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Arthritis mutilans
Arthritis mutilans
Arthritis mutilans
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Arthritis mutilans
SpecialtyRheumatology Edit this on Wikidata

Arthritis mutilans is a rare medical condition involving severe inflammation damaging the joints of the hands and feet, and resulting in deformation and problems with moving the affected areas; it can also affect the spine.[1] As an uncommon arthropathy, arthritis mutilans was originally described as affecting the hands, feet, fingers, and/or toes, but can refer in general to severe derangement of any joint damaged by arthropathy.[2] First described in modern medical literature by Marie and Leri in 1913, in the hands, arthritis mutilans is also known as opera glass hand (la main en lorgnette in French), or chronic absorptive arthritis.[3][4] Sometimes there is foot involvement in which toes shorten and on which painful calluses develop in a condition known as opera glass foot, or pied en lorgnette.[5][6]

Signs and symptoms

[edit]

For a person with arthritis mutilans in the hands, the fingers become shortened by arthritis, and the shortening may become severe enough that the hand looks paw-like, with the first deformity occurring at the interphalangeal and metacarpophalangeal joints. The excess skin from the shortening of the phalanx bones becomes folded transversely, as if retracted into one another like opera glasses, hence the description la main en lorgnette. As the condition worsens, luxation, phalangeal and metacarpal bone absorption, and skeletal architecture loss in the fingers occurs.[5]

Cause

[edit]

Arthritis mutilans occurs mainly in people who have pre-existing psoriatic arthritis, but can occur, if less often, in advanced rheumatoid arthritis; it can also occur independently.[5][6] Psoriasis and psoriatic arthritis are interrelated heritable diseases, occurring with greater heritable frequency than rheumatoid arthritis, primary Sjögren syndrome and thyroid disease.[7] Psoriasis affects 2–3% of the Caucasian population, and psoriatic arthritis affects up to 30% of those.[7] Arthritis mutilans presents in about 5–16% of psoriatic arthritis cases, involves osteolysis of the DIP and PIP joints, and can include bone edema, bone erosions, and new bone growth.[8] Most often psoriatic arthritis is seronegative for rheumatoid factor (occurring in only about 13% of cases[9]), and has genetic risk factor overlap with ankylosing spondylitis with HLA-B27, IL-23R77, and IL-1,[7] however, as of 2016, immunopathogenesis is unclear.[8]

Diagnosis

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Enthesitis can assist in differentiating arthritis mutilans' parent condition psoriatic arthritis from rheumatoid arthritis and osteoarthritis, with evidence in plain radiographs (x-rays) and MRI as periostitis, new bone formation, and bone erosions.[7] Dactylitis, spondylitis and sacroiliitis are common with the parent condition psoriatic arthritis, but are not in rheumatoid arthritis.[9] MRI bone edema scores are high in arthritis mutilans and correlate with radiographic measures of joint damage, although they may not correlate with disease activity.[10] A source of significant pain, bone marrow edema (or lesions, using newer terminology), can be detected on MRI or with ultrasonography by signals of excessive water in bone marrow.[11] Specifically, bone marrow edema can be detected within bone on T1-weighted images as poorly defined areas of low signal, with a high signal on T2-weighted fat-suppressed images.[12] Comparatively, with arthritis mutilans in rheumatoid arthritis, bone marrow edema often involves the subchondral bone layer, while the condition as a subtype of psoriatic arthritis includes a greater extent of marrow edema, expanding to diaphysis.[10][13]

Treatment

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Medication

[edit]

The bone edema in arthritis mutilans can be treated with TNF inhibitors in the short term: a 2007 study found that the bone edema associated with psoriatic arthritis (of which arthritis mutilans is a subtype) responded to TNF inhibitors with "dramatic" improvement, but the study was not determinative of whether TNF inhibitors would prevent new bone formation, bone fusion, or osteolysis (bone resorption).[10][14]

Surgical

[edit]

Although a 2011 research article stated that disagreements between hand surgeons and rheumatologists remain regarding the indications, timing and effectiveness of rheumatoid hand surgery,[15] arthritis mutilans may be successfully treated by iliac-bone graft and arthrodesis of the interphalangeal joints and the metacarpophalangeal joint in each finger.[5][16]

