Endosteum Does Not Compensate for Periosteal Loss in Cortical Bone Repair

Introduction: Osteo-progenitor cells reside in both the periosteal and endosteal compartments of bone. Recent studies have shown that periosteal cells are the primary contributors to fracture repair. This study was designed to determine whether endosteal osteogenesis compensates for periosteum (PO) loss in cortical bone repair. We hypothesized that endosteal bone formation will increase in periosteum-deficient defects.

Materials and Methods: Six adult dairy goats were used in the study. Under general anaesthesia, 6-mm circular unicortical defects were created in the lateral metacarpal IV diaphyses of both forelimbs. In one forelimb, the periosteum was stripped from the bone surface for application 2 cm beyond the cortical defect margins. The goats were euthanized after 6 weeks. Bone/defect samples were processed for histology. ImageJ software was used to measure defect infill, periosteal and endosteal callus depth at the dorsal and palmar defect margins. Outcomes were analysed by paired t-tests.

Results: All “PO intact” defects were bridged by new bone, whereas no defect in the “PO stripped” group had bridged. Defect infill was significantly higher in the “PO intact group” (76 ± 4% vs. 55 ± 6%). Periosteal callus was significantly thinner at the defect margins in the “PO stripped” group, however endosteal callus depth was almost identical in both groups.

Discussion/Conclusion: Periosteal stripping significantly reduced periosteal callus formation and defect infill. Endosteal callus formation was almost identical in both groups, disproving our hypothesis and emphasizing the critical importance of periosteum in fracture repair by callus formation.

Acknowledgment

This project was funded by a USDA Hatch Research Fund award.

Publication History

Article published online:
15 July 2025