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. 2024 Dec 17;63(Suppl 2):ii7–ii14. doi: 10.1093/rheumatology/keae568

Focusing on ligamentous soft tissue inflammation for the future understanding of early axial psoriatic arthritis

Kerem Abacar 1, Winston J Rennie 2, Siba P Raychaudhuri 3,4, Abhijit J Chaudhari 5, Dennis McGonagle 6,✉
PMCID: PMC12104146  PMID: 39700474

Abstract

Imaging has transformed the understanding of inflammatory and degenerative arthritis in both peripheral and axial disease. In axial inflammation, fat suppression magnetic resonance imaging (MRI) has unravelled the role of sub-fibrocartilaginous osteitis in axial spondyloarthritis and the role of peri-entheseal vertebral body osteitis and subsequent spinal new bone formation. Established or late-stage axial psoriatic arthritis (PsA) cases often exhibit impressive para-marginal or chunky syndesmophytosis on conventional X-ray that pathologically represents entheseal soft tissue ossification. However, the spinal entheseal soft tissue and contiguous ligamentous tissues are poorly visualized on MRI in subjects with early inflammatory back pain including those with axial PsA. In this article, we highlight the need for imaging modalities to discern the crucial soft tissue “ligamentous” component of axial PsA towards diagnosis, prognosis and therapy validation. We issue a clarion call to focus advanced imaging methodology on spinal ligamentous soft tissue that represents the last hidden backwater of PsA immunopathology that needs visualization to fully decipher axial PsA pathogenesis. This in combination with the existing ability to visualize ligamentous bony anchorage site osteitis is needed to define a gold standard test for axial PsA.

Keywords: early axial psoriatic arthritis, imaging, ligamentitis, soft tissue, therapy, diagnosis, osteitis

Rheumatology key messages.

  • In established axial psoriatic arthritis (PsA), para-marginal or chunky syndesmophytes are common on conventional radiography and point to prominent soft tissue ossification responses.

  • Osteitis in axial PsA is less common than osteitis in HLA-B27 positive axial inflammation including ankylosing spondylitis, but soft tissue changes are difficult to discern.

  • MRI or PET imaging has the potential to better delineate the role of soft tissue inflammation in PsA patients with axial inflammatory symptoms but much work is needed.

Introduction

A great interest has arisen in axial psoriatic arthritis (axPsA) that has been fuelled by the failure of IL-23 inhibitors in ankylosing spondylitis (AS), but clinical trial data and real-world evidence suggest that IL-23 inhibitors have a role in axPsA therapy [1–4]. Currently, expert panels, including the European League Against Rheumatism (EULAR) and the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA), recommend against the use of anti-IL-23, which can be used in peripheral PsA, in active axPsA despite this encouraging real-world evidence [4–8]. What hampers progress in this space is the inability to detect and thereby quantify axPsA on fat suppression magnetic resonance imaging (MRI) where most cases are reported to have ‘negative’ MRI scans in the face of inflammatory back pain [9].

There is no formal HLA-B27 or osteitis-centred classifications of axial PsA yet. Thus, in order to better describe the axial PsA spectrum, we first reinforce some definitions of axial spondyloarthritis (axSpA) and PsA.

  • AS: based on modified New York criteria for bilateral X-ray demonstrable sacroiliitis [10].

  • HLA-B27 positive non-radiographic axSpA: may be a forerunner of AS and is typified by diffuse bone marrow oedema on MRI.

  • HLA-B27-positive non-radiographic axPsA: Has the same imaging phenotype as HLA-B27 positive axSpA or AS with an association with diffuse bone oedema on MRI [11].

  • HLA-B27-negative axPsA: this may not be associated with bone marrow oedema on MRI. Hence, it is difficult to recognize in the early stages. Later stages show that ligamentous and entheseal ossification is common especially in the spine but not sacroiliac joints (SIJ). The focus of our article is on how to better define the latter pattern.

