Multiple Osteochondromas Comorbid With Enlarged Parietal Foramina, Elongated Styloid Processes, and Tibiofibular Synostosis: A Case Report and Review of Literature

• Published in: American journal of clinical pathology Vol. 156; no. 4; pp. 513 - 520
• Main Authors: Baugher, Elizabeth C, Batarseh, Tamara R, Becker, Ashley K, Cantu, Austin J, Carr, Evan W, Velavan, Sumathilatha Sakthi
• Format: Journal Article
• Language: English
• Published: Chicago Oxford University Press 01-10-2021
• Subjects: Cadavers; Comorbidity; Dysostosis; Femur; Fibula; Literature reviews; Medical students; Osteochondroma; Skull; Tibia; Vertebrae
• ISSN: 0002-9173; 1943-7722
• DOI: 10.1093/AJCP/AQAA282

Objectives: This study investigates a unique case of multiple osteochondromas (MO) comorbid with enlarged parietal foramina and correlates the findings with the existing literature. The aim of this study is to provide a deeper understanding of anatomic variation for physicians. Methods: A 66-year-old White male donor was examined during a routine cadaveric dissection performed by medical students in an anatomy laboratory. Detailed exploration of the skeleton and organs was performed, and photographs were taken. Tissue samples were obtained from multiple outgrowths, and histopathologic examination was done. Results: Bilateral bony growths were noted rising from the long bones of the upper and lower extremities (femur, tibia, fibula, and radius). An accessory muscle was found to be associated with the left radial bony growth. Histopathologic examination was positive for osteochondroma. Inspection of the skull revealed enlarged parietal foramina. Other findings included tibiofibular synostosis, abnormally shaped vertebral bodies and ribs, and elongated styloid processes of the skull. Conclusions: In combination with the histopathologic examination, the case report and literature review elucidate a more precise clinical picture for those affected with MO or similar disorders. This report also emphasizes the necessity of further investigation of the pathogenesis of MO and Potocki-Shaffer syndrome.