Tibial stress injuries have become an increasingly frequent reason for visits to sports medicine offices and clinics over the past decade. Unfortunately, these patients often leave the office with a diagnosis of shin splints. This nonspecific “diagnosis” has little clinical usefulness in light of the present day understanding of exercise-induced leg pain and, specifically, tibial stress injuries. The term “shin splints” merely describes a symptom of tibial stress injury and has little clinical or diagnostic value.
Researchers have proposed many alternative terms to shin splints over the years. Most terms have a more descriptive anatomic and/or pathophysiologic basis. These terms include tibial stress syndrome, medial tibial stress syndrome, medial tibial syndrome, posterior tibialis syndrome, soleus syndrome and tibial periostitis. Tibial stress syndrome or medial tibial stress syndrome are the terms that most authors and sports medicine clinicians currently favor since Mubarek introduced the term (credited to Drez) in 1982.1 A diagnosis of medial tibial stress syndrome (MTSS) specifically excludes exertional compartment syndrome and tibial stress fracture (TSF). It offers the most accurate description of the involved anatomy and presumed pathophysiology of this most common form of tibial stress injury.
With these points in mind, let us take a closer look at the diagnostic and therapeutic approach to MTSS. A familiarity with the current state of knowledge regarding exercise-induced leg pain, a logical, well directed history and physical, and appropriate special tests will help rule out other causes of exercise-induced leg pain that are beyond the scope of this article (see “Exercise-Induced Leg Pain: A Differential Diagnosis” below).2
Although one should not rule out any potential cause for chronic exercise-induced leg pain without a thorough history and physical, certainly one should have a higher index of suspicion for the most commonly encountered causes: MTSS, TSF and exertional compartment syndrome (ECS). Also keep in mind that two or more of these conditions may exist concurrently (e.g. MTSS and ECS) or sequentially (e.g. MTSS and TSF), causing symptoms to overlap and cloud the diagnosis. A thorough knowledge of anatomy and biomechanics as well as an understanding of the specific injuries will help the clinician sort these out.
The lower leg is second only to the knee as the most common site of running injuries.3 However, it has been difficult to establish the precise incidence of MTSS (particularly in the general population) due to inconsistent definitions of the condition and the varied use of terminology in the past. 
Recent studies report up to a 35 percent incidence of MTSS in actively training military recruits and 13 percent in civilian runners.4 Bennett looked at high school cross-country runners over the course of a season and found 12 percent developed MTSS (19 percent in females).5 Taunton’s retrospective analysis of over 2,000 running injuries ranked MTSS as the fifth most common injury and, when combined with TSF, would be the third most common injury behind only patellofemoral pain syndrome and iliotibial band friction syndrome.6
By any measure, tibial stress injuries represent a significant cause of exercise-induced leg pain. Most recent studies rank MTSS as the leading cause of chronic exercise-induced leg pain ahead of TSF and ECS. I have found this to be the case in my own experience as well.
Runners account for the majority of MTSS cases one sees in sports medicine practices although any running, jumping or cleated sport can contribute to MTSS cases.
Women are at least twice as likely to develop MTSS as men, particularly if they have a body mass index (BMI) of less than 21 kg/m2.5-7 However, female gender is only one of many factors for increased risk that researchers have proposed. Most of the studies that have looked at risk factors for tibial stress injuries have focused on TSF although MTSS can be linked to many of these as well. 
Typically, these studies have broken down these risk factors into extrinsic and intrinsic categories. Extrinsic factors include: training errors (with regard to frequency, duration and intensity); surface type and inclination; and shoe type and wear. Intrinsic factors include: endocrine factors (and their relationship to the female athlete triad of amenorrhea, disordered eating and osteoporosis); bone geometry and density; structural and biomechanical abnormalities; nutritional status; and previous running and injury history. Most of these risk factors have been well documented, particularly with regard to TSF. However, I would like to take a closer look at three specific risk factors that have an impact on MTSS. Indeed, some of these risk factors may help shed light on the relationship between MTSS and TSF.
Decreased regional bone marrow density. Recent studies have shown that athletes with MTSS demonstrated lower bone marrow density in the affected region of their tibias in comparison to non-athlete and athletic controls.4 However, this finding was truly regional in that the athletes with MTSS and decreased regional bone marrow density in fact had higher than normal bone marrow density in other regions as one would expect in athletes. Additionally, the decreased regional bone marrow density increased following recovery. However, it is uncertain as to whether this is a cause or a result of MTSS.