The predominant osteitis-centred presentation of AS has been well reviewed elsewhere [12]. The evidence that HLA-B27 defines a different entity to axPsA is also well described [11]. The strong correlation between HLA-B27 and osteitis may be explained by the relatively lower prevalence of osteitis in axial psoriatic arthritis (axPsA) and the reduced frequency of HLA-B27 positivity within this patient population. This suggests that the association between HLA-B27 and osteitis is more pronounced in conditions where the prevalence of HLA-B27 carriage is higher [11]. Moreover, we have previously highlighted that challenges in visualization of spinal soft tissue ligamentous inflammation or ‘ligamentitis’ and how such non-osteitic inflammation may underscore a substantial burden of axPsA [13]. Since most patients with chronic PsA have ligamentous soft tissue ossification on X-ray but many cases lack ligamentous insertion osteitis in early PsA, a case has been made for the importance of the ligamentous soft tissue pathology as a key early axSpA driver [13]. The purpose of this article is to delve into rudimentary spinal ligamentous anatomy and provide representative imaging of ligament related spinal pathology to better understand axPsA topography. We further discuss existing MRI technology for visualizing soft tissue pathology and potential emergent imaging using positron emission tomography/computed tomography (PET/CT) that allows the direct visualization of ligamentous soft tissue pathology towards the development of a gold standard modality to delineate axPsA.

Ligament anatomy

The spine is overrepresented with ligamentous tissues compared with the rest of the skeleton given the multiple bone-to-bone anchorage sites. There is a relative paucity of synovial joints in the spine that comprise the SIJ synovium, the facet joint synovium, the costotransverse and costovertebral joints synovium, the atlantoaxial joint and the synvial joints of Luschka in the lateral cervical spine. Many tendinous anchorage points are present in the spine with many of the tendon anchorage sites comprising small muscles. In chronic axPsA, most of the pathology occurs at the ligamentous insertions as evidenced by X-ray changes of ligamentous ossification (Fig. 1). Herein, we further focus on the role of ligaments in early axial PsA and the future need to image ligamentous soft tissue inflammatory changes.

Figure 1.

Figure 1.

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X-ray images of varying types of syndesmophytes seen in axial psoriatic arthritis patients. (A) Chunky prominent syndesmophyte at L1/L2 with mature bone proliferation and extension into the lateral paravertebral soft tissue in an HLA-B27-positive 46-year-old male with psoriasis. Note the preservation of disc space suggests that bulging of the annulus and ‘end-plate-related degenerative change’ are not the cause of extensive lateral growth. (B) A 63-year-old female with a history of skin psoriasis and HLA-B27 negative, on treatment presents with back pain and stiffness with resting pain. A single prominent syndesmophyte with a more typical ‘vertical’ growth pattern is seen at L1/L2. Note the normal sacroiliac joints on the radiograph. (C) Lateral lumbar vertebral X-ray image of a patient with axial PsA with inflammatory back pain. An example of a non-marrow-contiguous soft tissue ossification process that differs from the classic syndesmophyte. PsA: psoriatic arthritis

The anterior longitudinal ligament (ALL) runs along the anterior vertebral body from the base of the upper cervical vertebrae to the tip of the anterior coccyx and is thus a continuous structure. It tapers into the lateral vertebral body covering [14]. Ossification of the ALL as a distinct pathological process is evident on plain radiographs of diffuse idiopathic skeletal hyperostosis (DISH) that can be difficult to distinguish from axPsA and indeed there is clinical and imaging overlap in 10% of cases [15, 16]. Ossification in this topography accounts at least in part for PsA-associated lesions in established PsA that include ‘hanging syndesmophytes’, ‘chunky syndesmophytes’ and ‘para-marginal syndesmophytes’, that captures a soft tissue ossification process that is not contiguous with the bone marrow (Fig. 1) [13, 17–20].

In common with AS, ossification of the annulus fibrosis is also a ligamentous lesion that is evident in axPsA. The annulus fibrosis comprises large circumferential ligament structures or ‘the eternal enthesis’ from the cervical spine to the lumbosacral junction. In addition to a gelatinous nucleus pulposus these structures have remarkably thick fibrocartilage tissue in the annulus. Radiographic studies in axPsA often demonstrate prominent syndesmophytosis of these structures with a lateral pattern of growth and bone hyperostosis. Note in both cases the point of origin of the syndesmophyte is at the level of the end-plate although the final direction of growth maybe often parallel to the end plate (as in PsA or DISH) or perpendicular in the more classical form of syndesmophytosis as seen in AS (Fig. 1) [21].

There are several other important ligamentous structures in the spine including the posterior longitudinal ligament, the ligament flavum, the interspinous ligaments, multiple costovertebral and costo-transverse ligaments and also the supraspinal ligaments. At least on radiography as evidenced by the new bone formation in axPsA, these structures appear to be less often involved than the annulus and the ALL [22, 23]. Inflammation in these posterior elements with associated osteitis in axSpA is well recognized and compared with the ALL and annulus, soft tissue inflammation adjacent to these posterior elements is well recognized on MRI [24]. An especially interesting observation is that interspinous ligamentous soft tissue inflammation is a commonly recognized feature of acute polymyalgia rheumatica (PMR) on PET imaging, but this is less reported in SpA spectrum pathology [24–26]. The close juxta-position of these posterior element ligamentous tissue with more vascular peri-ligamentous soft tissue could be a factor in the ability to visualize soft tissue inflammation at these sites compared with the ALL or annulus fibrosis regions.

