Emerging Options for Biologic Enhancement of Stress Fracture Healing in Athletes

Timothy L. Miller, MD; Christopher C. Kaeding, MD; Scott A. Rodeo, MD

Disclosures

J Am Acad Orthop Surg. 2020;28(1):1-9. 

In This Article

Risk Stratification

Stress fractures result from an imbalance between the creation and repair of microtrabecular injury within bone that is caused by repetitive microtrauma. Commonly the term "stress reaction" is used to describe an overuse injury of bone that has not progressed to a radiographically identifiable fracture line. Because stress fractures occur along a continuum of severity and the clinical picture varies by location, a classification system is necessary to assess and effectively communicate regarding these injuries. In the early 2000s Boden and colleagues[3,4] stratified stress fractures as low-risk or high-risk. Injuries at high-risk sites require the most aggressive treatment to prevent complete fracture, delayed union, re-fracture, and osteonecrosis. These sites are listed in Table 1. High-risk sites require extended time to heal after diagnosis and typically occur where tensile forces are concentrated and/or vascularity is decreased.[3] More recently, Kaeding and Miller[5] have combined clinical and radiologic factors to create a grading system for severity of bony stress injuries (Table 2) that has shown high interobserver and intraobserver reliability among sports medicine and orthopaedic clinicians. In addition, this system has been shown to reliably predict time to healing and return to sports participation after the diagnosis of a stress fracture.[6,7]

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