Outcomes

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Arthritis mutilans' parent condition psoriatic arthritis leaves people with a mortality risk 60% higher than the general population, with premature death causes mirroring those of the general population, cardiovascular issues being most common.[9][17] Life expectancy for people with psoriatic arthritis is estimated to be reduced by approximately 3 years.[9]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Arthritis mutilans

View on Grokipedia
from Grokipedia
Arthritis mutilans is a rare and severe form of , characterized by aggressive osteolysis and that leads to profound shortening of the digits, telescoping deformities (often described as "opera glass hands"), and significant destruction, primarily affecting the interphalangeal and metacarpophalangeal s of the hands and feet. This condition results in severe pain, swelling, stiffness, and functional impairment, potentially deforming the fingers and toes to the point of impairing daily activities. It represents the most destructive of , with radiographic features including "pencil-in-cup" deformities, dissolution, and bone erosion. Arthritis mutilans occurs in approximately 3% to 6% of patients with , making it one of the least common subtypes, though prevalence estimates vary from 2% to 21% depending on diagnostic criteria. It is strongly associated with underlying psoriatic disease, often presenting alongside skin , nail changes such as and pitting, and sometimes axial involvement like . Risk factors include , as seen in familial clusters, and environmental influences like , though the exact involves chronic inflammation driven by immune dysregulation. Historically, it was first classified as a distinct subtype of by Moll and Wright in and is now recognized in the as "mutilating psoriatic arthritis." Early through clinical , radiographic , and assessment of psoriatic features is crucial to prevent irreversible , as the condition can progress rapidly without intervention. Treatment typically involves disease-modifying antirheumatic drugs (DMARDs) and biologic therapies targeting inflammatory pathways, with surgical options like digital lengthening considered in advanced cases to restore function. Despite advances in , arthritis mutilans remains a challenging condition with high rates if not addressed promptly.

Overview

Definition and Characteristics

Arthritis mutilans is recognized as the most severe and destructive form of , a seronegative spondyloarthropathy, characterized by progressive osteolysis that leads to extensive and irreversible destruction, predominantly affecting the small joints of the hands and feet. This condition results in marked deformity and functional impairment, distinguishing it from less aggressive patterns of psoriatic arthritis through its rapid and profound erosive nature. Key clinical characteristics include the development of telescoping digits, where the fingers or toes undergo significant shortening due to the collapse and resorption of phalangeal bones, often resulting in a characteristic "opera glass" or "main en " appearance. Radiographically, it is hallmark by the pencil-in-cup deformity, featuring concave cupping of the distal phalangeal heads with slender, pencil-like proximal shafts, indicative of severe marginal erosion and bone loss. While primarily involving the distal interphalangeal and proximal interphalangeal joints, the disease can extend to larger joints such as the wrists, ankles, and even the spine, exacerbating overall disability. Historically, mutilans was first described in modern in by Pierre Marie and André Leri, who coined the term "main en lorgnette" to depict the telescoping hand deformity observed in patients with chronic destructive associated with . Earlier accounts trace resorptive arthropathies linked to back to 1888 by Bourdillon, but the specific mutilans subtype gained recognition as a distinct entity within seronegative spondyloarthropathies in the early , emphasizing its unique osteolytic progression.

Epidemiology

Arthritis mutilans, the most severe subtype of (PsA), affects fewer than 5% of individuals with PsA, though estimates vary widely from 0.6% to 21% depending on diagnostic criteria. Globally, PsA has a of approximately 112 per 100,000 adults. In a population-based study from , the of arthritis mutilans was estimated at 3.69 cases per million adult inhabitants. This rarity underscores its limited impact compared to other inflammatory arthritides, though it imposes significant morbidity on affected individuals. Up to 30% of patients with develop PsA, with a small subset progressing to the mutilans form. The condition typically manifests in adulthood, with peak onset between ages 30 and 50 years, aligning with the age distribution of PsA. Some studies indicate a slight male predominance, with a male-to-female ratio of approximately 1.9:1, though data are constrained by the disease's infrequency. Rates are notably higher among populations with underlying , where the progression to PsA and subsequently to arthritis mutilans follows established demographic patterns of the precursor condition. Geographic and ethnic variations in arthritis mutilans are not well-characterized due to its low incidence, but reports suggest it is less frequently documented in Asian populations compared to those of European descent. Potentially higher occurrence in Northern European groups has been noted, though confirmatory data remain limited by diagnostic challenges and underreporting.