Interestingly, there was decreased bone marrow density in the unaffected leg among those with unilateral MTSS.4 This suggests the decreased regional bone marrow density preceded (and perhaps caused) the MTSS. In either case, there seems to be a clear association between MTSS and locally decreased tibial bone marrow density.
Bone geometry. Multiple studies have demonstrated a relationship between smaller tibial cross-sectional areas and tibial stress injuries.8-11 Long bones with narrow diaphyseal widths will bend to a greater extent when loaded than those with wider diaphyses. This supports the tibial bending theory of tibial stress injuries. This theory suggests that chronic repetitive loads that induce tibial bending cause bone stress around the site where maximum bending occurs. This corresponds to the most common location for MTSS. This theory also provides support for the pathophysiologic link between MTSS and TSF. 
Biomechanical abnormalities and structural malalignments. Despite the common acceptance of biomechanical/ structural contributions to the development of tibial stress injuries and other exercise-induced leg conditions, there continues to be conflicting data in the current peer-reviewed literature in regard to identifying specific biomechanical risk factors. Researchers have paid much attention to biomechanical abnormalities, particularly excessive subtalar joint pronation (in both degree and velocity) and its relationship to tibial stress injuries. However, only two prospective studies have demonstrated a relationship between excessive subtalar joint pronation and MTSS.5,7 Other studies have been inconclusive or conflicting in this regard.
Despite the general acceptance and broad use of foot orthoses in treating athletes with tibial stress injuries, the perceived benefits of these devices (reduction of injury frequency, improving skeletal alignment, impact cushioning and sensory feedback) are currently based on limited scientific evidence. Obviously, more research is needed in this area.
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.
Diagnosing MTSS is relatively straightforward although a well directed history and physical are required to rule out other causes of exercise-induced leg pain.
Athletes presenting with MTSS will typically complain of an aching pain at the middle to distal medial shin with activity (most commonly running). Medial tibial stress syndrome is similar to many overuse injuries in that athletes initially experience pain at the beginning of an activity. The pain then diminishes and often returns hours after completing the activity. These athletes generally achieve symptom relief with rest but the condition may progress to the point of causing pain even during inactivity.
Eventually, athletes may experience pain throughout the offending activity to the point of impaired performance. This is often the point where the athlete seeks medical attention. A common scenario is for an athlete to present one to two weeks into a new season or training program. Keep in mind that bone remodeling typically starts five days after stimulation and leaves the bone in a relatively weakened state for approximately eight weeks.7
The hallmark of the physical exam is tenderness over a 4 to 6 cm area at the posteromedial margin of the middle to distal third of the tibia. This is in contrast to TSF, which presents with well localized point tenderness. Refer to “How To Differentiate Between MTSS And TSF” below) for other diagnostic differences between MTSS and TSF.
The tenderness with MTSS may be exquisite and can often extend into the adjacent soft tissues. Mild soft tissue swelling and induration may be present. While researchers have described percussion, vibration with a tuning fork or using therapeutic ultrasound as adjunctive diagnostic maneuvers to help identify TSF, studies have shown these diagnostic tools have a low sensitivity.16 Passive stretch of the soleus, heel rises and unilateral hopping may reproduce symptoms. Radiographs are indicated to rule out TSF, infection or neoplasm but findings are generally normal with MTSS. Occasionally, one may observe cortical thickening due to chronic remodeling.
If the patient is a competitive athlete or if suspicion for TSF is high, obtaining a triple phase 99Tc bone scan (TPBS) is indicated. The triple phase bone scan is highly sensitive for tibial stress injuries with the added advantage of being able to distinguish between MTSS and TSF. MTSS will generally (although not always) be positive, displaying a longitudinally or vertically oriented diffuse uptake on the delayed images only. Whereas false negative findings may occur with MTSS, TPBS is virtually 100 percent sensitive for TSF, demonstrating a focal, intense uptake of tracer on all three phases.
