Background: The ongoing digital transformation of healthcare has enabled innovative technologies that improve diagnosis, treatment planning, and outcomes. Among these, three-dimensional (3D) printing has gained prominence in surgical disciplines for converting digital imaging data into patient-specific physical models. In orthopedics and traumatology, 3D printing is used to produce anatomical models, surgical guides, and custom implants, thereby enhancing preoperative planning, surgical precision, and interdisciplinary communication. Despite its growing adoption, integrating 3D printing into clinical workflows remains complex and requires stringent quality assurance. Each phase of the production process—from image acquisition and segmentation to material selection and post-processing—affects the safety and performance of the final product. Standardized quality approaches and regulatory frameworks are therefore essential to ensure reproducibility, biocompatibility, and patient safety. This systematic review consolidates current knowledge on quality standards and implementation strategies for 3D printing in orthopedic and traumatological care. It identifies practical pathways for clinical integration while highlighting challenges, opportunities, and areas for future research. Methods: A systematic literature search was conducted in PubMed, the Cochrane Library, and the Web of Science, following the PRISMA-P (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols) 2015 checklist and supplemented by manual searches. Reference management was performed using Rayyan QCRI (Qatar Computing Research Institute). Abstracts and full texts were analyzed with Voyant Tools to identify thematic focuses based on collocate analysis. Results: Nineteen publications met the inclusion criteria. The review highlights a focused but limited body of literature. Key factors influencing product quality include material choice, manufacturing accuracy, and adherence to validated quality control protocols. Discussion: With increasing digitalization and the integration of artificial intelligence, future quality initiatives will likely emphasize standardized preoperative planning, ethical oversight, and regulatory compliance to support personalized care models in orthopedics and traumatology.

Aim: To evaluate the efficacy and tolerability of febuxostat (FBX) and benzbromarone (BNZ) combination therapy in patients with difficult-to-treat (D2T) gout. Methods: This observational study was performed at two centers and included patients fulfilling the 2015 European Alliance of Associations for Rheumatology/American College of Rheumatology (EULAR/ACR) gout classification criteria, with clinical tophi and suboptimal response to standard urate-lowering therapy. A two-step treatment regimen was implemented: a 6-month dose escalation of the FBX dose followed by add-on BNZ. Demographic, clinical, and laboratory data—including cardiovascular risk factors (CVRFs), history of nephrolithiasis, liver enzymes, and estimated glomerular filtration rate (eGFR)—were recorded. Changes in serum urate (SUA) and eGFR were analyzed using paired t-tests. Results: The study population comprised 15 patients (87% male, median age 59 years) with longstanding gout [median 15 years, range 3–31; interquartile range (IQR) 8–25]. Baseline SUA was 10.3 ± 1.7 mg/dL; mean eGFR was 63.7 ± 23.6 mL/min. CVRFs were common (hypertension, 93%; dyslipidemia, 73%: major adverse cardiovascular events, 13%; diabetes, 7%). At 12 months, SUA had decreased significantly to 2.9 ± 1.1 mg/dL (Δ = 7.4 mg/dL; p < 0.01), with FBX alone contributing to a Δ of 5.4 mg/dL and BNZ an additional Δ of 2.1 mg/dL (both p < 0.01). Tophi resolved in 60% of patients. No serious adverse events or significant changes in liver or renal function were observed. One unrelated death was recorded. Conclusions: FBX + BNZ was effective and well-tolerated in patients with severe D2T gout, achieving a substantial reduction in SUA and clinically significant dissolution of tophi.

Aim: Osteoporosis (OP) is caused by imbalanced bone remodelling homeostasis. It is highly prevalent, especially in post-menopausal women, resulting in high risk of fracture and morbidity. Mesenchymal stromal cells (MSCs) are osteoblast progenitors, and orchestrate the function of surrounding cells including osteoblasts. Understanding MSC phenotype and function is therefore critical in discerning the aetiology of OP and developing superior therapies. Currently, adequate long-term therapeutic strategies are not available. Methods: Bioinformatic analysis of ribonucleic acid sequencing (RNA-seq) data revealed differential expression of genes primarily related to osteogenic differentiation and proliferation, followed by confirmatory in vitro analysis. Results: This study identified novel and previously proposed targets for therapeutic intervention in OP. Functional assessment demonstrated reduced MSC number and osteogenic capacity associated with OP. Proliferation was not affected but OP was unexpectedly associated with a reduction in MSC adipogenic differentiation capacity, correlating with donor age. Conclusions: These data indicate specific targets for further studies of future treatments for OP, including the assessment of modified MSCs as therapeutics. Advances in this area may contribute to reducing fracture-associated morbidity and mortality, and improving quality of life for the 200 million people living with OP globally.