Biomechanical Risk Factors of Tibial Stress Fractures

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Introduction/Overview[edit | edit source]

A tibial stress fracture (TSF) is a chronic injury that occurs when there is a disparity between external forces and the body’s ability to recover from them. Specifically, it occurs when the accumulation of repetitive submaximal forces to the tibia exceeds the bone’s ability to absorb the impact and remodel[1]. If not treated, this can result in microscopic cracks in the bone which can eventually lead to macroscopic fractures [1]. It is officially considered a fracture when there is visible indication of fracture of the bone from medical imaging [2]. Stress fractures can be categorized into 2 types: fatigue fracture or insufficient fracture. Fatigue fracture occurs when there are abnormal loads applied to a healthy aligned bone and are common in the athletic and healthy population [2]. Whereas an insufficient fracture occurs when average stress causes damage to clinically unhealthy bone[2]. Although stress fractures are not limited to the tibia, as it is also seen in the hip, tarsals, femur and even the ribs, it is most commonly occurring in the tibia [1].

Biomechanical Pathophysiology: Microscopic Level[edit | edit source]

The biomechanical pathophysiology of a tibial stress fracture can be explained via the Targeted Bone Remodelling Concept [3]. The vicious cycle begins with repetitive submaximal loading to the tibia, such as running, which causes stress to the bone. The stress disrupts the osteocytes which causes bone fatigue, micro damage and eventually cell apoptosis [3]. Osteoclasts arrive to the site of injury and remove the dead bone cells [3]. This results in a temporary negative bone space and a reduction in bone structural integrity [3]. Within the first few weeks, osteoblast recruitment occurs in the remodeling space and unmineralized bone is formed in the cavity. At this point, only 65-70% of the matrix is completely mineralized and mechanical stiffness is not completely restored [3]. From here, there are two fates of the bone: either the bone is fully mineralized, which can take up to a year to complete, or the submaximal loading continues [3]. If the loading persists, over time the microcracks can become microfractures and eventually a true fracture [3].

Intrinsic Risk Factors[edit | edit source]

Knee Stiffness[edit | edit source]

In a 2-year prospective study, which consisted of 300 runners, it was found that those who sustained an overuse running injury had significantly higher knee stiffness [4]. Messier et al. suggest that the knee acts like a shock absorber by dissipating forces during foot strike in the running gait cycle [4]. Thus, if the knee is stiffer, this results in less energy dispersion which can lead to damage in the surrounding area [4].

Sex[edit | edit source]

Sex is a highly recognized large contributor to risk of tibial stress fracture [5]. Female athletes have a 2.3x higher risk of stress fracture in comparison to males in sex-comparable sports such as baseball, basketball, cross country, lacrosse, soccer, and indoor/outdoor track [5]. This increase in risk could be attributed to Relative Energy Deficiency in Sport, formerly know as the Female Athlete Triad [6]. This is a decrease in caloric intake due to social pressures to maintain a certain appearance, menstrual disturbance/hormone imbalance and low bone mineral density. With low caloric intake, the body diverts limited calories and nutrients to more vital processes which can impair bone remodeling/abnormal bone turn over [7].

Anthropometrics and Body Composition[edit | edit source]

Tibial width is important as it is widely thought that wider bones provide a mechanical advantage such that they can disperse more forces due to the larger cross-sectional area [8]. Inversely, various studies indicate that those with narrower tibias had a higher risk of developing a stress fracture injury [8][9]. Additionally, females on average have more narrow tibias and thinner cortices suggesting lower biomechanical stress tolerance [8]. It has also been suggested that a smaller cross section of muscles in the thigh is a sign of risk due to increase in bone fatigue and can indicate low conditioning of the bone [8].

Bone Mineral Density[edit | edit source]

Bone mineral density has commonly been used as a marker for one of the characteristics of bone strength, thus it also makes a strong marker for risk of fracture. There is an inverse relationship where the lower the bone mineral density the higher the bone fragility. This results in an increased risk of insufficiency fracture [10]. Low calcium intake and hormonal disruption are linked to low bone mineral density[10].

Extrinsic Risk Factors[edit | edit source]

Sport of choice[edit | edit source]

The highest rates of stress fractures found amongst the endurance athlete population such as cross country, soccer, basketball, track and field, gymnastics, and dance [5]. Generally, any sport or activity that results in frequent jumping or loading of the lower limb is associated with an increase in tibial stress fracture [5].

Increase in training[edit | edit source]

A sudden increase in exercise intensity, rapid progression of exercise and duration can increase risk of developing a tibial stress fracture [5]. Increasing distance beyond 32 km (20 miles) per week was found to be associated with an increased rate of stress fractures [8]. Athletes with shorter preseasons had higher risks of injury due to heavy increase in conditioning and reduction in rest [5].

Training surface[edit | edit source]

Tibial strain in runners were 48-258% higher when running over ground compared to treadmills [11]. To decrease the stress subjected to the shank, avoid concrete running, and opt for treadmill, grass, or a rubber track.

Orthotics[edit | edit source]

Worn running shoes may increase the risk for stress fracture due to decreased shock absorption. There is an overall decrease in incidence of overuse injury and more site-specific reduction in the incidence of femoral and tibial stress fractures with the implementation of orthotic insoles [7].