Pathophysiology

Etiology and Risk Factors

Arthritis mutilans represents a severe autoimmune subtype of (PsA), characterized by immune-mediated that targets joint tissues, driven by a complex interplay between genetic susceptibility and environmental triggers. This condition emerges when dysregulated immune responses, influenced by both inherited and external factors, lead to progressive joint destruction, distinguishing it as a rare but destructive manifestation within the PsA spectrum. Key risk factors for developing arthritis mutilans mirror those of PsA, with family history of or PsA conferring a substantially elevated ; first-degree relatives of individuals with PsA face approximately a 50-fold higher likelihood compared to the general . Obesity in early adulthood, particularly with a greater than 30, increases the of PsA onset approximately 3-fold, potentially exacerbating inflammatory pathways that contribute to mutilans progression. has been linked to 1.5- to 2-fold higher odds of PsA in certain cohorts, though evidence is mixed and may vary by . Additionally, infections or physical trauma can act as precipitants, triggering flares in genetically predisposed individuals. Genetic underpinnings are prominent, with strong associations to and DQB1*02 alleles, which confer an increased risk specifically for arthritis mutilans among PsA patients. PsA, including its mutilans form, follows a polygenic pattern, as evidenced by genome-wide association studies identifying over 65 susceptibility loci (as of 2025) that modulate disease risk.

Disease Mechanisms

Arthritis mutilans, the most severe subtype of psoriatic arthritis, is driven by a dysregulated immune response dominated by T helper 17 (Th17) cells, which infiltrate the synovium and entheses, perpetuating chronic synovitis and enthesitis. This immune activation leads to the release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-17 (IL-17), and interleukin-23 (IL-23), which collectively amplify inflammation and orchestrate tissue destruction. TNF-α, in particular, is markedly elevated in the synovial fluid and tissue of affected joints, where it stimulates peripheral blood mononuclear cells to generate osteoclast precursors that migrate to sites of inflammation. IL-23 sustains Th17 cell differentiation and survival, while IL-17 directly promotes synovial fibroblast activation and cytokine production, creating a feed-forward loop of immune-mediated damage. The hallmark osteolysis in arthritis mutilans stems from this inflammatory milieu, initiating with marginal bone erosions at the pannus- interface that advance to profound central . Severe disrupts the balance of , with activation overwhelming activity, resulting in characteristic profound bone loss—a defining feature of the mutilans form. The receptor activator of nuclear factor kappa-B ligand () pathway is pivotal here, as upregulated by TNF-α and IL-17 on synovial fibroblasts and Th17 cells binds to on precursors, driving their maturation, survival, and resorptive function without the need for additional in some cases. This leads to aggressive bone dissolution, particularly in the distal interphalangeal joints, where resorb bone at markedly elevated rates compared to non-erosive . Disease progression in arthritis mutilans typically evolves from cutaneous , where initial immune dysregulation at the skin barrier may seed systemic T-cell activation, to axial and peripheral joint involvement marked by as an early . Over time, unrelenting cytokine-driven culminates in fibrotic of larger joints or the dramatic telescoping shortening of digits due to unchecked osteolysis. Certain HLA alleles, such as , confer genetic susceptibility that may accelerate this trajectory toward mutilating destruction.

