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Objectives: Although joint swelling is traditionally interpreted as synovitis, recent imaging studies showed that there is also inflammation of tenosynovium and intermetatarsal bursae in the forefoot. We aimed to increase our understanding of differences and similarities regarding forefoot involvement between ACPA-positive and ACPA-negative rheumatoid arthritis (RA) at diagnosis. Therefore, we (1) compared metatarsophalangeal (MTP) joint counts, walking disabilities and inflamed tissues between ACPA groups and (2) studied associations of joint swelling/tenderness and walking disabilities with underlying inflamed tissues within ACPA groups., Methods: 171 ACPA-positive and 203 ACPA-negative consecutively diagnosed patients with RA had a physical joint examination (swollen joint count-66/tender joint count-68), filled a Health Assessment Questionnaire including the domain walking and underwent MRI of the MTP joints at diagnosis. Synovitis, tenosynovitis, osteitis and intermetatarsal bursitis (IMB) were assessed. Findings in age-matched healthy controls were applied to define abnormalities on MRI., Results: While ACPA-negative RA patients had more swollen joints (mean SJC 8 vs 6 in ACPA-positives, p=0.003), the number of swollen MTP joints was similar (mean 1 in both groups); walking disabilities were also equally common (49% vs 53%). In contrast, inflamed tissues were all more prevalent in ACPA-positive compared with ACPA-negative RA. Within ACPA-positive RA, IMB was associated independently with MTP-joint swelling (OR 2.6, 95% CI 1.4 to 5.0) and tenderness (OR 3.0, 95% CI 1.8 to 5.0). While in ACPA-negatives, synovitis was associated independently with MTP-joint swelling (OR 2.8, 95% CI 1.4 to 5.8) and tenderness (OR 2.5, 95% CI 1.3 to 4.8). Tenosynovitis contributed most to walking disabilities., Conclusions: Although the forefoot of ACPA-positives and ACPA-negatives share clinical similarities at diagnosis, there are differences in underlying inflamed tissues. This reinforces that ACPA-positive and ACPA-negative RA are different entities., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Interosseous tendon inflammation (ITI) has been described in rheumatoid arthritis (RA). Whether ITI occurs in at-risk individuals before the onset of clinical synovitis is unknown., Objectives: To investigate, by MRI, ITI in anti-cyclic citrullinated peptide (CCP)-positive at-risk individuals (CCP +at risk) and to describe the anatomy, prevalence and clinical associations across the RA continuum., Methods: Hand MRI was performed in 93 CCP + at risk, 47 early RA (ERA), 28 established 'late' RA (LRA) and 20 healthy controls (HC) and scored for ITI, flexor tenosynovitis (TSV) and RA MRI scoring at the metacarpophalangeal joints (MCPJs). Cadaveric and histological studies were performed to explore the anatomical basis for MRI ITI., Results: The proportion of subjects with ITI and the number of inflamed interosseous tendons (ITs) increased along the disease continuum (p<0.001): 19% of CCP +at risk, 49% of ERA and 57% of LRA had ≥1 IT inflamed . ITI was not found in any HC. ITI was more frequently identified in tender MCPJs compared with nontender MCPJs (28% vs 12%, respectively). No IT tenosynovial sheath was identified in cadavers on dissection or histological studies suggesting MRI findings represent peritendonitis. Dye studies indicated no communication between the IT and the joint., Conclusions: ITI occurs in CCP + at-risk individuals and can precede the onset of clinical synovitis. The ITs may be important nonsynovial extracapsular targets in the development and progression of RA., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives: To use high-resolution imaging to characterise palindromic rheumatism (PR) and to compare the imaging pattern observed to that seen in new-onset rheumatoid arthritis (NORA)., Methods: Ultrasound (US) assessment of synovitis, tenosynovitis and non-synovial extracapsular inflammation (ECI) was performed during and between flares in a prospective treatment-naive PR cohort. MRI of the flaring region was performed where possible. For comparison, the same US assessment was also performed in anticyclic citrullinated peptide (CCP) positive individuals with musculoskeletal symptoms (CCP+ at risk) and patients with NORA., Results: Thirty-one of 79 patients with PR recruited were assessed during a flare. A high frequency of ECI was identified on US; 19/31 (61%) of patients had ECI including 12/19 (63%) in whom ECI was identified in the absence of synovitis. Only 7/31 (23%) patients with PR had synovitis (greyscale ≥1 and power Doppler ≥1) during flare. In the hands/wrists, ECI was more prevalent in PR compared with NORA and CCP+ at risk (65% vs 29 % vs 6%, p<0.05). Furthermore, ECI without synovitis was specific for PR (42% PR vs 4% NORA (p=0.003) and 6% CCP+ at risk (p=0.0012)). Eleven PR flares were captured by MRI, which was more sensitive than US for synovitis and ECI. 8/31 (26%) patients with PR developed RA and had a similar US phenotype to NORA at progression., Conclusion: PR has a distinct US pattern characterised by reversible ECI, often without synovitis. In patients presenting with new joint swelling, US may refine management by distinguishing relapsing from persistent arthritis., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