AxPsA pathology has a greater propensity for spinal involvement compared with early SIJ disease, something that can be conceptualized in relationship to sub-fibrocartilaginous osteitis that typifies sacroiliac joint inflammation in HLA-B27-positive subjects. Involvement of the SIJ is universal in AS but most cases with radiographic sacroiliitis do not progress to total spinal ankylosis [27]. Also, the earliest pathology in HLA-B27 positive axial inflammation in both AS and in HLA-B27-positive axPsA is an osteitis rather than a visible ligamentous soft tissue centric inflammatory process [11, 28]. Also, axial involvement in non-HLA-B27 axPsA appears to spare the SIJ but characteristically afflicts the spine [29]. Although desirable, the need to image SIJ ligamentous tissues in PsA is less pressing than for axial column territory involvement in PsA which is much more common (Fig. 1) [30].

Imaging spinal ligaments pre pathological ossification

On MRI ligamentous structures are inherently difficult to image due to the low water content and the restricted mobility of hydrogen atoms in the stiff ligamentous matrix. While inflammatory or degenerative changes within ligaments can be imaged in the peripheral skeleton using MRI this is down to the ability to place high-resolution coils over accessible joints [31]. However, in the spine, the ligaments are deeply seated, many are small and only large surface body coils can be used that restricts the ability of MRI to detect soft tissue pathology. Additionally, on fat saturation sequences that are designed to visualise fluid at sites of inflammation, the presence of high signal from juxta-vertebral aorta and inferior vena cava and adjacent paravertebral venous networks make the visualisation of ligament pathological changes difficult. The soft tissue oedema lesions reported in axial disease may occur within ligamentous but also typically merge into the peri-ligamentous soft tissue that is more vascular.

Soft imaging: MRI examples

Thus far MRI has been transformative in describing axial disease, but the vast majority of validated scoring pertains to osteitis lesions alone with little focus on soft tissue scoring. The exception to this is the description of soft tissue inflammation in the CanDen scoring system [32]. We provide images of soft tissue inflammation most of which are not formally included in MRI scoring systems in subjects with axPsA or axial SpA. However, it is first important to recognize that many subjects with axPsA also have osteitis or osteitis may be the only visible lesion (Figs 2 and 3). Paravertebral soft tissue change may be adjacent to the ALL and vertebral bodies may only be evident in the most lateral slices and can be difficult to differentiate from adjacent venous structures on MRI (Fig. 2). It is also evident that the soft tissue inflammation may be situated between the annulus and the ALL (Fig. 2) and be associated with the full gamut of other recognized SpA changes including corner fatty lesions and corner osteitis. However, compared with HLA-B27-positive AS or HLA-B27-negative axPsA, bone marrow oedema lesions are much less common [11].

Figure 2.

Figure 2.

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Extensive soft tissue inflammatory changes in the anterior soft tissue structures and fatty changes with syndesmophyte formation. (A and B) T1-weighted and corresponding short tau inversion recovery (STIR) para-sagittal, far lateral images thorough the thoracic spine in a 50-year-old male, HLA-B27 positive with psoriasis and inflammatory back pain. There is extensive soft tissue inflammatory change in the anterior lateral paravertebral tissues T8/9 and T9/10 (white arrows—2nd at T9/10), between the equatorial segmental spinal veins. Note the extreme lateral sequences may be the only images to demonstrate these changes and are critical for adequate assessment of extra osseous soft tissue changes seen in psoriatic axSpA. There is also soft tissue inflammation and osteitis of the transverse process at T3 on the left. (C and D) T1W central-sagittal and corresponding STIR thorough the mid-thoracic spine in a 50-year-old male with psoriatic arthritis. This demonstrates inflammatory ligamentitis along the deep fibres ‘trunk’ of the anterior longitudinal ligament annulus (white arrows on STIR image). This soft tissue inflammation is also associated with osteitis (arrow in panel D). On the corresponding TIW imaging, the ligament anchorage ‘roots’ of the vertebral bodies—anterior longitudinal ligament annulus early corner fatty lesions (arrows in C) and early syndesmophyte formation (D)

Figure 3.