Clinical Considerations[edit | edit source]

Since this is a chronic injury, it is important to recognize the symptoms and signs before the microcrack evolves into a true fracture. Take careful consideration of training regiment and rest periods when a client presents with “shin splints” or medial tibial stress syndrome [1]. For this is the early stage of a tibial stress fracture.

If a person presents with symptoms of tibial stress fracture, consider cross training of a sport that imparts less repetitive stress to the lower extremity. Consider golf, swimming, cycling or yoga for they have very low reported incidences of stress fractures [12].

In a prospective study of track and field athletes, 60% of those who sustained a fracture in the past, were reinjured within the year [13]. This could relate back to the idea that bone does not fully heal until approximately a year after injury. Be cautious to not return to maximal capacity immediately after perceived recovery.

If the person is an athlete presenting with symptoms of tibial stress fracture or medial tibial stress syndrome, consider other factors like Relative Energy Deficiency in Sport. Assess their nutrition, psychological state (self-efficacy, social pressures, body image) and menstrual cycle. Addressing these factors can aid in rehabilitation and recovery.

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 Kiel J, Kaiser K. Stress Reaction and Fractures. [Updated 2020 Aug 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507835/
  2. 2.0 2.1 2.2 Romani WA, Gieck JH, Perrin DH, Saliba EN, Kahler DM. Mechanisms and management of stress fractures in physically active persons. J Athl Train. 2002 Jul;37(3):306-14. PMID: 16558676; PMCID: PMC164361.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Hughes JM, Popp KL, Yanovich R, Bouxsein ML, Matheny RW Jr. The role of adaptive bone formation in the etiology of stress fracture. Exp Biol Med (Maywood). 2017 May;242(9):897-906. doi: 10.1177/1535370216661646. Epub 2016 Aug 5. PMID: 27496801; PMCID: PMC5407583.
  4. 4.0 4.1 4.2 Messier SP, Martin DF, Mihalko SL, Ip E, DeVita P, Cannon DW, Love M, Beringer D, Saldana S, Fellin RE, Seay JF. A 2-Year Prospective Cohort Study of Overuse Running Injuries: The Runners and Injury Longitudinal Study (TRAILS). Am J Sports Med. 2018 Jul;46(9):2211-2221. doi: 10.1177/0363546518773755. Epub 2018 May 23. Erratum in: Am J Sports Med. 2021 Feb;49(2):NP13. PMID: 29791183.
  5. 5.0 5.1 5.2 5.3 5.4 5.5 Rizzone KH, Ackerman KE, Roos KG, Dompier TP, Kerr ZY. The Epidemiology of Stress Fractures in Collegiate Student-Athletes, 2004-2005 Through 2013-2014 Academic Years. J Athl Train. 2017 Oct;52(10):966-975. doi: 10.4085/1062-6050-52.8.01. Epub 2017 Sep 22. PMID: 28937802; PMCID: PMC5687241.
  6. Bennell KL, Malcolm SA, Thomas SA, Reid SJ, Brukner PD, Ebeling PR, Wark JD. Risk factors for stress fractures in track and field athletes. A twelve-month prospective study. Am J Sports Med. 1996 Nov-Dec;24(6):810-8. doi: 10.1177/036354659602400617. PMID: 8947404.
  7. 7.0 7.1 Vannatta CN, Heinert BL, Kernozek TW. Biomechanical risk factors for running-related injury differ by sample population: A systematic review and meta-analysis. Clin Biomech (Bristol, Avon). 2020 May;75:104991. doi: 10.1016/j.clinbiomech.2020.104991. Epub 2020 Mar 14. PMID: 32203864.
  8. 8.0 8.1 8.2 8.3 8.4 Beck TJ, Ruff CB, Shaffer RA, Betsinger K, Trone DW, Brodine SK. Stress fracture in military recruits: gender differences in muscle and bone susceptibility factors. Bone. 2000 Sep;27(3):437-44. doi: 10.1016/s8756-3282(00)00342-2. PMID: 10962357.
  9. Hart NH, Newton RU, Tan J, Rantalainen T, Chivers P, Siafarikas A, Nimphius S. Biological basis of bone strength: anatomy, physiology and measurement. J Musculoskelet Neuronal Interact. 2020 Sep 1;20(3):347-371. PMID: 32877972; PMCID: PMC7493450.
  10. 10.0 10.1 Myburgh KH, Hutchins J, Fataar AB, Hough SF, Noakes TD. Low bone density is an etiologic factor for stress fractures in athletes. Ann Intern Med. 1990 Nov 15;113(10):754-9. doi: 10.7326/0003-4819-113-10-754. PMID: 1978620.
  11. Milgrom C, Finestone A, Segev S, Olin C, Arndt T, Ekenman I. Are overground or treadmill runners more likely to sustain tibial stress fracture? Br J Sports Med. 2003 Apr;37(2):160-3. doi: 10.1136/bjsm.37.2.160. PMID: 12663360; PMCID: PMC1724607.
  12. Bennell KL, Brukner PD. Epidemiology and site specificity of stress fractures. Clin Sports Med. 1997 Apr;16(2):179-96. doi: 10.1016/s0278-5919(05)70016-8. PMID: 9238304.
  13. Bennell KL, Malcolm SA, Thomas SA, Wark JD, Brukner PD. The incidence and distribution of stress fractures in competitive track and field athletes. A twelve-month prospective study. Am J Sports Med. 1996 Mar-Apr;24(2):211-7. doi: 10.1177/036354659602400217. PMID: 8775123.