Objectives The objective of this paper is to perform an ultrasonography (US) analysis of hands and wrists in two groups of patients with systemic lupus erythematosus (SLE), with and without Jaccoud's arthropathy, matched by age and disease duration and to correlate them with levels of CXCL13 clinical features, laboratory tests and disease activity score. Methods Sixty-four patients with SLE were enrolled, 32 with and 32 without Jaccoud's arthropathy. Each patient underwent physical examination, laboratory tests (including CXCL13 by ELISA) and bilateral US. Synovial hypertrophy, tenosynovitis and erosions were evaluated according to a semiquantitative grading system with a 0-3 rating. US findings were correlated with serum levels of CXCL13, other serological parameters and disease activity index. Results Synovitis was found in 25/64 patients (39%) and tenosynovitis in 14/64 (22%). These findings were more frequent in SLE patients with Jaccoud's arthropathy, particularly tenosynovitis ( p = 0.002) and synovitis ( p = 0.01). Median serum level of CXCL13 was 20.16 pg/ml in the whole population (23.21 pg/ml in the Jaccoud's arthropathy group and 11.48 pg/ml in the group without). There was an association between the presence of disease activity and high level of CXCL13 ( p = 0.004). However, no association was found between high levels of CXCL13 and "arthritis" in SLEDAI, swollen joints on physical examination or synovitis on US. Conclusions US findings in joints of SLE patients with Jaccoud's arthropathy confirm that synovitis and tenosynovitis are common in these patients. In addition, serum level of CXCL13 is associated with disease activity in SLE but does not seem to be a biomarker for arthritis in these patients.

Background: Scedosporium apiospermum, which can usually be isolated from soil, polluted stream water and decaying vegetation, is increasingly recognized as an opportunistic dematiaceous fungus. The mortality rate of infection in immunocompromised hosts is over 50%. S. apiospermum is commonly responsible for dermal and epidermal infections (i.e., mycetoma) after traumatic penetration., Case Presentation: A 73-year-old woman was admitted to our hospital complaining of painful swelling and tenderness on the dorsum of the proximal left wrist and hand. The symptoms had persisted for approximately 2 months. A physical examination revealed a 4 x 3 cm, poorly defined, erythematous papule, which was fluctuant, with pustules and crusts on the dorsum of the left hand., Conclusions: We report a very rare case of tenosynovitis caused by S. apiospermum infection. We identified the infectious agent via molecular DNA sequencing. The infectious agent was initially misidentified as an Alternaria species by microscopic examination with lactophenol cotton blue (LPCB) staining. The infection was successfully treated with debridement and adjuvant fluconazole therapy.

An immune reconstitution syndrome (IRS) occurs in between 10% and 25% of patients starting highly active antiretroviral treatment (HAART). A 49-year-old patient presents a tenosynovitis 6 weeks after HAART initiation. In our patient, exhaustive tests for infectious, inflammatory and drug-related causes of tenosynovitis were negative. The improvement obtained with high-dose Non-steroidal anti-inflammatory-drug (NSAID) therapy and the patient's immunovirologic profile, supported a diagnosis of tenosynovitis associated with immune reconstitution, a form of IRS that has not previously been described. This original case increase the broad spectrum of inflammatory rheumatologic disorders associated with HIV infection.