Clinical Features

Signs and Symptoms

Arthritis mutilans primarily manifests with severe , , and swelling in the interphalangeal joints (distal and proximal) of the hands and feet, often progressing rapidly and leading to significant functional impairment. Patients experience intense joint inflammation that erodes bone and , resulting in progressive digital shortening through a telescoping mechanism where bones collapse into one another, ultimately causing loss of and fine motor skills. Characteristic deformities include the "opera glass" or "main en lorgnette" appearance of the fingers and toes, where the digits become shortened and unstable due to and collapse, resembling the collapsible handles of old opera glasses. In advanced stages, a -in-cup deformity emerges, marked by central that leaves the resembling a pencil tip inserted into a cup, alongside possible ulnar deviation or swan-neck deformities that further distort hand function. Systemic symptoms accompany the joint involvement, including profound fatigue and prolonged morning stiffness lasting more than one hour, which exacerbates daily limitations. Occasional low-grade fever may occur during acute flares, intensifying the overall debilitating impact. As a subtype of psoriatic arthritis, it is often associated with psoriatic skin lesions, though these are secondary to the core joint pathology.

Associated Manifestations

Arthritis mutilans, as a severe subtype of psoriatic arthritis (PsA), is strongly linked to the broader psoriatic disease spectrum, with skin and nail involvement being hallmark extra-articular features. Plaque psoriasis affects 70-90% of individuals with PsA, often preceding joint symptoms by several years and contributing to the diagnostic criteria for the condition. Nail changes, including pitting, onycholysis, and dystrophy, occur in up to 80% of PsA cases and are particularly prevalent in mutilans due to the frequent distal interphalangeal joint involvement. Other associated manifestations in arthritis mutilans mirror those in PsA, reflecting shared inflammatory pathways, but may be more severe in this . , characterized by sausage-like swelling of digits, is common in early disease stages, with a of approximately 50% across PsA subtypes. , inflammation at sites such as the or , affects 27-50% of patients and underscores the entheseal pathology central to psoriatic disease. Axial spine involvement, including , occurs in 20-30% of cases, often asymmetrically and contributing to spondylitic features. Rare overlaps include and , which may share IL-23/IL-17 axis dysregulation with PsA. Comorbidities are elevated in arthritis mutilans owing to its chronic inflammatory burden. Metabolic syndrome is more prevalent in PsA than in the general population. These features can progress to joint deformities, such as telescoping digits, as part of the disease course.

Diagnosis

Clinical Evaluation

Clinical evaluation of begins with a detailed to identify patterns suggestive of this severe subtype of (PsA). The onset is typically insidious, progressing over several years, with often preceding articular symptoms by 5 to 10 years in the majority of cases. Family should probe for or PsA, as genetic predisposition increases risk. Symptom progression commonly starts with dactylitis or enthesitis, evolving into polyarticular involvement and eventual digital mutilation, characterized by progressive joint destruction. Patients frequently report significant impact on activities of daily living, such as difficulty with fine motor tasks like buttoning clothes or walking due to foot deformities. Physical examination focuses on identifying characteristic deformities and associated features. tenderness is assessed through , often less pronounced than in , while is evaluated to detect or flail joints in affected interphalangeal, metacarpophalangeal, or . Digital shortening is measured by comparing affected digits to contralateral ones or historical norms, revealing telescoping appearances clinically, with "pencil-in-cup" deformities confirmed radiographically. Concurrent evaluation for includes inspection of skin for plaques, particularly in hidden areas like the , umbilicus, or , and nail changes such as pitting or , present in up to 80% of PsA cases. Classification relies on the CASPAR criteria for PsA, requiring inflammatory musculoskeletal disease with a score of at least 3 points from features like current psoriasis (2 points), personal history of psoriasis (1 point), family history of psoriasis (1 point), dactylitis (1 point), juxta-articular new bone formation (1 point), and negative rheumatoid factor (1 point). For the mutilans subtype, clinical suspicion arises from evidence of severe, erosive disease causing significant joint destruction, though radiographic confirmation is essential for definitive categorization. While there are no validated specific criteria for the arthritis mutilans subtype, it is diagnosed in patients meeting PsA classification (e.g., CASPAR) with radiographic evidence of severe destructive arthropathy. Exclusion of rheumatoid factor helps differentiate from rheumatoid arthritis, as PsA is typically seronegative.

