When considering disc pathology, one of the most-asked questions is, “How do you determine causality and age-date the lesion?” Medical literature has purposefully avoided answering this type of question to apparently avoid any appearance of pandering to the medical-legal community, as evidenced by Fardone and Milette (2001) reporting, “The term herniated disc does not infer knowledge of cause, relation to injury or activity, concordance with symptoms, or need for treatment” (p. E108).

Yet 14 years later, upon further evidence, Fardon et al. (2014) reported the following:

The category of trauma includes disruption of the disc associated with physical and/or imaging evidence of violent fracture and/or dislocation and does not include repetitive injury, contribution of less than violent trauma to the degenerative process, fragmentation of the ring apophasis in conjunction with disc herniation, or disc abnormalities in association with degenerative subluxations. Whether or not a ‘less than violent’ injury has contributed to or been superimposed on a degenerative change is a clinical judgment that cannot be made on the basis of images alone; therefore, from the standpoint of description of images, such discs, in the absence of significant imaging evidence of associated violent injury, should be classified as degeneration rather than trauma. (p. 2531)

As described by Fardone above, the definition and understanding of “violent injury” becomes an important arbiter in determining causality and lends an important understanding to age-date the herniation and/or bulge. In understanding the nature of Fardone’s tag of “violent,” science gives us answers rather than intuitive perceptions or rhetoric, and the quantification of energy transferences to victims in accidents gives us those answers.

The rate of change in speed (“acceleration,” or “ΔV”) of any free-moving body is what contributes to quantifying energy transfer and can be directly correlated to injury. Brault, Wheeler and Siegmund (1998) reported that in rear-end collision testing, it was determined whiplash could occur with a change in speed as low as 2.49 mph ΔV where there was no visual damage to the automobile.

Krafft, et al. (2002) reported symptoms at a ΔV of 12.5 km (7.77 mph) and an injury mean threshold of 4.2 g-force for males and a ΔV of 9.6 km (5.97 mph) with a mean of 3.6 g-force for females. Using this data, a corresponding window of time can be calculated between .084 seconds for males and .080 seconds for females (verifying that females are more at risk than males), resulting in a mean of .082 seconds. As evidenced above, acceleration (ΔV) is important as it is part of the physics determining g-force that explains injury thresholds and gives a numerical value to Fardone, et al.’s (2014) use of the descriptor “violent injury.”

The risk for injury is present in a vehicle no matter the initial speeds or damage to the protective equipment, as transference of force is the prime factor in accidents. Additionally, low-speed collisions have a history of little to no damage; therefore, little or no energy is absorbed by the safety equipment and design of the vehicles, yet the occupant is subject to this force even with safety restraints. Because of these factors, only a few pieces of information are needed to quantify the energy transfer an occupant is subjected to:

• The SPEED just before the collision of each vehicle involved.
• The WEIGHT of each vehicle and its occupants.
• The TIME (t) involved (in the case of the above example…082 seconds)

Here are two examples:

Example A: A 6,100-pound SUV traveling at 7 mph rear-ends a 4,200-pound car stopped at a red light, and the SUV stops as a result of the collision. The car (and its occupants) will experience a resultant ΔV of 10.67 mph (…which is not to be confused with the speed of the bullet vehicle that struck the target vehicle).

Example B: A 30,000-pound truck and trailer backing up at 2 mph backs into the rear of a 4,800-pound occupied parked van, and the truck stops as a result of the collision. The van (and its occupants) will experience a ΔV of 12.5 mph.

Regarding the Krafft, et al. (2002) tables 1-4 (pg. 3): In both examples above, the acceleration threshold for injury of males and females was exceeded. Both collisions would be traditionally classified as low speed with potentially no deformity of the vehicles.

(Just to underscore the injury potential at low speeds, the second example occurred at 2 mph where the physics of the crash offered demonstrable evidence of threshold forces sufficient to cause bodily injury.)

Because Fardone et. al. (2014) uses the word “violent” with no qualifying parameters, the above examples offer insight through science on how transferred forces impact the human body with a predictable threshold for injury. Since the word “violent” is a subjective descriptor, one must utilize science and not consider generalities as illustrated by the low speed examples above.

Del Grande, Maus and Carrino (2012) reported, importantly, that although there were varying reports of asymptomatic herniations in the literature, only a post-traumatic finding of radicular, or nerve root, pain can be definitive for determining causality.

