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

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.

This study investigates the periosteum's contribution to spinal fusion and how electrocautery, commonly used for subperiosteal dissection, impacts this contribution.

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.

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.

Bone formation was significantly lower on the cauterized side (p=.0002; p<.0001) 6 weeks after surgery. Sharp dissection without electrocautery triggered a periosteum-driven regenerative process similar to fracture repair, involving both endochondral and intramembranous ossification. Electrocautery abolished this response and significantly decreased periosteum-derived chondrogenesis (p=.0009). Angiogenesis was also reduced on the cauterized side (p=.0367). Without surgical decortication, new bone integrated into the native cortex through biological remodeling, indicating that surgical decortication may not be necessary.

The periosteum is a potent driver of PSF bone formation through combined endochondral and intramembranous ossification, achieving integration without surgical decortication.

Monopolar electrocautery can destroy key regenerative contributions of the periosteum in PSF, cautioning the excessive use of monopolar electrocautery in surgical practices. More research is needed to determine the impact of alternate means of achieving hemostasis such as bipolar on bone formation, as these may better preserve periosteal tissue.