Revisiting hemostasis strategy: the impact of excessive monopolar electrocautery on periosteal-driven spinal fusion

BACKGROUND CONTEXT: The common surgical approach in posterior spinal fusion (PSF) conflicts with basic principles of bone repair and may lead to high failure rates. In recent years, experimental data has shown that the periosteum plays an indispensable role in fracture bone repair both for skeletal stem/progenitor cells (SSPCs) and for angiogenesis promotion. However, the role of the periosteum in spinal fusion remains experimentally poorly defined. Furthermore, current surgical approach often involves electrocautery to achieve subperiosteal dissection. However, the impact of this electrocautery remains not fully defined. We hypothesize that the periosteum is a potent driver of spinal fusion, and that its excessive ablation through electrocautery can be a significant iatrogenic contributor to reduced bone formation. PURPOSE: This study investigates the periosteum's contribution to spinal fusion and how electrocautery, commonly used for subperiosteal dissection, impacts this contribution. STUDY DESIGN: A nondecorticated murine PSF model compared bone formation after sharp dissection with electrocautery (Caut) versus sharp dissection without electrocautery (Sharp). A nondecorticated model was utilized to isolate the contributions of the periosteum without decortication as a confounding variable. METHODS: Bone formation and integration were evaluated using microCT and histology. Pulse-chase lineage tracing in Aggrecan CreERT2+/Ai9+ mice tracked skeletal stem/progenitor cell (SSPC) source and differentiation pathway. This model identifies mostly cells committed to the chondrogenic lineage during regeneration. Angiogenesis was assessed with Microfil, including 2D and 3D reconstructions. RESULTS: Bone formation was significantly lower on the cauterized side (p=.0002; p