Del Grande, Maus and Carrino (2012) wrote:

Only a close concordance, a key in lock fit, of an imaging finding and an individual patient’s pain syndrome can suggest causation, which further implies that the imager must know the nature of a radicular pain syndrome if he/she is to suggest a causal lesion. Close communication between clinician and imager via the medical record, an intake document at the imaging site detailing the pain syndrome, or direct patient interview by the imager is necessary. (p. 640)

Therefore, it is critical to ensure that patients have a complete history taken and an examination performed by a credentialed health care provider that is trained in trauma care. Many practitioners are licensed to treat the trauma case, but many are ill equipped in training and experience to ensure an accurate diagnosis and determine proper relationship to causality.

Beyond radiating symptomatology, although as Del Grande, Maus and Carrino (2012) have reported as an accepted parameter for determining herniation causality, it is important to realize that radiating clinical symptoms arising from an injury to an intervertebral disc are dependent on the anatomical positioning of the injured and inflamed disc material. It is only when the disc herniation is of a lateralized nature that the segmental nerve root is compressed or inflamed, producing radiation of axial symptoms to the corresponding upper or lower extremity. To discuss radiation as a primary indicator of acute traumatic injury to the intervertebral disc omits central disc herniations, which in and of itself do not typically produce extremity symptomology. When it comes to acute injury in the absence of radiating symptoms, local symptomatology should also be considered in approaching a mechanism and timing of the injury. Furthermore, one must also look at the morphology or architecture of the individual vertebrae as demonstrative evidence to age-date disc pathology inclusive of both herniations and traumatically induced, directional, non-diffuse bulges, as described by Fardon et al. (2014).

This is Wolf’s Law, as described by Isaacson and Bloebaum (2010): “Physical forces exerted on a bone alter bone architecture and is a well-established principle.…”(p. 1271). This has been understood and accepted as a general principle since the late 1800s and has been verified through the past century’s research, inclusive of contemporary research. Simply put, if a bone has abnormal stresses, it will change morphology or shape within expected parameters. Since these changes are “expected,” the question becomes, “How does Wolf’s Law apply to traumatic external forces and acute disc injury and how does this relate to causality?”

In order to fully understand the process, it is critical to understand the biochemical reaction (functional adaptation) that occurs with abnormal stresses on bone, which centers on bioelectric changes that occur at the cellular level.

According to Issacson and Bloebaum (2010), when tissue is damaged, the injury potential creates steady, local electric fields that result from ion flux (positive and negative charges moving through local cellar membranes) that are an integral part in the regeneration/remodeling of bony tissue. Bone remodeling is a tightly coupled functional system and is strongly influenced by age, activity level and mechanical loading. This functional adaptation of bone demonstrates the unique ability of bone to alter its trabecular (structural bone tissue) orientation as a result of loading conditions. According to Frost (1994), bone remodeling is a direct response to mechanical influences and strains on the osseous system. This can occur as a normal process to strengthen bone, or as a response to altered anatomy, biomechanics or direct traumatic injury. Since this is a predicable scenario, we can identify specific factors that will help us to determine whether the response was present over time or is at the beginning phase of remodeling. That is the fundamental basis for putting a causally related date to the injury.

Isaacson and Bloebaum (2010) note that in regard to the remodeling of bone, the successful growth of additional supporting bone results from a combination of competent mechanical strain stimuli and endogenous electrical currents (bio-electrical changes). Simply put, it is the mechanical stresses and the flow of the bioelectric compounds that work in conjunction with one another to strengthen or produce additional bone to functionally “buttress” the joint segment.  The above mentioned endogenous electrical current/bioelectrical changes are more commonly known as the “piezoelectricity,” or the body’s electrical reaction to pressure or mechanical stress. It is this electrically and mechanical-based system that subsequently controls osteogenic (osteo=bone; genic=to create) activity. The amplitude or amount of electrical potential is dependent upon on the magnitude of the mechanical bone loading, while polarity (meaning, the application of the bioelectric charge) was determined by the direction of the deformed bone. Isaacson and Bloebaum (2010) reported, “The specific loading pattern of bone has been documented as an important piezoelectric parameter since potential differences in bone have been known to be caused by charge displacement during the deformation period” (p. 1271). What this means is that application of Wolf’s Law to a bony segment is dependent on the amount of mechanical stresses as well as the direction of those forces, and is therefore based on basic engineering principles in the body. The extent and direction of the bone’s response to these forces is predictable and expected.

