Canine appendicular osteosarcoma (OSA) is typically managed by limb amputation. However, this approach may be suboptimal in dogs with concurrent osteoarthrosis (OA). Limb-sparing surgery using three-dimensional (3D)-printed patient-specific implants (PSIs) may be an alternative, although evidence on implant durability and revision strategies remains limited, in particular for proximal humeral reconstructions. This report describes a 9-year-old, overweight dog referred for a 4-week history of persistent left forelimb lameness. Computed tomography (CT) confirmed a lesion affecting the proximal humerus and severe bilateral hip OA. Fine-needle aspiration cytology supported a presumptive diagnosis of OSA. Limb-sparing surgery with 3D-printed PSIs was chosen instead of amputation due to overweight status and OA. Patient-specific guides (PSGs) and endoprosthesis (PSE) were designed based on preoperative CT. Histopathology of the resected tumour confirmed OSA with complete surgical margins. Postoperative functional recovery was favorable, with progressive return to weight-bearing and mild residual lameness up to 8 months. At 9 months, implant failure occurred due to fracture at the distal humeral fixation region. Revision surgery was performed using a novel 3D-printed modular PSE integrating the retained proximal component, allowing restoration of limb function for an additional 6 months. The dog was euthanized at 15 months due to pulmonary metastases. Post-mortem macroscopic and histological visual semi-quantitative assessment of peri-implant tissue suggested advanced osseointegration, with no local recurrence or infection. This report suggests that PSI-based limb-sparing reconstruction may be feasible in proximal humeral OSA and highlights mechanical fatigue as a key limitation. The modular revision approach suggests the potential of additive manufacturing for salvage strategies after implant failure.

The information available on cervical myelopathies (CMs) and cervical pain (CP) in non-chondrodystrophic breeds remains limited compared to chondrodystrophic breeds. The expression of CP in CMs may depend on lesion type, severity and onset of clinical signs. This retrospective single-centre study reviewed the medical records of 112 purebred non-chondrodystrophic dogs referred for neurological evaluation, in which C1-T2 lesions were subsequently confirmed by magnetic resonance imaging (MRI). Clinical onset was categorised as acute (≤7 days) or chronic (>7 days). Neurological grade was classified into four neurological groups (G1–G4). CP was graded using a study-specific, non-validated five-point ordinal clinical scale. Multifactorial analysis of variance (ANOVA), odds ratios with 95% confidence intervals, and multivariable binomial logistic regression were performed. ANOVA showed significant effects of group (p < 0.0001), disease category (p < 0.05), and clinical onset (p < 0.02) on CP scores. Post-hoc comparison showed significantly lower CP scores in chronic onset than in acute onset (p < 0.0001). Acute onset was associated with CP in G2 (OR = 71.0; p < 0.0002) and remained associated with CP after adjustment for groups (adjusted OR = 4.42; 95% CI: 1.28–15.28; p = 0.019). These findings suggest that clinical onset may contribute to CP expression in non-chondrodystrophic dogs with CMs. Acute onset, particularly in ambulatory myelopathic patients, appears more frequently associated with CP. However, due to the retrospective design, the heterogeneous diagnostic composition, and the study-specific nature of the CP score, these associations should be interpreted cautiously.