Figure 3.

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Lateral band of anterior longitudinal ligament soft tissue inflammation and Andersen lesions detected on MRI. (A and B) A 28-year-old male patient with psoriasis and inflammatory back pain and HLA-B27 positive. (A) White block arrow denotes extensive psoriatic soft tissue inflammation in peri-facetal left L2/3 region which is rich in ligaments and entheseal attachments. Note the Andersen’s central end-plate erosion with bone marrow oedema at the same level (short arrow). (B) Interspinous ligament inflammation C6/7 (White block arrow). (C and D) Short tau inversion recovery (STIR) images through mid-thoracic spine—a central STIR sagittal slice through the thoracic spine demonstrates central band of the anterior longitudinal ligament inflammation (short white arrow). There is lateral band of anterior longitudinal ligament soft tissue inflammation (long white arrows in D). Costovertebral osteitis is also shown in D (short white arrow in D)

Figure 3 has four panels all of which show soft tissue inflammation. Figure 3A demonstrates perifacetal soft tissue oedema and facetal bone oedema. Figure 3B illustrates prominent interspinous ligamentous soft tissue oedema without osteitis at that level (Fig. 3B). Finally, Fig. 3C and D shows marked anterior vertebral region oedema and also posterior element costovertebral region osteitis. Figure 4 also shows anterolateral vertebral body soft tissue inflammation in subjects with PsA in addition to costovertebral osteitis. Figure 4C–F shows similar anterior soft tissue changes in a subject where CT demonstrates an early syndesmophyte again illustrating the importance of the soft tissue.

Figure 4.

Figure 4.

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Soft tissue inflammation, costovertebral junction inflammatory changes and oedema corresponding to ligamentous soft tissue undergoes ossification without bone marrow oedema. (A and B) A 36-year-old HLA-B27-negative male patient with inflammatory back pain. In consecutive parasagittal slices, there are paravertebral soft tissue inflammation (arrows in A) and costovertebral junction osteitis and other inflammatory changes (arrows in B). (C–F) A 50-year-old male patient with inflammatory back pain without psoriasis or SpA-associated clinical features. The CT scan shows early syndesmophyte formation at the L2–3 level. The corresponding MRI scan demonstrates oedema corresponding to the ligamentous soft tissue that is undergoing ossification but without bone marrow oedema

More extensive vertebral body imaging with coronal, axial imaging and novel sequences or wider coverage with sagittal imaging or contrast use may help better delineate these soft tissue changes better going forward. Additionally, in Fig. 5, it can be seen that the soft tissue involvement in the axPsA patient regressed with treatment. Therefore, soft tissue involvement in axPsA and its resolution with therapy is something that could ascertained with MRI in future studies.

Figure 5.

Figure 5.

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Soft tissue involvement regressed after treatment in psoriatic arthritis patient. The soft tissue involvement circled in the upper row (A and B), detected on MRI in the psoriatic arthritis patient, decreased after treatment, as shown in the lower row (C and D)

Positron emission tomography/computed tomography

PET has demonstrated the capability to probe molecular and metabolic targets along the proliferative-inflammatory cascade of autoimmune diseases [33], including PsA [34–36]. When combined with X-ray CT, which provides correlative anatomical information, and the radiotracer [18F]-Fluorodeoxyglucose ([18F] FDG), which images altered glucose metabolism and thus inflammation, PET/CT has emerged as an imaging modality that allows for direct interrogation of soft tissue and entheseal activity in PsA [35, 37, 38].

The recent advent of total-body PET/CT scanners has further advanced the field, with tangible benefits for PsA. These systems capture the entire body (therefore, the whole spine) in a single field-of-view, at a high spatial resolution (<3 mm), and they can do this within a scan time of 20-min or less and at ultra-low dose [34, 35]. With these aforementioned imaging characteristics, these scanners provide the opportunity to assess total spinal inflammatory load in PsA, while emphasizing regional ligamentous pathology (Fig. 6). These benefits could be capitalized upon to potentially define a soft tissue phenotype for PsA, and hence differentiate it from AS. Conventional PET, despite limitations in field-of-view and sensitivity compared with total-body PET, has been integrated with MRI, enhancing the value of the latter by providing the capability to quantify the cellular activity of pathologies of interest in arthritis imaging, such as oedema [39, 40].

Figure 6.

Figure 6.

