Osteoarthritis (OA) is increasingly conceptualized as a whole-joint disorder, in which pathological processes across articular cartilage, subchondral bone, synovium, and periarticular tissues are tightly interconnected. Within this context, miRNAs have emerged as central post-transcriptional regulators capable of integrating mechanical, inflammatory, and metabolic cues at the network level. In human OA, extensive evidence links miRNA dysregulation to cartilage catabolism, impaired stress adaptation, inter-tissue communication, and the emergence of extracellular and circulating miRNA (cmiRNA) signatures with diagnostic and translational relevance. In contrast, miRNA research in canine OA remains limited, despite dogs developing a naturally occurring form of the disease that closely mirrors human OA in clinical presentation, joint pathology, and biomechanical drivers. To date, only a single pilot study has systematically investigated miRNA expression in spontaneous canine OA, underscoring both the feasibility of miRNA profiling and the substantial gaps that persist in tissue validation and functional characterization. This review critically synthesizes miRNA-mediated regulatory mechanisms in human OA and leverages this evidence to define research priorities in canine OA, where experimental validation remains limited. By focusing on shared molecular contexts rather than assumed equivalence, the review defines a comparative framework highlighting cmiRNAs as promising non-invasive translational targets.

Background: Osteoarthritis (OA) is a chronic whole-joint disease involving extracellular matrix remodeling, inflammatory signaling, immune–stromal interactions, and sensory-associated processes. MicroRNAs (miRNAs) may contribute to post-transcriptional regulation within these interconnected molecular domains, but concurrent mRNA and miRNA expression patterns remain insufficiently characterized in naturally occurring canine OA. Methods: A total of 12 formalin-fixed, paraffin-embedded (FFPE) canine tissue specimens were classified as osteoarthritic joint tissues (OA; n = 7) and control joint tissues without radiographic or histopathological evidence of OA (C-JT; n = 5). RT-qPCR was used to quantify 17 selected mRNAs involved in extracellular matrix remodeling, chronic inflammatory signaling, immune–stromal interactions, and neuroinflammatory and sensory-associated processes, together with five miR-30 family members. Statistical comparisons were performed on ΔCq values using two-sided unpaired Welch’s t-tests followed by Benjamini–Hochberg false discovery rate correction. Results: Compared with C-JT, OA tissues showed significantly higher expression of ADAMTS5, MMP2, MMP13, COL2A1, SPARC, HP, VEGFA, IGFBP6, and ASIC3 after false discovery rate correction. MMP9, IL1B, IL1R1, IL1RAP, JAK2, TYK2, NGFB, and NTRK1 did not differ significantly between the two joint-tissue groups. MiR-30b was significantly downregulated in OA, whereas miR-30c, miR-30d, and miR-30e were significantly upregulated; miR-30a did not differ significantly. Exploratory database-supported miRNA–gene connectivity was used for candidate prioritization but was not interpreted as evidence of direct regulation in canine joint tissue. Conclusions: Canine osteoarthritic capsulosynovial tissues exhibit concurrent alterations in selected mRNAs and miR-30 family members across matrix-remodeling, immune–stromal, and sensory-associated molecular domains. These findings identify OA-associated expression patterns but do not establish pathway activation, direct miRNA–mRNA regulation, or disease progression. They provide a focused molecular basis for future mechanistic studies of post-transcriptional regulation in naturally occurring canine OA.

Rupture of the Achilles (common calcaneal) tendon remains one of the most demanding soft-tissue injuries in canine orthopaedic surgery, and recent large-cohort evidence confirms that no single surgical or postoperative strategy is clearly superior across all cases. This article first provides an updated, critical review of the anatomy, aetiology, diagnosis, and surgical management of Achilles tendon rupture in dogs, covering core suture patterns, biological and synthetic augmentation techniques, and postoperative immobilisation strategies, together with their respective biomechanical evidence and clinical limitations. It then presents a clinical case of chronic, complete Achilles tendon rupture in a dog, repaired using a Three-Loop Pulley suture pattern combined with a polypropylene mesh sleeve incorporated directly into the core suture passes—a “mesh-in-stitch” technique—supported by temporary transarticular external skeletal fixation. Over a follow-up period extending to 33 months postoperatively, serial clinical, ultrasonographic, and orthopaedic evaluations showed progressive structural remodelling of the tendon, stable mesh integration, and complete functional recovery without major complications. Taken together, the reviewed literature and this clinical outcome suggest that combining intraoperative mechanical reinforcement with a scaffold for tissue ingrowth may represent a viable option for reconstructing severe, chronically ruptured tendons in dogs.