Additionally, Isaacson and Bloebaum (2010) noted that increased pressure surround the bone inhibits specific hormones preventing the uptake of calcium in the blood…which, in turn, results in the additional uptake of calcium within bone itself, causing additional bone to be produced.

Now that we understand what is happening from a physiological perspective when the bone responds to normal or abnormal mechanical stresses, the aging processes, or an acute traumatic injury, the question becomes, “Can we objectively predict this process in the human spine?”

He and Xinghua (2006) studied the predictability of bone remodeling, which included both the external shape and internal bone density distribution. They extended the simulation of the external shape of bones to determine and to predict pathological changes in bone: specifically, the osteophyte on the edge of a bone structure. They reported, “The significance of this work were [sic]: (1) it confirmed that osteophyte formation was an adaptive process in response to the change of mechanical environment, which can be simulated numerically by combining quantitative bone remodeling theory with finite element method; and (2) it can help to better understand the relationship between bone morphological abnormity and the mechanical environment.” (p. 96)

He and Xinghua (2006) also reported that with load-bearing bones such as the femur and vertebrae, mechanical factors are crucial to the morphology and changes in boney structures that relate closely to changes in mechanical environments. In addition, changes in bone structure morphology are slowly progressing processes unless other factors such as trauma or inflammation are included, at which time the processes will be accelerated to change the bone structural morphology. What that means is that there is a “genetic timing” to the remodeling process that can be altered (increased) by the presence of specific conditions such as an acute injury or inflammation.

According to He and Xinghua (2006), when only the local mechanical environment changes or a directional change in force coefficients is present, then only part of the vertebrae will remodel leaving the rest of the vertebrate unchanged. Meaning, if there is a one-sided lesion creating pressure unilaterally, only that side of the disc will create an osteophyte. This is very similar to the formation of a callus on your hand or foot. “In this paper, the main pathology of osteophyte formation was associated with the structural deterioration of intervertebral disc.” (He and Xinghua, 2006, p. 97)

These researchers further discuss that the remodeling process will continue until the biomechanical failure is resolved and the body has reached a biomechanical equilibrium by placing an osteophyte on the edge of the vertebrae, one whose size and strength is based upon the influencing mechanical imbalance. They concluded that only the bone in the area of mechanical imbalance would be compromised.

Although individuals have different formation rates and the osteophytes may vary in size, everyone is subject to morphological changes depending upon mechanical imbalances in the spine. He and Xinghua (2006) concluded that, “…it will actually take about more than half a year to observe the bone morphological changes…” (p. 101). This indicates that it takes approximately 6 months for an osteophyte to be a demonstrable post-mechanical failure or imbalance. This again gives a time frame to better understand if pathology of the intervertebral disc has been present for a long period of time (pre-existing) or has been produced as the direct result of the specific traumatic event by lack of the existence of an osteophyte, meaning the disc pathology is less than 6 months in duration.

In conclusion, we would like to remind you readers that, by definition, a disc is a ligament, connecting a bone to a bone, and it has the structural responsibility to the vertebrate above and below to keep the spinal system in equilibrium. Damage to the disc through a tear (herniation or annular fissure) or a directional, non-diffuse bulge will create abnormal load-bearing or biomechanical failure on the side of the disc lesion. Since we have previously defined the term “violent trauma” as not being dependent upon the amount of damage done to those structures either around or containing the victim, and we have determined there were ample force coefficients to produce injury to the spine, then based upon the current literature, we can now accurately predict in a demonstrable manner the timing of causality of the disc lesion. This is both based upon the symptomatology of the patient and/or the morphology of the vertebral structure and is a subject that can no longer be based upon rhetoric.

Now we will discuss how spinal experts document causality with disc and ligament injuries….

“The clinical presentation is a disc bulge in their neck and some arthritis, so their neck symptoms are not related to the crash. There is a low back herniation but lots of people have those and don’t have pain.  It is our opinion it was there before the crash.”

