Meningioma Hyperostotic Subtype Defines a TRAF7-Associated Phenotype

BackgroundMeningioma-induced hyperostosis (MIH) is a frequent radiographic finding, yet its underlying mechanisms remain poorly understoodWhile hyperostosis has traditionally been treated as a binary phenomenon, the aim of this study was to determine whether MIH represents a heterogenous process with distinct radiological subtypes associated with genetic associations. MethodsWe retrospectively reviewed the records and imaging of patients with meningiomas resected between 2021-2024 at a single institution. Somatic mutations identified through next-generation sequencing were analyzed. CT images were analyzed for bone involvement and hyperostosis subtype. Type I hyperostosis was defined by destruction of cortical architecture while Type II hyperostosis was defined by the preservation of cortical structure. Associations with TRAF7 mutations were assessed using univariate testing, multivariable logistic regression, and supervised machine-learning models. Quantitative bone density analysis was performed using region-of-interest grayscale histogram analysis. ResultsAmong 384 tumors, 54 (14.1%) exhibited hyperostosis--23 Type I and 31 Type II. TRAF7 mutations were significantly enriched in Type I hyperostosis compared with Type II and non-hyperostotic tumors (78.3% vs 25.8% vs 17.0%, p<0.001). Type I hyperostosis independently predicted TRAF7 mutations (OR:18.73, p=0.001), along with skull base location, smaller tumor size, homogeneous contrast enhancement, and extensive T2 hyperintensity. Gradient boosting achieved the highest predictive accuracy (AUC=0.854). Quantitative bone density analysis demonstrated preserved cortical-cancellous architecture in Type II hyperostosis, whereas Type I showed architectural disruption. ConclusionsMIH is a radiographically heterogenous phenomenon. Hyperostosis with disrupted cortical architecture is strongly associated with TRAF7 mutations and may represent a key feature of this mutations radiographic phenotype.