Objective: To assess the value of gray-scale ultrasound (US), color Doppler ultrasound (CDUS), contrast-enhanced CDUS, and magnetic resonance imaging (MRI) in the diagnostic evaluation of the hands in patients with remitting seronegative symmetrical synovitis with pitting edema (RS3PE)., Methods: Eight patients (5 men, 3 women; mean +/- SD age 69.3 +/- 7.2 years) with clinical diagnosis of RS3PE syndrome underwent US, CDUS, contrast-enhanced CDUS, and MRI. US was performed with a linear array transducer operating at 12 MHz. The US contrast agent (SHU 508; Levovist, Schering, Germany) was intravenously infused in a concentration of 300 mg/ml at a rate of 1 ml/minute., Results: All patients showed symmetric subcutaneous edema and synovitis of tendons and finger joints on both US and MRI. Vascularity was detected subcutaneously in tendon sheaths and in the joint synovia on CDUS and MRI. Detection of increased vascularity was improved after contrast administration compared with unenhanced CDUS (P < 0.01)., Conclusion: Ultrasound, CDUS, contrast-enhanced CDUS, and MRI are valuable tools in the diagnostic evaluation of involved anatomic structures in patients with RS3PE. Contrast-enhanced CDUS is superior to CDUS in assessment of inflammatory edema, effusion, and synovitis.

Avian leukosis virus subgroup J has a high tropism for myeloid lineage cells and frequently induces neoplastic transformation of myelocytes. The impact of congenital avian leukosis virus subgroup J infection on the function of circulating heterophils and susceptibility to staphylococcal infection was investigated. Six-week-old broiler chickens negative for exogenous avian leukosis viruses or congenitally infected with avian leukosis virus subgroup J were inoculated intravenously with 10(6) colony-forming units of Staphylococcus aureus, and pre- and postinoculation heterophil function was assessed. All chickens developed a leukocytosis with heterophilia after inoculation, but total leukocyte and heterophil counts were significantly higher in leukosis-negative chickens than in virus-infected chickens. Tenosynovitis was more severe in leukosis-negative chickens, and 2/10 (20%) of the virus-infected chickens had no histologic evidence of tenosynovitis. Osteomyelitis in the tibiotarsus or tarsometatarsus developed in 5/10 (50%) of the chickens in each group. S. aureus was recovered from the hock joint of 6/10 (60%) of the chickens in each group. Heterophils from all chickens exhibited similar phagocytic ability pre- and postinoculation. Heterophils from virus-infected chickens exhibited less bactericidal ability preinoculation than did heterophils from leukosis-negative chickens. However, postinoculation bactericidal ability was similar in both groups. Avian leukosis virus subgroup J provirus was present in heterophils isolated from congenitally infected chickens. Heterophils isolated from broiler chickens congenitally infected with avian leukosis virus subgroup J exhibit no significant functional deficits, and infected and uninfected chickens exhibit similar susceptibility to staphylococcal infection.

Avian reoviruses are ubiquitous among poultry flocks. Although infection is usually present without disease, reoviruses may occasionally be involved in several disease syndromes of which viral arthritis/tenosynovitis in chickens is the most important, particularly in broiler breeds. While reoviruses have been isolated from turkeys and several other species of birds with various conditions, the presence of the virus has been conclusively linked with disease in relatively few instances. In chickens in particular, avian reoviruses with a wide spectrum of pathogenic capability have been isolated and several antigenic types exist. Diagnosis is dependent on the detection of the virus in clinical samples, although the presence of the virus does not necessarily confirm that this is the cause of the disease, except where reoviruses are detected in affected joints. Serological tests are usually difficult to interpret in view of widespread and frequently harmless reovirus infection. The principal approach to control of viral arthritis/tenosynovitis is by vaccination using attenuated vaccines in young birds, followed by inactivated preparations for breeders intended to protect chicks by maternal antibodies. Many vaccines are based on the S1133 strain isolated in the United States of America, but these may not be effective against antigenic variants.

