Conquering Medial Tibial Stress Syndrome
What Research Reveals About The Pathophysiology Of MTSS
Though the anatomic site of MTSS is well known, neither the exact pathophysiologic mechanism nor the specific pathologic lesion are completely understood. Traditionally, researchers believed the underlying mechanism was repetitive microtrauma to the periosteum and fascial attachments as a result of traction forces from the soleus (primarily) and the flexor digitorum longus.12 However, recent MRI and histiologic studies have not supported this periosteal traction-based theory of MTSS. In fact, these studies fail to demonstrate periosteal inflammation.13,14 There is a growing body of evidence that suggests MTSS, like TSF, is a bone stress reaction caused by chronic repetitive loads that induce tibial bending forces. Keep in mind that maximal tibial bending occurs at the narrowest diaphyseal width (middle to distal third of the tibia), which corresponds to the anatomic site of MTSS. Beck states that “when the tibia experiences chronic and repetitive strain in a pattern that involves abnormal or exaggerated bending, it is stimulated to deposit new bone on its periosteal surface at the level of the narrowest diaphyseal cross-section (junction of the middle and distal thirds) to reduce potentially injurious strains at this site in the future.”9 Beck’s tibial bending theory is gaining increasing acceptance among authors and clinicians who treat exercise-induced leg pain. Some authors consider MTSS and TSF to be conditions on a bone stress-failure continuum upon which MTSS is a mild expression and TSF the severe extreme. Why then do some athletes develop chronic refractory cases of MTSS (which never progress to TSF) and others develop TSF without ever demonstrating signs or symptoms of MTSS first? It is not universally accepted that MTSS is simply a mild form of or a precursor to TSF. Many authors believe that although MTSS and TSF may be induced by similar activities, they represent two unique pathologic lesions. Beck goes on to state that “persistent and increasing strain on porous (remodeling) bone incites a positive feedback loop that restimulates remodeling. This results in a protracted hypermetabolic state within the bone. This chronic remodeling in cortical bone, mediated via the periosteum (with or without periostitis or periosteal avulsion), probably represents the pathologic lesion of MTSS.”9 This model would explain why a subset of athletes develops protracted, refractory cases of MTSS that cannot be explained as a self-limiting inflammatory condition of the periosteum or crural fascia. For those athletes who recover in a normal time frame, it is likely that these reparative processes occur rapidly enough to accommodate ongoing tibial loads without triggering this positive feedback loop.9,15 Further research is needed in this area. However, these studies do shed additional light on the pathophysiology of tibial stress injuries and, more specifically, the relationship between MTSS and TSF.