Ultrasound findings in finger flexor tendons in systemic sclerosis: A cross-sectional pilot

study

Michael Hughes1, 2, Joanne Manning3, Tonia Moore3, Ariane L Herrick2,4 and Sarang Chitale1,5

1. Department of Rheumatology. Wrightington, Wigan & Leigh NHS Foundation Trust,

Wigan, UK.

2. Centre for Musculoskeletal Research, The University of Manchester, Salford Royal

NHS Foundation Trust, Manchester Academic Health Science Centre, Manchester,

UK.

3. Department of Rheumatology, Salford Royal NHS Foundation Trust, Salford, UK.

4. NIHR Manchester Biomedical Research Centre, Manchester University NHS

Foundation Trust, Manchester Academic Health Science Centre, UK.

5. Edge Hill University, Omskirk

Corresponding author:

Dr Michael Hughes PhD MRCP (UK) (Rheumatology)

ORCID ID: 0000-0003-3361-4909

Consultant Rheumatologist

Department of Rheumatology, Royal Hallamshire Hospital, Sheffield Teaching Hospitals NHS

Foundation Trust, Sheffield, UK.

Michael.hughes-6@postgrad.manchester.ac.uk

Telephone: +44 (0)114 271 1900

Word count = 1777/2000.

Key words: Systemic sclerosis; Scleroderma: Ultrasound; Flexor tendon; Pulley, Calcinosis.

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Abstract (n=265)

Objective: Finger flexion contractures are an important cause of disability in patients with

systemic sclerosis (SSc); however, their pathophysiology is poorly understood Our aim was

to assess feasibility of scanning finger flexor tendons in patients with SSc and explore the

ultrasound findings in these tendons, including measurement of finger flexor tendon

complex (FFTC).

Methods: Grey Scale and Power Doppler ultrasound assessment of the FFTC including

tendon structure and surrounding soft tissue. Measurements of the FFTC (A1 pulley, tendon

and palmar plate) were made. Feasibility was assessed by the number of fingers which could

be measured.

Results: We studied the second to fifth flexor tendons (n=160) of both hands in 20 patients

with SSc, including early and established disease. We were able to assess the FFTC and make

measurements of the flexor tendon and palmar plate in all (n=40) and A1 pulley in almost all

(n=39) of the studied fingers. Common pathologies identified included peritendinous (n=12)

and soft tissue (n=8) calcification. Tendon thickening was seen in 6 patients, but

synovitis/tenosynovitis was rare. The A1 pulley was thickened in patients with SSc

(0.46mm), in particular, those with diffuse cutaneous SSc (0.50mm).

Conclusion: We were able to successfully assess, including making measurements of, the

FFTC in patients with SSc. Our study showed calcifications in the peritendinous areas and

soft tissue and thickening of the A1 pulley. These findings may play a role in the

pathophysiology of SSc-hand contractures by causing mechanical impingement of the finger

flexion mechanism. This pilot study will guide future research to look for potential

(treatable) causes of finger flexion contractures in patients with SSc.

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Introduction

Finger flexion contractures are an important cause of disability in many patients with

systemic sclerosis (SSc); however, the pathophysiology behind these is poorly understood. In

some patients, finger flexion contractures can progress very quickly (i.e. over months rather

than years) and may persist even in later disease when the skin may atrophy. Previous

studies [1–4] using ultrasound (US) and magnetic resonance imaging (MRI) have

demonstrated evidence of synovitis and tenosynovitis (both have a reported frequency of

up to 50 %) [1,2], including erosive disease in patients with SSc. Whether inflammation is

important in the development of contractures in SSc is currently unknown. In addition,

calcinosis is common in patients with SSc, and this could also have a potentially contributory

role in the development of hand deformities/contractures in SSc.

Against this background, the primary aim of our study was to determine the feasibility of

assessing the finger flexor tendon complex (FFTC) in patients with SSc and a broad spectrum

of both disease duration and subtype. Our secondary aim was to describe ultrasonographic

findings of the FFTC, including measurements of the A1 pulley, flexor tendon and palmar

plate in patients with SSc.