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Ligamentous involvement in PsA via [18F] FDG PET/CT. (A–D) (A) Magnified coronal CT and (B) fused [18F] FDG PET/CT sections demonstrating radiotracer uptake at some components of the cruciform ligament around the atlanto-axial joint (B, arrows). The CT component showed no corresponding changes at these sites. (C and D) Magnified coronal views of the same joint in the same subject demonstrating ossification of the anterior atlanto-occipital membrane and plausibly the anterior longitudinal ligament (C, arrowheads), with corresponding activity on the fused [18F] FDG PET/CT images (D, arrowheads). Study participant was a 42-year-old man with PsA. (E and F) Sagittal section through the CT scan (left) and fused [18F] FDG PET/CT image (right) of a 33-year-old male PsA patient acquired using a total-body PET/CT scanner. Images demonstrate marked supra- and interspinous ligament involvement at the C6/C7 and L5/S1 levels (arrows). Elevated radiotracer uptake was also noted at ligamentous sites in the upper and mid-thoracic levels (arrowheads). The corresponding CT images (bone window) demonstrated no abnormality. FDG: [18F]-fluorodeoxyglucose

Future directions

While it is well recognized that a significant proportion of axPsA cases exhibit spinal bone marrow oedema, there remain numerous instances in which these lesions are absent. The challenge in visualizing soft tissue abnormalities in symptomatic axPsA patients is likely a key factor contributing to the lack of positive imaging findings in such cases. This suggests that limitations in current imaging modalities may obscure underlying pathology, rather than an absence of inflammatory activity. Herein we have emphasized the soft tissue ligamentous changes in the spine in axPsA as depicted on fat suppression MRI and FDG PET. Imaging outcomes need to systematically evaluate soft tissue changes in axPsA including an evaluation of MRI contrast agents and machine learning approaches.

It is possible that artificial intelligence and machine learning applied to spinal CT may be useful in extracting information about ligamentous thickening and early ossification or dual-energy CT may have a role in the evaluation of inflammatory changes. In the case of PET imaging, novel contrast agents including fibroblast activation protein might have a role for fibroblast imaging [41]. Finally, careful evaluation of age-related changes and other diseases that lead to imaging changes in the spine also needs consideration including osteoarthritis, DISH and PMR in order to better define the role of imaging towards the development of an imaging gold standard biomarker for axPsA.

Conclusions

We believe that a dichotomous classification of axial pathology as predominantly bone based (AS-like) or more soft tissue centric (PsA like) exists and the purpose of this article is to highlight the evolving role of imaging in telling both apart. This model appears to be supported by translational therapeutics where blocking of IL-23 in myeloid red marrow that is afflicted in AS was not linked to efficacy in AS [42]. We believe that the key to unlocking the spinal pathology in axPsA is the recognition of the importance of soft tissue ligamentous centric pathology following by concerted imaging efforts to better define such pathology.

Acknowledgements

Authors SPR and AJC would like to thank Dr Yasser Abdelhafez of the University of California, Davis for his help with creating the PET/CT images used in this article. DM work is funded by the Leeds NIHR Biomedical Research Centre.

Contributor Information

Kerem Abacar, NIHR Leeds Biomedical Research Centre, Chapel Allerton Hospital, Leeds Teaching Hospitals NHS Trust and Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK.

Winston J Rennie, Department of Radiology, University Hospitals of Leicester, Leicester Royal Infirmary, Leicester, UK.

Siba P Raychaudhuri, Department of Internal Medicine—Rheumatology, University of California Davis, Sacramento, CA, USA; Northern California Veterans Affairs Medical Center, Mather, CA, USA.

Abhijit J Chaudhari, Department of Radiology, University of California Davis, Sacramento, CA, USA.

Dennis McGonagle, NIHR Leeds Biomedical Research Centre, Chapel Allerton Hospital, Leeds Teaching Hospitals NHS Trust and Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK.

Data availability

No new data were generated or analysed in support of this article.

Author contributions

K.A., W.J.R., S.P.R., A.J.C. and D.M. conceived of the manuscript concepts and manuscript structuring. K.A., W.J.R., S.P.R., A.J.C. and D.M. wrote the manuscript.

Funding

No specific funding was received from any bodies in the public, commercial or not-for-profit sectors to carry out the work described in this article.

Disclosure statement: D.M. has received grant funding and honoraria from Abbvie, Janssen, Lilly, Novartis, and UCB. K.A. is funded by Amgen under the PARTNER fellowship program. All other authors declare no competing interests.

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