MRI has become an increasingly utilized modality for assessing tibial stress injuries in athletes. It has also shed new light on the relationship between MTSS and TSF. Tibial stress fractures are clearly delineated on MRI and the sensitivity is similar to that of TPBS. In cases of acute MTSS, MRI will demonstrate findings consistent with tibial stress injury. However, chronic MTSS often demonstrates normal findings. Obtaining a MRI can also be helpful in differentiating MTSS from rarer longitudinal tibial stress fractures. With superior anatomic visualization, decreased radiation exposure and reasonable cost for a limited study, MRI is becoming a first line study for tibial stress injuries in many sports medicine practices.
Short-term management of MTSS is centered around relative rest and activity modification. Rest is the most effective, though often prolonged, treatment approach. Athletes must be aware that many cases of MTSS require upward of four months of relative rest or altered training. In my experience, scintigraphically negative MTSS may resolve in as little as three to six weeks with proper treatment but scintigraphically positive MTSS generally takes eight to 16 weeks. Cross training options during this period include cycling, swimming, deep water/pool running or upper body ergometry.
Institute ice and NSAIDs (for pain control) early on in treatment. If symptoms are present even with daily activities, patients can use a cast boot or pneumatic leg splint for two to four weeks. Physical therapy is a key component of treatment and may include soft tissue management, massage, electric stimulation, ultrasound or iontophoresis. Some clinicians have used bone growth stimulators (electric, pulsed electromagnetic fields or ultrasonic) on tibial stress injuries in athletes. However, keep in mind that the only randomized controlled trial that evaluated the effect of bone stimulators on TSF in athletes found no difference in healing times.17
Cold laser treatment is a relatively new option although it is largely unproven. Acupuncture is another alternative treatment for particularly refractory or painful cases. Surgery for chronic, refractory cases of MTSS is an option although results are variable at best. Performing a release of the fascial attachments to the posteromedial tibial margin has had reported success rates of 29 to 86 percent.17 However, a recent study reported that only 41 percent of athletes returned to pre-surgery levels of participation.18 There is also an interesting case study describing a college athlete who was able to get through her soccer season following a sympathetic block for refractory MTSS.19
Long-term management of MTSS is centered on prevention. Eliminating training errors is the cornerstone of preventing MTSS. Doing “too much too soon” at the start of a training program or sports season is the most common training error scenario. The highest incidence of bone stress injuries occur in the first month, which corresponds to the most porous phase of the bone remodeling cycle.9
Practitioners also need to address surface and terrain issues. Grass, sand and road shoulders are not universally preferable to road running due to their irregular surfaces. A level uniform surface of moderate firmness is optimal for minimizing injury risk.15 Shoes should be sport-specific and patients should change running shoes every 250 to 300 miles. Studies have shown that a running shoe may lose greater than 60 percent of its shock-absorbing capacity after as little as 250 miles.3,20
Establishing normal strength, endurance and flexibility of calf and leg musculature is also important. A tight or overly strong triceps surae can impart an increased bending moment on the tibia. Weak or fatigued leg muscles may also result in up to a 25 percent increase in ground reactive forces.9
One should also address biomechanical abnormalities and structural malalignments but keep in mind that investigators have found few statistical relationships between alignment measures and overuse injuries. However, two recent studies do support an association between excessive subtalar joint pronation and MTSS in runners.5,7
Finally, do not overlook hormonal and nutritional factors. The female athlete triad (amenorrhea, disordered eating and osteoporosis) has been linked to decreased bone marrow density and increased risk for bone stress injuries.15 It is important to note that the female athlete triad is not limited to elite athletes and that many athletes with these issues will not always meet the classic definitions or criteria.16
Nutritional assessments and diet counseling may be indicated even for athletes without disordered eating. Insufficient protein or calcium intake relative to the caloric demands of the athlete’s specific activity may be present.16
The return to activity for athletes after treatment for MTSS must be gradual and individualized. Athletes must adhere to the “start low and go slow” mantra. Once athletes are asymptomatic, they can typically start at 50 percent of their baseline training load and increase the frequency/intensity/duration by 10 to 15 percent per week. They should avoid back-to-back days of repetitive impact activity for the first two to four weeks, depending on the severity of the case.
If symptoms recur, two additional weeks of rest are recommended and should be followed by a “downgraded” training regimen. Patients can often achieve a return to full, unrestricted activity in three to six weeks. However, a delayed return is not uncommon for this often refractory condition.
Dr. Hester is a Fellow of the American College of Foot and Ankle Surgeons. He is in private practice with Sports Medicine Associates and Pro Sports Orthopedics, and is the team podiatrist for the Boston Celtics.
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