Material and Methods

Study design

We examined the FFTC in 20 patients (160 fingers) with SSc and a spectrum of both disease

subtype and duration. Patients with SSc were recruited from a UK tertiary referral centre. All

patients had a confirmed diagnosis of SSc and fulfilled the American College of

Rheumatology/ European League Against Rheumatism classification criteria [5]. Our study

design sought to include 10 patients with ‘early’ and 10 patients with ‘late’ SSc, where

‘early’ SSc was defined as ≤ 5 years from the onset of skin thickening. Within both groups we

sought to include equal numbers of patients with both limited and diffuse cutaneous SSc

(lcSSc and dcSSc) [6]. Key exclusion criteria included patients with diabetic

cheiroarthropathy and a history of extensive hand surgery including sympathectomy (as

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these can cause hand contractures), known overlap inflammatory arthritis, and significant

hand contracture where the probe could not make physical contact with the hand to

perform the scan. Baseline clinical and demographic data were collected. SSc-related hand

involvement was assessed by the finger to palm distance (FPD) (measured in mm) and mean

finger Rodnan skin score (mRSS), the latter of which is scored between 0 (not involved) and

3 (severe thickening). The study was approved by the North of Scotland Research Ethics

Service (REC reference – 17/NS/0061) and all patients signed informed consent.

Ultrasound assessment and measurement of the FFTC

Ultrasound was performed by a Rheumatologist/Ultrasongrapher (SC) with over 10 years’

experience of musculoskeletal ultrasound, and who was blinded to the clinical findings (i.e.

ultrasonographer did not know whether patient had limited or diffuse, early or late disease,

and any other disease-related characteristics). Logic E (GE®) portable US machine with a

high-frequency (8-18 MHz) hockey stick probe was used to perform the study scans. The

second to fifth flexor tendons in both hands were assessed on the volar aspect in the

longitudinal view, from just proximal of the metacarpophalangeal (MCP) joint to the

insertion distal to the distal interphalangeal (DIP) joint, including the proximal

interphalangeal (PIP) joint. The patients were scanned in a ‘neutral’ position as discussed

below. Grey-scale assessment was performed looking at tendon structure, tenosynovitis,

calcification, joint (MCP/PIP/DIP) abnormalities. Any abnormalities of the flexor tendon

were confirmed in a cross-sectional view. Whereas, any joint abnormalities were confirmed

using a dorsal longitudinal scan.

Measurements were performed of the third (middle) finger (as this is the finger commonly

used to measure finger to palm distance) at the level of the MCP joint for: 1. A1 pulley, 2.

Flexor tendon, 3. palmar plate. The pulley was measured at the widest/thickest portion.

Feasibility was assessed by the number of fingers which could be measured. Doppler US was

performed if there was grey-scale evidence of tenosynovitis and/or synovitis, which was

graded semi-quantitatively (0-3), using a well-validated scoring system [7,8]. In brief, 0= no

synovitis, 1= mild synovitis not extending beyond the joint line, 2= extending the joint line

but concave, and 3= extending the joint line and bulging upwards. Examples of normal

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tendon structure and measurement of the FFTC are provided in Figure 1. The soft tissue

structure was also assessed during the scans (e.g. for the presence of calcification).

Normal values (mean, SD) for the thickness of the A1 pulley have been previously published

[9] in healthy controls in both ‘neutral’ and ‘hooked’ (akin to contracted SSc fingers) grip

positions: 0.38 (0.15) and 0.37 (0.15) mm, respectively [8] and these ‘hooked’ values were

used in our study for comparison with SSc patients.

Statistical analysis

Data are presented as descriptive statistics. Where appropriate, the mean values of the right

and left hands were used in the analysis. For ultrasonographic assessment of the FFTC, we

provide the number of patients with that finding (e.g. tenosynovitis) and the maximum

number of fingers (in at least one patient) which were involved.

Results

Study population

The demographic and clinical characteristics of the patients are provided in Table 1.

Assessment of feasibility of assessing the FFTC by US

We were able to assess the FFTC and make measurements of the flexor tendon and palmar

plate in all (n=40) the studied fingers. The A1 pulley could be measured in almost all

(n=39/40) of the studied fingers.

