Abstract Background/Aims Enthesitis is a hallmark clinical feature of psoriatic arthritis (PsA) with the most commonly affected site being the Achilles tendon (AT) insertion into the posterior calcaneum. There is overlap in the clinical and ultrasound (US) pathological presentation of Achilles enthesitis and Achilles tendinopathy, however their treatment guidelines differ significantly. AT pain in PsA is complex, with the potential interplay of mechanobiology and inflammation. The aim of this study was to assess the structure and function of the AT in individuals with PsA to inform the future development of a non-pharmacological intervention. Methods A single-centre, cross-sectional observational study was conducted. People with PsA with (PsA+AT) and without (PsA-AT) AT pain were age and sex-matched with healthy controls (n = 11 per group). AT structure and function were assessed by clinical examination (Leeds Enthesitis Index and AT tendinopathy tests), B-mode and Power Doppler (PD) US, the Victorian Institute of Sports Assessment - Achilles (VISA-A) questionnaire, the bilateral heel raise test and 10-metre walk test (10MWT). Patient-reported outcome measures were used to evaluate local and global disease activity, impact, and quality of life. Group membership associations and between-group differences for domains of interest were evaluated using Pearson’s Chi-squared, one-way ANOVA, Mann-Whitney or Kruskal-Wallis tests. Results All groups were comparable in terms of sex, age and BMI. PsA disease duration was longer in the PsA-AT group (mean [SD], 20.1 years [13.1]) compared to the PsA+AT group (7.4 [6.3]). Structural changes at the enthesis on US were detected in all groups; however inflammatory features were significantly more prevalent in the PsA+AT group (p<0.001). PD signal was only detected in the PsA+AT group. Mid-portion and myotendinous AT pathology, including diffuse thickening, altered echogenicity and partial tears were also present, irrespective of the presence of enthesitis. PsAID-12 and HAQ-DI scores were significantly worse in the PsA+AT compared to the PsA-AT group (p=0.018 and p=0.001, respectively). The PsA+AT group walked slower (mean=17.89 seconds for 10MWT) compared to the PsA-AT group (12.23) and controls (11.55), could perform significantly less heel raises until the point of fatigue (PsA+AT mean=19.45, PsA-AT=39.18, controls=51.55, p=0.007) and had significantly worse VISA-A scores (PsA+AT mean=33, PsA-AT=71, controls=92, p<0.001), indicative of impaired AT function. In the PsA+AT group, AT pain was persistent and disabling despite pharmacological management in line with current guidelines and <30% had received treatment from podiatry or physiotherapy services. Conclusion People with PsA and AT pain exhibit severe functional limitations as demonstrated by the bilateral heel raise test, 10MWT and VISA-A scores. The diversity of US imaging features detected, and the inconsistencies in treatment provided, highlights an opportunity to develop individualised non-pharmacological management strategies stratified by US features and performance-based testing. Disclosure A. Patience: None. M.P. Steultjens: None. S. Siebert: None. G.J. Hendry: None.