Imaging and Laboratory Findings

Imaging in arthritis mutilans primarily relies on radiographic evaluation to identify characteristic structural damage, with advanced modalities like MRI and providing insights into early inflammatory processes. Conventional X-rays of the hands and feet reveal hallmark features such as the pencil-in-cup , where the distal end of one appears sharpened and articulates with a cup-shaped in the adjacent , typically affecting the distal interphalangeal joints. Marginal , often asymmetric and well-defined in early stages, progress to irregular patterns with periosteal new bone formation, while severe osteolysis leads to significant , including acro-osteolysis of phalangeal tufts and telescoping digits. These changes indicate advanced disease, with osteolysis often resulting in profound loss in affected phalanges. MRI enhances detection of subclinical in mutilans, visualizing as synovial thickening and enhancement, bone marrow signaling active , and at ligamentous attachments, which may precede radiographic damage. This modality is particularly valuable for assessing disease severity in periarticular structures and monitoring progression in mutilans variants. complements these by identifying soft tissue , such as and dactylitis-related hyperemia, offering a dynamic, non-invasive view of peripheral involvement without . Laboratory investigations in arthritis mutilans reflect underlying activity but lack disease-specific markers. Elevated (ESR) and (CRP) levels occur in approximately 40% of cases during active inflammation, serving as non-specific indicators of systemic involvement. and anti-cyclic citrullinated peptide (anti-CCP) antibodies are typically negative, distinguishing it from , though low-titer positivity may occur in 2-10% of patients. positivity is observed in about 20% of cases with axial features, less frequently than in . Diagnosis of arthritis mutilans subtype requires radiographic confirmation of severe destructive changes, including pencil-in-cup deformities and severe osteolysis leading to significant and telescoping of digits, often involving multiple joints in the hands or feet. These criteria emphasize functional impairment alongside , building on clinical suspicion to confirm the mutilans form.

Treatment

Pharmacological Management

Pharmacological management of arthritis mutilans, a severe destructive form of , primarily focuses on controlling inflammation, alleviating symptoms, and preventing further damage through disease-modifying antirheumatic drugs (DMARDs). Initial therapy often involves nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen or naproxen, to provide symptomatic relief from and swelling in mild flares, though their use is limited to short durations (up to 4 weeks) due to limited impact on disease progression. Corticosteroids, administered systemically or intra-articularly, are employed for rapid control of acute inflammation but are used cautiously to avoid exacerbating psoriasis. Conventional synthetic DMARDs (csDMARDs), particularly at doses of 15-25 mg weekly, serve as first-line agents to reduce and flares by inhibiting inflammatory pathways, with supporting their role in slowing radiographic progression in early disease. For severe cases like arthritis mutilans, biologic DMARDs (bDMARDs) form the cornerstone of treatment, targeting key cytokines in the inflammatory cascade. (TNF) inhibitors, including (50 mg subcutaneous weekly) and (40 mg subcutaneous every two weeks), are recommended as initial biologic therapy due to their efficacy in halting and improving function, with studies demonstrating significant improvement in symptoms in mutilans patients over two years. Interleukin-17 (IL-17) inhibitors, such as (150-300 mg subcutaneous monthly after loading) or bimekizumab (320 mg subcutaneous every 4 weeks), offer robust control of both axial and peripheral symptoms, particularly in patients with prominent , and are preferred when skin involvement is severe; bimekizumab, a dual IL-17A/F inhibitor approved for in , has shown sustained efficacy through 3 years as of 2025. IL-23 inhibitors, exemplified by (100 mg subcutaneous at weeks 0, 4, and every 8 weeks thereafter), have shown significant inhibition of structural damage in active , as evidenced by the 2025 phase 3b APEX trial, which reported a 2.5-fold lower rate of progression versus at week 24. In refractory arthritis mutilans, targeted synthetic DMARDs (tsDMARDs) like (JAK) inhibitors, including (5 mg orally twice daily), provide an oral alternative by modulating multiple downstream inflammatory signals, with comparable efficacy to biologics in musculoskeletal manifestations per EULAR guidelines. Emerging strategies emphasize early aggressive with these agents, often using with a csDMARD and a bDMARD for non-responders. Disease activity is monitored using validated tools such as the Disease Activity Score 28 (DAS28) for joint involvement or Psoriatic Arthritis Response Criteria (PsARC) for overall response, guiding treatment escalation.