Ultrasongraphic assessment of the FFTC

Any thickening of the finger tendons (by visual inspection, including hypoechogenicity within

the tendon fibres), and on direct measurement was observed in 6 patients (30%) (maximum

number of fingers involved in any patient =6). Tenosynovitis was rare (n=2, 10%) (maximum

of 2 fingers). Tendon calcification was seen in over half (n=12, 60%) (maximum of 3 fingers)

of patients. Osteoarthritis was present in a quarter (n=5) of patients (maximum of 3 fingers).

Synovitis was rare (n=3, 15%) (maximum of 3 fingers) and was low-grade (grade 1) in the

majority of joints (grade 2 in one PIP joint only). Almost half of patients had evidence of

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minor joint effusion particularly in PIP joints on grey scale (n=8, 40%) (maximum of 7

fingers), which was not clinically relevant. Joint calcification was seen in 6 patients (30%)

(maximum of 3 fingers). Soft tissue calcification was observed in 8 patients (40%) (maximum

of 6 fingers). Example images of abnormal tendon structure including thickening of the FFTC,

as well as tendon and soft tissue calcification, are provided in Figure 1.

Measurement of the FFTC

Measurements (A1 pulley, tendon and palmar plate) of the FFTC are presented in Table 2.

The mean (SD) measurement of the A1 pulley was 0.46 (0.13) mm and was higher in

patients with dcSSc compared to lcSSc, but similar in those with early and late disease.

Mean (SD) tendon measurement was 3.5 (0.04) mm, and with no important differences

between patients with lcSSc and dcSSc or early or late disease. Mean (SD) palmar plate was

2.9 (0.5) mm and with no important differences between patients with lcSSc and dcSSc or

early and late disease.

Discussion

To our knowledge this is the first study to explore abnormalities of finger flexor tendons as a

potential cause for finger flexion contractures. This study demonstrated the feasibility of

studying the FFTC complex with ultrasound, with measurements possible in almost all

patients with SSc.

Over half of patients had evidence of tendon calcification. Furthermore, around half of

patients had evidence of soft tissue calcification and a number of patients also had joint

calcification. Active tenosynovitis/synovitis with Doppler was rare. In this study, the A1

pulley was thickened, in particular, in dcSSc.

The A1 pulley is an important mechanism of the flexor apparatus of the digit and has been

reported to be involved (thickened) in patients with trigger finger [9,10]. Therefore, focal

abnormality (including through enlargement) of the A1 pulley could result in progressive

impingement and with eventual persistent sticking/failure of the FFTC.

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It is important to highlight that the presence of tenosynovitis and inflammatory arthritis in

our cohort was lower than has been previously reported [3,12]. For example, in our previous

study, which included 17 patients with SSc and with no known overt inflammatory arthritis,

at baseline and 6 months, tenosynovitis was seen in 46% and 47% of patients, and synovitis

in 6% and 23% [3]. This may be explained by the fact that in the previous study [3] we

studied patients with small joint arthralgia. In our current study, the presence of minor joint

effusion was observed in around half of patients, which is in keeping with a previous Italian

study in which joint effusion was found in 49% (n=45) of patients as assessed by US [1]. The

role of inflammatory tendon disease in SSc requires further investigation, as this may also

contribute to the development of hand contractures (e.g. through fibrosing stenosing

tenosynovitis).

Our study has a number of important limitations. This was a cross-sectional study with the

primary aim to determine the feasibility of US to assess the FFTC in SSc. Although the

patient sample size was limited, we examined patients with a wide spectrum of disease. In

this study, we did not include a healthy control (comparator) group and used previously

published values (normal and abnormal) for the A1 pulley.

In future studies, larger numbers of patients, including specific patient subgroups, in

particular, early dcSSc should be studied, including longitudinal assessment of the FFTC. It

will also be important to include patients with contractures, so see whether measurements

are feasible in the presence of contractures. In our study, we chose pragmatically to study

the index to ring fingers inclusive, and performed measurements only of the middle (3 rd)

finger FFTC as this finger is commonly used to calculate FPD. However, in future studies, the

thumb should also be assessed as this may be an important determinant in predicting future

hand function and disability. Furthermore, the extensor finger tendons should also be

examined as these might also have an important role in the development of hand

contractures. In future research, a matched control group should be used including to

define normal/abnormal values of the tendon and palmar plate. Intra- and inter-observer

reproducibility should also be assessed.

