease Activity Score (PASDAS), and comprehensive ultrasound assessment of 52 joints, 40 tendons, and 14 entheses. Patients with PsA and concomitant fibromyalgia had significantly higher clinical scores, suggesting greater disease activity, but their ultrasound scores were similar to those without fibromyalgia. Ultrasound findings correlated with clinical indices in PsA patients without fibromyalgia, but not in those with it, demonstrating that ultrasound provides a more objective measure of true inflammation and helps distinguish PsA from overlapping pain syndromes that can inflate clinical assessments [40].

OA, especially its erosive form, may also mimic PsA, particularly when affecting the proximal and distal interphalangeal joints [4]. Ultrasound may detect inflammatory features such as synovitis or erosions within a single affected joint; however, this alone cannot reliably distinguish OA from PsA. The distinction becomes clearer when evaluating other joints and entheses: PsA typically shows patterns of inflammation such as enthesitis, tenosynovitis, dactylitis, and peritendinitis at sites beyond the initially affected joint, which are generally absent in OA. Importantly, although ultrasound cannot definitively differentiate PsA from OA, detecting inflammatory signs or central bone erosions in OA—particularly in its erosive form—may have implications for disease management, including the consideration of conventional disease-modifying anti-rheumatic drugs (DMARDs) in more inflammatory cases [41].

Although PsA and RA share features such as synovitis, ultrasound can help differentiate them by evaluating the pattern and distribution of inflammation. In RA, synovitis is generally a primary, intra-articular process, whereas in PsA it is considered to arise from entheseal inflammation, consistent with the “synovio-entheseal complex”. Extra-synovial manifestations, such as enthesitis, tenosynovitis, and peritendinitis, are more common in PsA and provide important distinguishing clues. These lesions frequently occur at mechanically stressed sites, including annular pulleys, extensor tendons, and adventitial bursae, which have fibrocartilaginous structures similar to entheses [42]. Flexor tendon tenosynovitis is the second most frequent ultrasound finding in PsA after synovitis, and although peritendinitis of the finger extensor tendon is less common, it is considered relatively specific for PsA [43, 44]. By assessing both intra-articular and extra-synovial involvement, ultrasound offers an objective, non-invasive method to distinguish PsA from RA, even when synovitis appears morphologically similar in both conditions [45, 46].

Crystal-induced arthritis should also be considered in the differential diagnosis of PsA, particularly because both conditions often present with mono/oligoarthritis. Ultrasound has demonstrated excellent ability in diagnosing crystal-induced monoarthritis, thus aiding in the differential diagnosis from other types of arthritis. In a recent study in patients with acute mono/oligoarthritis, ultrasound findings showed specificity > 90% and good sensitivity for both gout and crystal pyrophosphate deposition disease (CPPD) using a targeted scanning protocol of two joints bilaterally (gout: knee and first metatarsophalangeal joint; CPPD: knee and wrist) in addition to the symptomatic joint, achieving overall diagnostic accuracy greater than 90% for both conditions [47]. The differential diagnosis between PsA and gout remains challenging, especially as many studies have reported cases in which the two conditions coexist (referred to as “Psout”) [48]. Hyperuricemia is indeed more common in patients with PsO or PsA compared to the general population. The presence of hyperuricemia in PsA patients could potentially influence patient characteristics and treatment outcomes, but stronger data is needed to confirm this relationship [49, 50]. Similarly, in patients with polyarticular involvement, where clinical distinction between PsA and crystal-induced arthritis may be particularly difficult, ultrasound is extremely helpful, as it can visualize urate (or CPPD deposits) and distinguish between the two conditions, with very important implications for patient management (Fig. 3).

Fig. 3

Ultrasound in the differential diagnosis of psoriatic arthritis. Legend. A man was referred to rheumatology with polyarticular joint pain and swelling. He had a previous diagnosis of gout (serum urate <400 µmol/L on allopurinol 300 mg/day) and a family history of PsO, raising suspicion for PsA. No cutaneous tophi were present. (a–c, d) Dorsal longitudinal images of the metacarpophalangeal region showing hyperechoic deposits within and adjacent to the extensor tendon and over the proximal phalanx, consistent with monosodium urate (MSU) crystal deposition, including cloud-like deposits (outlined in white in figure a) and small urate aggregates, which are pointed out by arrows in b and c. Dorsal longitudinal images of the metacarpophalangeal joints demonstrate intra-synovial MSU crystal aggregates (arrows in d), intra-tendinous and peri-tendinous deposits (e) and crystal deposition along the cartilage surface consistent with a double contour sign (f). Acronyms: et: extensor tendon; mcp: metacarpophalangeal; pp: proximal phalanx

Finally, it is important to acknowledge that entheseal ultrasound abnormalities may be influenced by non-inflammatory factors. Obesity, increasing age, and metabolic comorbidities such as diabetes mellitus and hypercholesterolaemia are associated with a higher prevalence of entheseal structural changes, including enthesophytes, which may confound interpretation in PsA and PsO [51,52,53]. In addition, recent mechanical loading and physical exercise can transiently increase PD signal at entheses [54]. These factors highlight the need to interpret entheseal ultrasound findings within the broader clinical and metabolic context, particularly when assessing subclinical disease or differential diagnoses.

New Insights into the Ultrasound Assessment of Enthesitis in PsA

Enthesitis—inflammation at sites where tendons, ligaments, or joint capsules insert into bone—is a hallmark feature of spondyloarthritides (SpA), including PsA [55].

In PsA, enthesitis plays a central role in disease pathophysiology and is closely linked to clinical symptoms and long-term outcomes, with prevalence estimates ranging from 35% to 74%, depending on diagnostic criteria and study populations [56,57,58]. Clinically, enthesitis typically manifests as persistent pain, stiffness, and functional impairment, significantly affecting quality of life and frequently guiding therapeutic decisions, including escalation to biologic therapies when conventional treatments are insufficient [59, 60].