A matched case-referent study was undertaken to assess whether rheumatoid factor (RF) is associated with repeating tenosynovitis or peritendinitis and whether HLA-B27 predisposes to epicondylitis. The study subjects consisted of 25 workers in manually strenuous jobs with a history of at least two episodes of tenosynovitis or peritendinitis in the wrist or forearm, or humeral epicondylitis, and their matched referents. The latex agglutination test was positive in seven of the 23 cases with tenosynovitis and in one of the referents (p = 0.03). The corresponding figures for IgM-RF by enzyme immunoassay were ten and two, respectively (p = 0.008). HLA-B27 antigen was found in five of the 13 workers with epicondylitis and in one worker with no such history (p = 0.13). It is possible that RF-positive repeating tenosynovitis represents an incomplete form of rheumatoid disease.

Data that are relevant to the general understanding of the juvenile-onset spondyloarthropathies are reviewed here. Seronegative enthesopathy and arthropathy syndrome is considered the earliest recognizable form of juvenile-onset spondyloarthropathy, from which other syndromes and diseases emerge. The group also includes juvenile-onset ankylosing spondylitis, a disease defined in adult-based terms when definite changes have occurred in the axial joints; ankylosing tarsitis, a complex disorder in which foot problems resemble those of the spine in ankylosing spondylitis; Crohn's disease and ulcerative colitis-related peripheral and, especially, HLA-B27 axial disease; reactive arthritis and Reiter's syndrome, which might be further classified according to its cause; and juvenile psoriatic arthritis, a disease that resembles juvenile rheumatoid arthritis more than does juvenile-onset spondyloarthropathy.

Heterophil function was evaluated in 16 healthy chickens and in 46 chickens with experimentally induced staphylococcal tenosynovitis. In paired blood samples, heterophils from chickens with tenosynovitis had a significant increase in adherence, chemotaxis, phagocytosis, and bacterial killing of Staphylococcus aureus compared to heterophils from healthy chickens. The percent adherence of heterophils to nylon fiber columns increased significantly from a 78.4% mean +/- 6.6% standard deviation to 87.6% +/- 3.2% after induction of staphylococcal tenosynovitis. Heterophil movement following in vitro exposure to saline or endotoxin was increased in chickens with tenosynovitis; 3 +/- 1 heterophils/0.25 mm2 to 10 +/- 6 heterophils/0.25 mm2 and 136 +/- 29 heterophils/0.25 mm2 to 340 +/- 74 heterophils/0.25 mm2, respectively. Endotoxin-activated serum was chemoattractive for heterophils from all chickens. Flow cytometry was used to define the heterophil population on light scatter histograms, evaluate individual cell phagocytosis of latex beads, and quantitate the number of beads phagocytosed per heterophil. When incubated with increased numbers of beads, only heterophils from chickens with tenosynovitis phagocytosed higher numbers of beads. At heterophil to bead ratios of 1:10, the percentage of heterophils that phagocytosed beads increased from baseline values of 37.8% +/- 9.0% to post-infection values of 67.3% +/- 7.5%. Using 1:20 heterophil to bead ratios, heterophil phagocytosis increased from 38.7% +/- 9.9% to post-infection values of 79.8% +/- 7.3%. Heterophils from all chickens were able to phagocytose and kill log phase staphylococcal bacteria. After phagocytosis, the heterophils from chickens with staphylococcal tenosynovitis rapidly decreased the number of viable bacterial colony forming-units per milliliter by approximately one log.(ABSTRACT TRUNCATED AT 250 WORDS)

Immunization of breeder chickens by eyedrop with viral arthritis/tenosynovitis vaccine strain S1133 (73rd egg passage) gave no immunity against day-old oral challenge of their progeny at 1 week postvaccination of the breeders, but progeny immunity was observed at 3, 4, 5, 6, and 7 weeks postvaccination of the breeders. Oral cross-challenge of immune progeny with viral isolates from Connecticut, West Virginia, California, Indiana, Pennsylvania, and Minnesota showed that in vitro neutralization of an isolate by anti-S1133 antiserum correlated with in vivo immunity of the progeny against oral day-old challenge with such an isolate.

