Background/Objectives: To evaluate the association between adjunct tendon vibration and changes over 12 months in dual-energy X-ray absorptiometry (DXA)-derived bone mineral density (BMD) T-score and bone turnover markers in older adults with osteoporosis receiving standard care in a non-randomised controlled cohort study. Methods: This 12-month prospective non-randomised controlled cohort study included 100 adults aged ≥60 years with DXA-confirmed osteoporosis recruited from orthopaedic clinics in the Greater Thessaloniki area. Fifty participants received adjunct tendon vibration therapy in addition to usual care, while 50 received usual care alone. Usual care consisted of calcium and vitamin D supplementation. The primary outcome was post-intervention BMD T-score, analysed using analysis of covariance (ANCOVA) adjusted for baseline T-score. Secondary outcomes included changes in bone turnover markers and calcium/phosphate metabolism. Sensitivity analysis was conducted using a linear mixed-effects model with repeated BMD measurements. Results: Baseline characteristics were comparable between groups. Over 12 months, the intervention group showed greater improvement in BMD T-score than controls (median change 0.90 [0.70–1.00] vs. −0.10 [−0.10–0.10], p < 0.001). The adjusted between-group difference was 0.871 (95% CI 0.773–0.968; p < 0.001). Results remained consistent after adjustment for age and sex. The mixed-effects model confirmed a significant group × time interaction (β = 0.922, 95% CI 0.806–1.038; p < 0.001). Bone resorption markers decreased more in the intervention group. The magnitude of the observed BMD improvement (~0.9 T-score units) is notable for a non-pharmacological intervention and should be interpreted cautiously. Conclusions: Adjunct tendon vibration was associated with a more favourable BMD trajectory and changes in bone turnover markers in older adults with osteoporosis receiving standard care. Given the non-randomised design and potential residual confounding, these findings should be interpreted as associative rather than causal.

Primary bone vascular neoplasms comprise a rare and biologically heterogeneous group of endothelial tumors encompassing benign, intermediate, and malignant entities with distinct clinicopathological, molecular, and prognostic characteristics. These tumors remain diagnostically and biologically challenging because of overlapping histopathological features, heterogeneous clinical behavior, evolving molecular landscapes, and limited disease-specific evidence. Advances in bone pathology, immunophenotyping, molecular diagnostics, and genomic profiling have substantially improved tumor classification and biological characterization. Importantly, contemporary classification and molecular studies have also highlighted the biological heterogeneity of vascular lesions involving bone, distinguishing well-defined vascular neoplasms from vascular malformations and identifying additional molecularly defined entities relevant to osseous disease and differential diagnosis. Concurrently, increasing recognition of the bone microenvironment and osteoimmunology provides a broader framework for understanding interactions among endothelial, skeletal, stromal, and immune populations and the extracellular matrix, with potential relevance to angiogenesis, bone remodeling, and tumor biology. Previous authoritative syntheses have established the classification, molecular features, diagnosis, and clinical management of these neoplasms. However, comparatively limited attention has been devoted to integrating tumor-intrinsic alterations with vascular–bone crosstalk, extracellular-matrix and mechanobiological signaling, osteoimmune regulation, and emerging precision-oncology strategies. Building on these foundations, this review integrates current evidence on classification, molecular pathogenesis, the skeletal microenvironment, osteoimmunology, biomarkers, and precision oncology. Where relevant, molecularly defined vascular neoplasms and vascular anomalies involving bone are discussed to clarify classification, molecular context, and differential diagnosis without conflating these lesions with the principal WHO-defined primary vascular neoplasms of bone. Findings directly demonstrated in primary bone vascular neoplasms are distinguished from mechanistic concepts extrapolated from physiological bone biology, other bone tumors, or non-osseous vascular neoplasms. Through this evidence-calibrated approach, we propose an integrated vascular–bone–immune framework, identify key knowledge gaps, and define priorities for disease-specific translational research and more individualized patient management.