Mechanical modulation of bone fracture repair and restoration to its structural strength must rely on the fundamental physical concept of remodeling according to the type of stress applied to immature or undifferentiated tissue. This article proposes the possible mechanisms of interaction between physical factors and cellular responses in healing long bone fractures and speculates on the advantages and limitations of different experimental models in evaluating these interactions. A revised classification system of fracture union types based on histomorphologic characteristics is introduced here as a reference standard in the studies of possible accelerating factors. Bone fracture union can follow more than one or two pathways, with various combinations of bone formation mechanisms, whereas there may be only one bone remodeling principle. There are definite mechanical and operative interventions that can provide effective enhancement to fracture healing. However, different intervention may limit its association to a specific healing mechanism. The key element in establishing these interactions is defining the precise cellular and molecular mechanisms in a quantitative manner. This can be achieved best by interdisciplinary research collaborations working on a higher level of expertise in each related field using standardized experimental models. Not only a basic understanding of the associated cellular reactions is necessary, but also the specific forms of mechanical stimulation, the dose effect, and its application timing must be determined and validated. Without this basic research effort, it would be difficult to transform such an augmentational modality into effective and reliable therapeutic regimens for clinical application. Furthermore, successful fracture repair enhancement must have proper new bone formation maintenance and remodeling through physiologic loading, or the initial stimulation process may be short lived and unable to reestablish the required biomechanical strength of the long bone. Finally, there is no substitute for a well organized and carefully controlled prospective clinical trial in establishing the validity of any bone fracture healing enhancement modality, regardless of its nature and form of application.
Reprint requests to Edmund Y.S. Chao, PhD, Orthopaedic Research, The Johns Hopkins University, Room 225, Ross Building, 720 Rutland Avenue, Baltimore, MD 21205-2196.
From the Biomechanics Laboratory, Department of Orthopaedic Surgery, The Johns Hopkins University, School of Medicine, Baltimore, MD.