A crystallizing IgG-lambda cryoprotein was found in the synovial fluid of a patient with peripheral erosive arthritis and tenosynovitis. The same crystallizing paraprotein could be demonstrated in serum incubated at 4 degrees C, but its formation could be inhibited by the in vitro addition of D-penicillamine. Crystals were present in synovial tissue and appeared to be initiating an inflammatory reaction via complement activation. Slit lamp examination showed crystals in Bowman's membrane. Plasmapheresis led to temporary improvement in the synovitis and tenosynovitis.

Fifty-seven patients with arthritis associated with non-gonococcal genital infection have been studied. Synovitis characteristically affected one or a few joints, expecially the knee, ankle or metatarsophalangeal joints and was accompanied by tenosynovitis and enthesopathies--each in about one third of the patients. A quarter of the patients had ocular, cutaneous, or mucous membrane lesions (Reiter's syndrome). Although six patients developed a chronic or relapsing course, average duration of the acute episode in the majority was three to five months. Available evidence strongly suggests that infection following sexual intercourse, usually but not always with a new partner, was instrumental in the initiation of the disease. We have suggested the term 'sexually acquired reactive arthritis (SARA)' to emphasize the mode of acquisition of the disease, and note that similar syndromes are seen associated with gut infection. We consider that usage of the term Reiter's syndrome is correctly applied to only those cases which exhibited the characteristic triad of urethritis, arthritis and conjunctivitis with or without other cutaneous and mucous membrane lesions. Thirty-six of the 54 patients who were HLA typed (67 per cent) possessed the antigen HLA-B27. Of 30 who presented directly to a rheumatology unit 25 (82 per cent) were HLA-B27 positive. The other 24 patients initially attended a venereology clinic and only 11 (46 per cent) of these bore the antigen. This appears to reflect disease severity, HLA-B27 positive patients having a significantly longer duration of disease symptoms and a higher frequency of extra-articular manifestations, than those lacking this antigen.

A viral agent that was isolated from livers of commercial turkey poults that died at approximately two weeks of age was characterized as a reovirus. Experimental infection of day-old chickens with this reovirus isolate resulted in the development of tenosynovitis, hepatitis, and myocarditis. In vitro neutralization of the turkey reovirus isolate by antiserum against chicken reovirus correlated with in vivo protection of maternally immune chickens from day-old oral challenge with the turkey reovirus isolate.

Three patients with IgG (kappa) paraproteinaemia in association with inflammatory polyarthritis are described. Two of the patients had an erosive deforming arthritis, and the third had a non-erosive arthritis and necrotizing vasculitis. Possible aetiological relationships between the paraproteinaemia, arthritis and vasculitis are discussed.

The effect of cyclosporine A on reovirus-infected male broiler chickens was studied. Beginning at 1 or 10 days of age, 3 groups of 15 broilers were injected in the pectoral muscle with 50 mg of cyclosporine A (CSA) in oil per kg body weight every 3 days until 28 days. Controls were injected with olive oil. Two CSA-injected groups and one untreated group were orally infected with 1000 TCID50 of reovirus at 1 day of age. Cell-mediated immunity was evaluated at 17 and 24 days by a delayed-wattle-response test to injected phytohemagglutinin (PHA-M). Cyclosporine A and reovirus significantly (P less than 0.001) depressed the wattle response following the first injection of PHA-M but not the second. At necropsy 28 days postinoculation (PI), no gross lesions were apparent. Histologic lesions in birds infected with reovirus were lymphocytic pericarditis and tenosynovitis; synovial cells were hyperplastic, and heterophils and fibrin were in synovial spaces. Thymic medullary diameters were significantly (P less than 0.001) smaller in all CSA-treated birds. Although CSA suppressed cell-mediated immunity somewhat, there were no apparent differences in severity of microscopic lesions among reovirus-infected groups.

