# Psoriatic Arthritis: Developments in 2025

**Authors:** Christina Spanopoulou, Pelagia Katsimbri

PMC · DOI: 10.31138/mjr.200925.per · 2026-01-08

## TL;DR

This review discusses recent developments in understanding and treating psoriatic arthritis, focusing on early diagnosis and personalized management to improve patient outcomes.

## Contribution

The paper provides a comprehensive overview of 2025 advancements in PsA, including risk identification and new therapeutic approaches.

## Key findings

- New insights into the transition from psoriasis to psoriatic arthritis have been identified.
- Advancements in pathogenesis understanding are leading to more individualized treatment protocols.
- Improved diagnostic methods are helping prevent functional disability in PsA patients.

## Abstract

Psoriatic arthritis (PsA) a complex, multifaceted autoimmune disease involving the skin and joints, presents a diagnostic and therapeutic challenge due to its heterogenous nature and existence of comorbidities. Early diagnosis is essential to prevent functional disability and achieve disease remission. The previous year has seen further advancements in the better understanding of PsA that include identifying patients at risk and the phases of transition from psoriasis (PsO) to PsA as well as new insights in pathogenesis and the development of newer treatments and therapeutic protocols. These developments are paving the way for more individualised management protocols aiming for further improvement in the quality of life for patients living with PsA. In this narrative review article, we reviewed the literature from major scientific databases for PsA from June 2024 to September 2025.

## Linked entities

- **Diseases:** psoriatic arthritis (MONDO:0011849), psoriasis (MONDO:0005083)

## Full-text entities

- **Genes:** IL23A (interleukin 23 subunit alpha) [NCBI Gene 51561] {aka IL-23, IL-23A, IL23P19, P19, SGRF}, APOF (apolipoprotein F) [NCBI Gene 319] {aka Apo-F, LTIP}, albumin [NCBI Gene 102531966], TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IL12B (interleukin 12B) [NCBI Gene 3593] {aka CLMF, CLMF2, IL-12B, IMD28, IMD29, NKSF}, JAK3 (Janus kinase 3) [NCBI Gene 3718] {aka JAK-3, JAK3_HUMAN, JAKL, L-JAK, LJAK}, IL-17A [NCBI Gene 102529779], CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, JAK1 (Janus kinase 1) [NCBI Gene 3716] {aka AIIDE, JAK1A, JAK1B, JTK3}, CD79A (CD79a molecule) [NCBI Gene 973] {aka IGA, IGAlpha, MB-1, MB1}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, AHR (aryl hydrocarbon receptor) [NCBI Gene 196] {aka FVH3, RP85, bHLHe76}, TYK2 (tyrosine kinase 2) [NCBI Gene 7297] {aka IMD35, JTK1}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL17F (interleukin 17F) [NCBI Gene 112744] {aka CANDF6, IL-17F, ML-1, ML1}
- **Diseases:** herpes zoster (MESH:D006562), pain (MESH:D010146), spondylitis (MESH:D013166), skin and joint disease (MESH:D012871), immune-mediated inflammatory diseases (MESH:C567355), articular disease (MESH:D057072), Inflammatory Arthritis (MESH:D001168), vitiligo (MESH:D014820), skin and nail disease (MESH:D009260), ankylosing spondylitis (MESH:D013167), Inflammation (MESH:D007249), diabetes (MESH:D003920), metabolic syndrome (MESH:D024821), depression (MESH:D003866), PsO (MESH:D011565), TREATMENT (MESH:D016609), axial involvement (MESH:C537791), cardiovascular disease (MESH:D002318), uveitis (MESH:D014605), PsA (MESH:D015535), immunological dysregulation (MESH:D007154), weight loss (MESH:D015431), of Disease (MESH:D004194), functional disability (MESH:D003291), swelling (MESH:D004487), Dysbiosis (MESH:D064806), chronic pain (MESH:D059350), rheumatoid arthritis (MESH:D001172), arthralgias (MESH:D018771), Hashimoto thyroiditis (MESH:D050031), chronic bronchitis (MESH:D029481), malignancies (MESH:D009369), systemic lupus erythematosus (MESH:D008180), synovitis (MESH:D013585), IBD (MESH:D015212), autoimmune disease (MESH:D001327), obesity (MESH:D009765), infection (MESH:D007239), thromboembolic or cardiovascular complications (MESH:D013923), Crohn's disease (MESH:D003424), DIP joint tenderness (MESH:D010003), bone erosion (MESH:D014077), thyroid disease (MESH:D013959), cytopenias (MESH:D006402), immune dysregulation (OMIM:614878), enthesitis (MESH:D001171), hypertension (MESH:D006973)
- **Chemicals:** BA (MESH:D001647), MTX (MESH:D008727), MDA (MESH:D015104), vedolizumab (MESH:C543529), Bimekizumab (MESH:C000625981), infliximab (MESH:D000069285), adalimumab (MESH:D000068879), Tofacitinib (MESH:C479163), prebiotics (MESH:D056692), Risankizumab (MESH:C000601773), Ixekizumab (MESH:C549079), Apremilast (MESH:C505730), IL-23i (-), TMAO (MESH:C005855), SCFA (MESH:D005232), Guselkumab (MESH:C000588857), lipid (MESH:D008055), Deucravacitinib (MESH:C000628674), Secukinumab (MESH:C555450), Ustekinumab (MESH:D000069549), Upadacitinib (MESH:C000613732), glucose (MESH:D005947), tryptophan (MESH:D014364)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395]

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Source: https://tomesphere.com/paper/PMC12835932