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In conclusion, this study shows that calcification of both tendon and soft tissue is common in

patients with SSc, and also thickening of the A1 pulley. Inflammatory joint and tendon

disease was rare. We propose that soft tissue calcification and A1 pulley thickness should

be assessed in future studies as potential non-inflammatory causes of finger flexor

contractures. Longitudinal studies are required to further examine the role of these

local/mechanical factors in the development of hand contractures in SSc. Better

understanding of the pathophysiology of finger flexion deformities may, in the future,

inform new treatment approaches.

Conflicts of interest: None.

Acknowledgement: This study was supported by the NIHR Manchester Biomedical Research

Centre.

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musculoskeletal ultrasonography detect and characterize covert inflammatory

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(2003) Interobserver agreement in ultrasonography of the finger and toe joints in

rheumatoid arthritis. Arthritis Rheum 48: 955–62.

8. Scheel AK, Hermann K-GA, Kahler E, et al (2005) A novel ultrasonographic synovitis

scoring system suitable for analyzing finger joint inflammation in rheumatoid arthritis.

Arthritis Rheum 52: 733–43.

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tendon between in neutral and in flexed positions of trigger finger. Open Orthop J 10:

36–40.

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fingers. J Ultrasound Med 27: 1407–13.

11. Tinazzi I, McGonagle D, Aydin SZ, Chessa D, Marchetta A, Macchioni P (2018) “Deep

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Sex (F:M) 15:5

Age in years (Mean, SD) 54.2 (15.2)

Diagnosis (n) lcSSc: dcSSc 11:9

Early: late 10:10

RP duration (mean, SD) (years) 11.9 (8.8)

Disease duration, from first non-RP clinical manifestation) (mean, SD)

(years)

9.6 (9.5)

SSc-associated

autoantibodies (n)

Anticentromere 6

Anti-Scl-70 6

Anti-RNA polymerase III 4

SSc-related hand

involvement (n)

Finger mRSS (mean, SD) 1.8 (1.8)

Finger to palm distance in mm (mean, SD) 11 (20)

Organ complications (n) Pulmonary fibrosis 5

Pulmonary hypertension 1

Drug therapies (n) Oral vasodilators (CCBs) 14 (13)

Immunosuppression 1

Previous hand surgery (n) 4

Table 1: Demographic and clinical characteristics of the 20 patients. Disease subtype as

defined by LeRoy et al [6]. Finger modified Rodnan skin score (mRSS) data are presented as

the mean of both fingers (range 0 to 3). lcSSc and dcSSc: limited and diffuse cutaneous SSc;

CCBs: calcium channel blockers; SSc: systemic sclerosis.

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Measurement All SSc Subset Disease

duration

Comparative

values from [8]

lcSSc dcSSc Early Late

A1 Pulley 0.46

(0.13)

0.41

(0.12)

0.50 (0.15)

0.43

(0.14)

0.48

(0.12)

0.37

(0.15)

Tendon 3.5

(0.04)

3.6

(0.6)

3.5

(0.4)

3.5

(0.6)

3.6

(0.5)

-

Palmar plate 2.9

(0.5)

2.8

(0.5)

2.9

(0.6)

2.9

(0.6)

2.9

(0.3)

-

Table 2. Measurement of the FFTC. Data are presented as the mean (SD) for all the studied

patients and by disease/subset disease duration. Previously published normal values for the

A1 pulley are provided for comparison [8]. lcSSc and dcSSc: limited and diffuse cutaneous

SSc.

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Figure 1: FFTC assessment including measurement by US in patients with SSc. Panoramic

view of a normal (A) Finger Flexor tendon (FFT) (arrowheads) and demonstrating extra-

tendinous soft tissue calcification (B) (arrows). Normal transverse view (C) of the FFTC

identifying the flexor tendon and proximal phalynx (PP). Tendon intrasubstance (D), soft

tissue (D), and next to the finger flexor tendon (E) calcification. Measurement of the pulley

(F) (enlarged), finger flexor tendon and palmar plate. DIP: Distal interphalangeal. MCP:

metacarpophalangeal. PIP: proximal interphalangeal.

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