A 10-year-old male neutered domestic shorthair cat was presented with a 5-month history of ambulatory paraparesis that progressed to non-ambulatory paraparesis 2 weeks prior to referral. Vertebral column radiographs performed by the referring veterinarian revealed an expansile osteolytic lesion of the L2-L3 articular facet joint (Figure 1a). The cat was treated with meloxicam (0.05 mg/kg q24h PO [Loxicom; Norbrook]) and frunevetmab (1 mg/kg SC q28 days [Solensia; Zoetis]) for suspected spinal arthritis, and the cat's activity level increased initially.
General examination at our referral centre was unremarkable. On neurological examination, the patient had normal mentation and cranial nerve examination. The cat was non-ambulatory paraparetic with delayed postural reactions, normal withdrawal and hyperactive patellar reflexes on both pelvic limbs. Lumbar hyperaesthesia was detected. Neurological findings were consistent with a T3-L3 myelopathy. Based on the radiographic findings, a vertebral neoplasm (primary or metastatic) was considered the most likely differential.
Haematological parameters were unremarkable. Serum biochemistry revealed only slight hyperglycaemia (9.66 mmol/l; reference interval [RI] 3.95-8.84). Advanced imaging was indicated. MRI of the thoracolumbar spine was performed under general anaesthesia using a 1.5 Tesla MRI unit (Siemens Symphony Tim system). There was a single, well-defined, expansile extradural mass lesion (1.2 height x 1.4 length x 1 cm width) affecting the caudal half of the L2 lamina, caudal articular processes and right pedicle, which was expanded abaxially. The mass extended into the vertebral canal leading to severe right dorsolateral spinal cord compression. There was a focal, ill-defined intramedullary T2-weighted hyperintensity at this level. The mass had a heterogeneous appearance and was hypointense/isointense in T2-weighted images and isointense on T1-weighted sequences, with mild homogeneous contrast enhancement after gadolinium injection (0.1 mmol/kg [Dotarem; Guerbet Laboratories]) (Figure 1b,c). Images of the remaining neuroaxis revealed no further abnormalities.
CT (160-slice Aquilion Prime; Toshiba) with ioversol contrast (2 ml/kg [Optiray 300; Guerbet Laboratories]) of the neck, thorax and abdomen was performed for the purpose of staging. In agreement with the MRI findings, CT identified an aggressive osteolytic lesion at L2 with strong ioversol contrast uptake (Figure 1d,e). Slight spondylosis deformans was present in between the L1 and L2 vertebrae. Other CT findings considered not clinically relevant included multifocal anaesthesia-related atelectasis, splenic parenchyma changes consistent with a benign process and bilateral elbow osteoarthrosis. There were no additional neoplastic foci.
Differential diagnosis of vertebral neoplasms included osteosarcoma (OSA), fibrosarcoma, chondrosarcoma, haemangiosarcoma, plasma cell tumours (multiple myeloma, plasmacytoma), histiocytic sarcoma and lymphoma. A benign bone tumour such as solitary or aneurysmal bone cysts could not be entirely excluded. The owner elected to pursue surgical management.
Preoperative surgical planning was performed by determining screw orientation and insertion within the bone corridors using a three-dimensional slicer software (Surgical Planning Lab, Harvard Medical School, Harvard University; www.slicer.org). A midline dorsal approach to the L1-L4 vertebrae was performed. The mass was removed by en bloc resection. A dorsal laminectomy was performed from the caudal portion of the L2 spinous process to caudal to the L3 spinous process, extending ventrolateral to the L2-L3 articular facet joints.   Vertebral stabilisation was performed using 1.5 mm titanium screws, which were placed bilaterally on the pedicles of L1, L2, L3 and L4 and embedded in polymethylmethacrylate (PMMA) cement. Implant entry points were estimated by visual approximation from the preoperative surgical planning video recording of the three-dimensional reconstruction, and drilling direction was guided by premeasured numeric values of inclination angles and osteotomy wedge gauges.
Haemostasis was controlled using Surgicel SNoW (Original Absorbable Hemostat; Ethicon). The exposed spinal cord was protected with local haemostatic agent (Lyostypt; Braun) and routine closure was performed.
Postoperative CT demonstrated correct placement of the implants and macroscopic resection of the tumour (Figure 2). The cat was discharged 5 days postoperatively, and, on discharge, was ambulatory paraparetic with moderate proprioceptive ataxia.
Histopathological examination of the mass demonstrated a densely cellular neoplasm expanding the vertebral bone. There was a thin cap of reactive woven bone around the periphery, and the neoplasm appeared contained within this. The neoplasm was formed of two cell populations: spindle cells and multinucleated giant cells (Figure 3a,b). Spindle cells predominated, and were arranged in a tightly interwoven storiform pattern surrounding small vessels and multifocally associated with islands and thin trabeculae of woven mineralised bone (Figure 3c). The spindle cells showed only mild pleomorphism without significant nuclear atypia. The multinucleated giant cells were sparse or densely scattered, and contained numerous (up to 50) nuclei that lacked significant atypia. Less than one mitosis was detected in 2.37 mm   (equivalent to 10 high-power fields) in both populations. Vascular invasion was not detected.
Immunohistochemistry with a histiocytic marker (ionised calcium binding adaptor molecule 1 [Iba1]; monoclonal AIF19mouse anti-Iba1 [Merck Millipore]), a general mesenchymal marker (vimentin [monoclonal mouse anti-vimentin, Clone V9; Dako]) and an osteoblast-specific transcription factor marker (osterix [polyclonal rabbit anti-Sp7/osterix; Abcam]) was performed. The multinucleated giant cells exhibited weak cytoplasmic labelling with Iba1 (Figure 3d), suggestive of a monocyte/macrophage lineage. Most of the spindle cells showed nuclear labelling with osterix and both cell populations showed cytoplasmic labelling with vimentin (Figure 3e,f).
Based on the combined histological and immunohistochemical findings, the differential diagnosis included giant cell tumour of bone (GCTB) and giant cell-rich OSA. In consideration of the bland morphology of the cells, the absence of detectable mitotic activity and the apparent expansile rather than infiltrative growth pattern, a GCTB was favoured.
On re-examination 3 weeks postoperatively, the cat was ambulatory paraparetic with pelvic limb ataxia. Six months postoperatively, the cat returned to outdoor activity and had a good quality of life, although with a reduced ability to jump. The patient was ambulatory with subtle paraparesis. A postoperative full-body CT suggested instability of the L1-L4 spinal stabilisation construct demonstrated by multifocal PMMA fracturing and L2 implant loosening. Moderate periosteal reaction was present along the ventral/ventrolateral margins of L2-L3. There was no evidence of disease recurrence or metastasis.