Traditionally, assessment relies on physical examination using standardized scoring systems such as the Leeds Enthesitis Index (LEI) and the Maastricht Ankylosing Spondylitis Enthesitis Score (MASES) [61, 62]. However, these methods are limited by their reliance on subjective pain, which can be influenced by mechanical factors or conditions such as fibromyalgia, making it challenging to distinguish true inflammatory enthesitis from non-inflammatory causes of pain. Over the past two decades, ultrasound has emerged as a sensitive, non-invasive, and dynamic tool for entheseal evaluation, providing detailed visualization of both anatomy and pathology [11, 63]. Several ultrasound scoring systems, including GUESS, the Madrid Sonographic Enthesis Index (MASEI), and GRAPPA-based methods, have been developed to standardize imaging assessment across different entheses and lesion types [64].

The OMERACT ultrasound task force further refined definitions of key lesions, distinguishing features of active inflammation, such as entheseal thickening, hypoechoic areas, and PD signal, from structural damage, including enthesophytes, calcifications, and bone erosions [65]. Enthesitis is defined as a hypoechoic and/or thickened tendon insertion within 2 mm of the cortical bone, with PD signal if inflamed, whereas structural lesions reflect chronic or prior disease. Thickening and hypoechoic changes are not entirely specific to inflammatory disease and may be observed in fibromyalgia, OA, obesity, or physically active individuals [12]. Moreover, reliability of certain features can vary, as shown in web-based scoring exercises, highlighting the importance of standardized training and reference image atlases [66].

Ultrasound has been shown to help differentiate inflammatory enthesitis from other causes of tenderness. In the ULISSE study, clinical examination identified enthesitis in 92% of patients with fibromyalgia; however, ultrasound findings were more specific for PsA-related enthesitis, with only 75% showing both tenderness and ultrasound-detected entheseal involvement [67].

The Defining Enthesitis on Ultrasound in Spondyloarthritis (DEUS) initiative evaluated the reliability and clinical relevance of the OMERACT lesions of enthesitis, and developed the DEUS Enthesitis Index (DEI), a combined clinical-ultrasound scoring system [68]. DEUS studies demonstrated that features such as PD signal and bone erosions strongly distinguish SpA-related enthesitis from mechanical or fibromyalgia-related tenderness, with the Achilles tendon identified as the most discriminative enthesis in over 400 SpA patients and nearly 300 disease controls [69]. An example of active, erosive enthesitis of the Achilles tendon in a patient with PsA is shown in Fig. 4.

Fig. 4

Ultrasound detected enthesitis in psoriatic arthritis. Legend. (a) Image showing active, erosive enthesitis at the calcaneal insertion of the Achilles tendon. Note the presence of entheseal thickening, hypoechoic areas (outlined by white line), and power Doppler signal at the enthesis, including filling of cortical bone erosions pointed out by arrows (dorsal longitudinal view). Acronyms: at: Achilles tendon; cal: calcaneal bone

DEUS also highlighted marked discordance between clinical and ultrasound findings, with approximately 70% of clinically tender entheses showing no ultrasound evidence of active inflammation, and around 15% of non-tender sites demonstrating subclinical disease [70]. This discordance may reflect differences in tissue biology, whereby pain at the enthesis can arise from mechanical load or microdamage in a structure with limited vascularity, meaning that symptoms and inflammatory activity may not fully overlap, in contrast to the synovium in RA. In addition, these observations underscore that clinical signs may be influenced by mechanical factors or central sensitization, whereas ultrasound can detect subclinical disease that may be clinically relevant and guide treatment strategies.

Recognizing the complementary strengths of clinical and imaging assessments, the DEI was the first tool designed to combine both modalities for the evaluation of enthesitis [71]. The DEI assesses five key lower-limb entheses bilaterally, scoring each site for clinical tenderness and ultrasound-detected lesions to generate a total score ranging from 0 to 20. This composite approach allows the DEI to capture both patient-reported symptoms and objective imaging findings, correlating with markers of disease activity, structural damage, and systemic inflammation. By integrating these dimensions, the DEI provides a more comprehensive and reliable measure of enthesitis than either clinical or imaging assessment alone. Its sensitivity to change, however, still requires further demonstration in longitudinal studies.

Beyond active inflammation, ultrasound assessment of structural damage provides insight into SpA phenotypes. DEUS studies showed a high prevalence of enthesophytes, calcifications, and erosions, with distinct patterns in PsA versus axial SpA [72]. Enthesophytes were most common in PsA and associated with clinical enthesitis and PsO, erosions reflected inflammation-driven disease, and calcifications correlated with age and metabolic comorbidities. These findings highlight the potential of ultrasound-detected lesions to inform disease severity and phenotypic stratification in SpA.

Ongoing studies, such as the DUET project, are further exploring these findings, aiming to improve ultrasound standardization and establish its potential use in clinical practice, ensuring more precise and consistent assessment of enthesitis in SpA patients [73]. In addition, increasing attention has been directed toward assessing smaller entheses, particularly those in the hands, which will be discussed in a dedicated paragraph.

Patients with established PsAAssessing Response to Therapy

Ultrasound is a sensitive tool for evaluating therapeutic response in patients with established PsA. Studies consistently demonstrate that ultrasound can detect changes very early after treatment initiation, sometimes within the first week, and that these changes correlate with improvements in patients treated with DMARDs [74,75,76,77,78]. In one study including 25 patients (9 with PsA and 16 with SpA), ultrasound detected significant improvements in both the MASEI and OMERACT PD scores at three- and six-month follow-up [