Surgical Interventions

Surgical interventions for arthritis mutilans are indicated in cases of irreversible joint destruction resulting in severe , , or profound functional impairment that does not respond to pharmacological . These procedures primarily target end-stage structural damage, particularly in the hands and feet, to salvage function and prevent further mutilation. Pre-surgical medical optimization to suppress active is crucial for improving operative outcomes. Key procedures focus on stabilizing destroyed joints and reconstructing lost bone and . , or joint fusion, is commonly performed on digits to provide stability and halt progressive shortening, often using intramedullary fixation to maintain alignment despite poor bone quality. , involving joint replacement with prosthetic components, is employed for larger joints such as the or ankle to restore mobility and alleviate pain. releases and transfers address fixed contractures and imbalances, enhancing hand or foot positioning for better grasp or ambulation. techniques, including and iliac crest autografts, repair osteolytic defects and elongate shortened phalanges, preserving digital length essential for pinch and grip. Outcomes of these surgeries demonstrate functional gains in select cases, with reports of increased pinch strength (from 1.5 to 8 pounds) and (from 40 to 60 pounds) following digital lengthening procedures. In broader cohorts including mutilans cases, approximately 48% of patients undergo orthopedic interventions, achieving pain relief and improved daily function in many instances, though overall remains elevated compared to non-surgical patients. However, success is tempered by high complication rates, including (historically elevated in hand surgeries), graft resorption, and non-union, attributable to compromised stock and ongoing disease activity.

Prognosis

Long-term Outcomes

Arthritis mutilans, the most severe form of , exhibits a progressive natural history characterized by rapid joint destruction if left untreated, often leading to severe functional within 10 years through osteolysis and telescoping deformities. In a Nordic of patients with psoriatic arthritis mutilans, 21% reported significant impairment in and daily activities, with a mean of 8.2 mutilated joints per patient and gross deformities in 16%. Furthermore, patients with , including those with mutilans, face a 43% increased risk of compared to the general population, contributing to elevated morbidity and potential premature mortality. Early initiation of biologic therapies has demonstrated substantial benefits in altering disease trajectory, with agents such as TNF inhibitors and IL-17 inhibitors inhibiting radiographic progression in patients compared to , as evidenced by reduced erosions and space narrowing in clinical trials. For instance, and have shown low rates of radiographic progression over 2 years in responders achieving early clinical improvement. Full remission is uncommon in severe forms of psoriatic arthritis such as arthritis mutilans, though minimal disease activity is achievable in a subset of patients with sustained treatment, supporting better long-term functional preservation. Key prognostic factors include the timing of diagnosis and treatment adherence; delays exceeding 6 months from symptom onset are associated with irreversible joint erosions and poorer functional outcomes. Poor adherence to therapy accelerates progression and exacerbates disability, whereas consistent early intervention is critical for mitigating structural damage. High baseline joint burden and comorbidities such as smoking further worsen prognosis by increasing the risk of severe disability fourfold.

Complications

Arthritis mutilans, as a severe subtype of , leads to profound destruction in the hands and feet, resulting in and significant functional impairment that often fosters dependency on assistive devices or caregivers for daily activities. Furthermore, individuals with , including those with arthritis mutilans, face an elevated risk of cardiovascular events, with studies indicating a 68% increased risk of compared to the general . Treatment with biologic agents, particularly inhibitors (TNFis), carries risks of serious infections, including reactivation of , necessitating pre-treatment screening in endemic areas. Surgical interventions for joint reconstruction or replacement in arthritis mutilans are complicated by the underlying inflammatory state, leading to heightened chances of implant failure, delayed , and postoperative infections due to compromised tissue integrity. Systemically, the disfiguring deformities of arthritis mutilans contribute to elevated rates of depression and anxiety, affecting 30-50% of patients with , often linked to diminished and . Additionally, chronic inflammation in longstanding cases can rarely precipitate secondary , a condition associated with poor and multi-organ involvement. Poor adherence to therapy may exacerbate these complications, influencing overall prognostic trajectories.

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