Previously untreated chicks and those treated neonatally with either cyclophosphamide (CY) or infectious bursal disease virus (IBDV) were subcutaneously inoculated with viral arthritis virus ( VAV ) to determine whether suppression of humoral immunity would affect VAV pathogenicity. No difference was apparent in the disease process that occurred in the immunosuppressed versus the nonimmunosuppressed chickens. However, in the immunosuppressed birds, VAV was recovered from the heart and tendon tissues earlier in the postinoculation (PI) period. Also, VAV inoculated immunosuppressed birds carried higher levels of serum gamma globulins at certain PI intervals than the VAV inoculated positive controls or the untreated negative control chickens. It is suggested that the suppression of the bursa of Fabricius (BF) by CY or IBDV did not interfere in the antibody production to VAV , but the antibody produced was qualitatively defective.

Two viruses serologically related to the tenosynovitis virus of chickens were isolated from two flocks of turkeys experiencing outbreaks of tenosynovitis. Both viruses produced a tenosynovitis when injected into the foot pad of young turkeys. Staphylococcus aureus was not isolated from either flock, nor was there any evidence of Mycoplasma synoviae antibody in either flock.

Rabbits were first immunized and later challenged with the same antigen (bovine serum albumin, or ferritin) by injection into the tibialis anterior tendon. Inflammatory changes of the tenosynovium and epitenon included infiltration by neutrophils (early) and mononuclear cells (later) over a 6-week course of tenosynovitis. A pattern of antigen entrapment in the tendon together with immunoglobulin was shown by use of radiolabelled antigen and immunochemical staining. Half-life of antigen in the tissues averaged 5 days over the 6-week period. Changes in the epitenon included cellular necrosis, appearance of phagocytic cells, and disruption of the collagen matrix. Tissues of control animals (challenged without prior immunization) showed minimal changes and significantly less retention of antigen (P greater than 0.005). The model is relevant to the mechanism of tendon damage associated with antigen-driven chronic inflammation, as may be the case in rheumatoid arthritis.

The cellular immune responses of 12 patients with culture-proved Mycobacterium marinum infection involving deep tissues were studied. Of the 12 patients, 11 failed to respond to M. marinum antigens. All of the patients had, however, normal blastogenic responses to concanavalin A, phytohemagglutinin, pokeweed mitogen, and the antigens tetanus toxoid and Candida albicans. In contrast, 9 of 14 healthy fishermen responded to the M. marinum antigens with significant in-vitro blastogenesis. Infection of deep tissues with M. marinum is associated with antigen-specific T-cell anergy to M. marinum antigens.

When chicks with maternal antibodies against infectious tenosynovitis (viral arthritis) virus were inoculated orally at 1 day old with tenosynovitis virus, they were protected against developing active tenosynovitis lesions 3 weeks later. They were not protected against subcutaneous inoculation, however. Breeder vaccination against tenosynovitis resulted in immunity of the progeny against oral infection at 1 day old, whereas progeny from unvaccinated breeders were susceptible to such a challenge.

Idiopathic inflammation and rupture of the posterior tibial tendon (PTT) has received much attention in the recent literature. In this report of the presentation of PTT dysfunction as a manifestation of seronegative inflammatory disease, we describe the clinical and laboratory features of 76 patients with inflammation and/or rupture of the PTT. Analysis of all patients identified two discrete groups. Group A patients were younger (mean age 39 years) and had multiple manifestations of inflammation at other sites of ligament and tendon attachments (enthesopathy). Other features of a systemic inflammatory disorder such as oral ulcers, conjunctivitis, colitis, and especially psoriasis were common in the latter patients and their families. Group B consisted predominantly of elderly patients (mean age 64 years) with isolated dysfunction of the PTT. These two groups differed widely in the manner of clinical presentation, demographic data, family history, HLA data, and surgical pathology. These distinctions suggest different pathogeneses for posterior tibial tendinitis. Group A demonstrated local manifestations of a systemic inflammatory disease, whereas group B exhibited the effects of mechanical trauma and degeneration.