Case report: Nonsimultaneous bilateral triceps tendon rupture and surgical repair in a healthy dog.

A 7-year-old female spayed Australian shepherd dog was presented for an acute onset of inability to stand. On physical examination, the dog was unable to support weight on the thoracic limbs. On neurological examination, the thoracic limbs had absent hopping and paw placement and reduced withdrawal reflexes bilaterally. The remainder of the neurological examination was normal. The anatomic lesion localized to the C6-T2 spinal nerve roots, spinal nerves, or the named nerves of the thoracic limb, bilaterally. A lesion affecting the ventral gray column of the C6 through T2 spinal cord segments was considered less likely. In an effort to exclude an orthopedic disorder from consideration, radiographs of the shoulders, elbows, and manus were normal. Magnetic resonance imaging of the cervical and cranial thoracic vertebral column was normal. Analysis of synovial fluid from the carpi, elbows, and shoulders were normal. Ultrasonography of the triceps muscle and tendon of insertion revealed bilateral, acute-subacute tears of the tendon at insertion of the triceps muscles, bilaterally. Magnetic resonance imaging of both elbows revealed complete avulsion of the triceps tendons bilaterally. Surgical repair of both tendons was performed using the Arthrex FiberLoop system combined with autologous conditioned plasma soaked in a collagen sponge. Postoperatively, external coaptation was provided using Spica splints for 6 weeks followed by the use of soft padded orthotic braces for an additional 6 weeks. Concurrently, a front support wheelchair was used for 10 weeks postoperative. By 10 weeks postoperative, the dog was able to ambulate without support. To the authors' knowledge, this is the first report of bilateral triceps tendon avulsion in a dog. Tendon avulsion occurred without a known history of trauma or predisposing metabolic abnormalities. Magnetic resonance imaging provided excellent anatomical detail that aided in surgical repair.

Mesenchymal stromal cells donate mitochondria to articular chondrocytes exposed to mitochondrial, environmental, and mechanical stress.

Articular cartilage has limited healing capacity and no drugs are available that can prevent or slow the development of osteoarthritis (OA) after joint injury. Mesenchymal stromal cell (MSC)-based regenerative therapies for OA are increasingly common, but questions regarding their mechanisms of action remain. Our group recently reported that although cartilage is avascular and relatively metabolically quiescent, injury induces chondrocyte mitochondrial dysfunction, driving cartilage degradation and OA. MSCs are known to rescue injured cells and improve healing by donating healthy mitochondria in highly metabolic tissues, but mitochondrial transfer has not been investigated in cartilage. Here, we demonstrate that MSCs transfer mitochondria to stressed chondrocytes in cell culture and in injured cartilage tissue. Conditions known to induce chondrocyte mitochondrial dysfunction, including stimulation with rotenone/antimycin and hyperoxia, increased transfer. MSC-chondrocyte mitochondrial transfer was blocked by non-specific and specific (connexin-43) gap-junction inhibition. When exposed to mechanically injured cartilage, MSCs localized to areas of matrix damage and extended cellular processes deep into microcracks, delivering mitochondria to chondrocytes. This work provides insights into the chemical, environmental, and mechanical conditions that can elicit MSC-chondrocyte mitochondrial transfer in vitro and in situ, and our findings suggest a new potential role for MSC-based therapeutics after cartilage injury.