Case report: Sintilimab combined with anlotinib as neoadjuvant chemotherapy for metastatic bone tumor resection in patients with PSC.

Background: Pulmonary sarcomatoid carcinoma (PSC) is a rare subtype of non-small-cell lung cancer (NSCLC), which is resistant to chemotherapy and radiotherapy with a poor prognosis. PSC is highly malignant and is prone to recurrence even after surgery. The programmed death-ligand 1 (PD-L1) tumor cell proportion score (TPS) 5%, TERT and TP53 gene mutations were detected in this patient accompanied by multiple metastatic sites. The anlotinib is a novel multitarget tyrosine kinase inhibitor (TKI) that could be effective for advanced NSCLC and some sarcoma patients. Limited clinical trials and case reports have shown that PSC patients with gene mutations and PD-L1 expression have good responses to multitarget antiangiogenic drug and immune checkpoint inhibitors (ICIs). In this article, we reported a case with metastatic PSC diagnosed by Computed Tomography (CT)-guided needle biopsy treated with immunotherapy combined with antiangiogenic drugs as a neoadjuvant chemotherapy (NACT). PSC is controlled and the patient achieves successfully limb salvage treatment by surgical resection. Therefore, targeted therapy and immunotherapy can provide sufficient surgical opportunities for limb salvage in the treatment of metastatic PSC patients. Case summary: A 69-year-old male diagnosed with malignant bone tumor in the proximal femur was admitted to our hospital in June 2022 with recurrent fever as well as swelling and pain in the left thigh for twenty days. The initial computed tomography (CT) scan of the chest showed a pulmonary cavity (20 mm × 30 mm) and scattered lung masses. Subsequently, he underwent a CT-guided needle biopsy to distinguish the essence of osteolytic bone destruction and soft tissue mass in the left proximal femur which showed metastatic sarcomatoid carcinoma histology. Genetic testing revealed TERT c.-124C mutation (abundance 8.81%), TP53 p.R342 mutation (abundance 11.35%), tumor mutational burden (TMB) 7.09 muts/Mb, microsatellite stability (MSS), and PD-L1 (SP263) TPS 5% were also detected. The patient was tentatively treated with a combination of antiangiogenic drug and PD-1 inhibitor. After one course, the tumor volume significantly reduced in magnetic resonance imaging (MRI) and pathological fracture occurred in the femur after combined treatment. The patient received proximal femoral tumor resection and prosthesis replacement after defervescence. Sequentially sintilimab with anlotinib were administered for over 1 year. Finally, the local tumor was well controlled, and no obvious drug-related adverse reactions were observed. The lesions in the lung remained in partial response (PR) for more than 16 months and complete response (CR) of metastatic tumor in the proximal femur was observed through imaging examinations. Conclusion: This is the first reported case of a metastatic PSC in femur showing a favorable response to the treatment consisting of anlotinib combined with sintilimab. This case suggests that antiangiogenic therapy combined with immunotherapy may benefit patients with metastatic PSC in the preoperative adjuvant therapy for limb salvage.

Using 3D Printing Technology to Design Split-Piece Sleeve Prosthesis in the Revision Surgery of Tumor-Type Total Elbow Prosthetic Fractures: A Case Report.

BACKGROUND: Revision of tumor-type prosthetic fractures is very challenging in clinical work. Traditional repair methods may not be able to meet the needs of complex cases or cause greater bone damage. Therefore, more effective and reliable solutions need to be found. CASE PRESENTATION: This study presents a novel revision technique for managing fractures of tumor-type total elbow prostheses. A 57-year-old female patient was diagnosed with a left distal humeral bone tumor accompanied by pathological fracture and underwent customized tumor-type total elbow prosthesis arthroplasty. After 5 years, she experienced pain and encountered difficulty in flexing the left elbow while lifting heavy objects. The X-ray examination revealed a fracture of the distal humeral prosthesis. As a response, the elbow joint was initially explored, and the damaged component of the prosthesis was extracted. Subsequently, we utilized 3D printing technology to design a split-piece sleeve prosthesis and effectively restored the fractured left distal humerus implant. During the 2-year follow-up, The X-ray demonstrated satisfactory positioning of the prosthesis, which remained securely affixed without any indications of loosening. The Mayo Elbow Performance Score (MEPS) reached 80 points, the Musculoskeletal Tumor Society (MSTS) attained a score of 28 points, and the range of motion of the elbow was measured between 25° and 110°, revealing favorable functional outcomes. CONCLUSION: The utilization of a 3D printed split-piece sleeve prosthesis presents a viable clinical treatment strategy for addressing fractures in tumor-type elbow prostheses.

Young thoracic vertebra diffuse idiopathic skeletal hyperostosis with Scheuermann disease: A case report.

BACKGROUND: Diffuse idiopathic skeletal hyperostosis (DISH) is a disorder characterised by the calcification and ossification of ligaments and entheses. It is a frequent occurrence in elderly males, but rarely encountered in younger individuals. CASE SUMMARY: A 24-year-old male was admitted to the hospital due to low back pain accompanied with numbness in both lower limbs for 10 d. Upon clinical examination and imaging tests, the patient was diagnosed with DISH with Scheuermann disease and thoracic spinal stenosis. Before the operation and medical treatment, the patient had hypoesthesia of the skin below the xiphoid process. Afterward, a standard laminectomy was conducted using ultrasonic bone curette and internal fixation was applied. Subsequently, the patient was given corticosteroids, neurotrophic drugs, hyperbaric oxygen and electric stimulation. As a result of the treatment, the patient's sensory level decreased to the navel level and there was no major change in the muscle strength of the lower limbs. During follow-up, the patient's skin sensation has returned to normal. CONCLUSION: This case is a rare instance of DISH co-existing with Scheuermann's disease in a young adult. This provides a valuable reference point for spine surgeons, as DISH is more commonly observed in middle-aged and elder adults.

Monosodium iodoacetate-induced subchondral bone microstructure and inflammatory changes in an animal model of osteoarthritis.

The monosodium iodoacetate (MIA)-induced osteoarthritis (OA) may lead to cartilage degeneration and histopathological lesions. However, the correlation between inflammatory reaction and subchondral bone remodeling in a rodent osteoarthritic model is ambiguous. In this study, intra-articular injection of MIA was performed in 36 four-week-old specific pathogen-free male Wistar rats to induce OA. After 4 weeks of intervention, changes in intrinsic structural properties of the subchondral bones were measured, and the histological evaluation, as well as biochemical analysis, was conducted. We found that intra-articular injection of MIA increased chondrocyte apoptosis and promoted cartilage matrix degradation, such as cartilage surface defects and shallow or disappearing staining. MIA also induced inflammation, improved the expression of IL-1ß, TNF-α, and matrix metalloproteinase, and decreased the expression of cartilage-specific proteins with the extension of modeling time. Meanwhile, the MIA also significantly accelerated the subchondral bone remodeling, as shown by the decreased subchondral bone density, thinning of trabeculae, disordered cartilage structure, and morphology. In conclusion, we have shown that MIA-induced rodent osteoarthritic model would cause decreased subchondral bone density, sparse trabecular bone, and other manifestations of osteoporosis accompanied by an inflammatory response, which would worsen with the progression of modeling time. Our results suggest that different phases of MIA-induced OA are associated with the changes in subchondral bone microstructure and the progression of local inflammation.