That statement from an adjuster is an argument that has been made for years, allowing insurance companies to inappropriately reduce settlements to their clients based on the client’s inability to prove when or how their injury really occurred. To factually counter this type of statement, one must use imaging and age dating, with an understanding of biomechanics, in order to demonstrably discuss causality. Without medical experts utilizing the current medical and academic research available, it will continue to be difficult for any argument to be made explaining the nature and long-term effects of these injuries based on scientific fact vs. rhetoric

Imaging of the spine is critically important in all cases of injured clients. In traumatic cases, imaging is necessary for diagnosis, triage and proper co-management of bodily injuries. Imaging needs to be performed as per the current academic and contemporary medical/chiropractic standards to ensure an accurate diagnosis. The most common injuries in car accidents are spinal related, and the basic imaging available includes x-rays, CAT scans and magnetic resonance imaging (MRI), allowing medical providers to make an accurate diagnosis, when clinically indicated.

Every medical provider in Colorado, from MD to DO to DC—for diagnosis/prognosis purposes—has a license to see and treat car related injuries. However, a “license” is not the same as “specialization.”  By way of illustration, although psychiatrists are MDs and might have a license to do heart surgery, it would not be in the best interest of the patient.  Nor would I go to a spine surgeon for psychological concerns even though they are fully licensed to treat medical conditions. In spinal trauma, certain providers specialize in connective tissue injuries of the spine, allowing us to go one step further in diagnosis, prognosis and management…including “age-dating” these commonly found disc and ligament injuries.

To understand age dating, one needs to have a basic medical understanding of anatomy and physiology, as well as what tissue is commonly injured and the probable “pain generator.”  Since neck injuries are the most common injuries seen in car crashes, cervical spinal joints will be our focus. Related to anatomy, every set of two vertebrae in the neck is connected with three joints: one disc and two facet joints. These joints allow for normal movement of the spine (mobility). Additionally, there are multiple ligaments that hold these joints together and are responsible for stability. The proper balance of mobility and stability is critical when looking at the biomechanical part of patient’s injuries…meaning that too much or too little movement in spinal joints can cause pain, secondary to damaged tissue. The tissue most commonly injured in a car crash is muscle/tendon, ligament, disc, facet, and nerve. Spinal cord and bone injuries also occur although less frequently. To determine causality, the provider should comment on what tissue is injured, and also use imaging to help determine when this injury occurred (i.e., age-dating).

There are two basic problems that must be addressed. Fardon and Milette (2001) reported, “The term ‘herniated disc’ does not infer knowledge of cause, relation to injury or activity, concordance with symptoms, or need for treatment” (p. E108).  Simply having the presence of a disc herniation, without a physical exam or without proper symptom documentation, does not allow one to comment on the cause of the injury. In a rear-impact collision for example, even when the diagnosis is confirmed, additional criteria need to be met to answer the question, “Was there enough force generated into the vehicle and the occupant to cause the cervical/lumbar herniation?” Fardon, in a follow-up study (2014) reported that disc injury “in the absence of significant imaging evidence of associated violent injury, should be classified as degeneration rather than trauma” (p. 2531).  So, we must more objectively define the subjective connotations of “violent injury” and address the issue of “degeneration rather than trauma.” Although this statement can often be misleading, it gives the trauma-trained expert doctor a basis in going forward, understanding that every patient’s physiology is unique and not subject to rhetoric, but clinical findings.

Violent injury to the occupant can occur when there are sudden acceleration and deceleration forces (g-force) generated to the head and neck that overwhelm connective tissue or bring them past their physiological limit. To determine the acceleration force, “delta V” (ΔV as it appears in equations) is used.  Delta V is the change in velocity of the occupant vehicle when it is hit from behind (i.e., going from a stopped position to seven miles per hour in 0.5 seconds due to forces transferred from the “bullet” vehicle to the “target” vehicle).  Using these data, research allows us to make specific comments related to violent injury. For the purpose of this article, we are oversimplifying because the cervical spine is exposed to compression, tension and shearing forces. In addition to g-force and the elastic nature of most rear impact crashes makes it nearly impossible to find a true minimum threshold for injury although the literature has given us many examples of low-speed crashes that are dependent not simply on speed, but the mass (weight) of the subject vehicles. Each person’s susceptibility to injury is unique.  As stated previously,  while g-force alone isn’t insufficient to predict injury, Krafft, et al. (2002) reported that in low-speed collisions there is an injury threshold of 4.2 g-force for males and 3.6 g-force for females.  Krafft’s research is unique in that she has access to insurance data that is inaccessible to most researchers. Panjabi (2004) showed that forces as low as 3.5 g-force impacts would cause damage to the front of the disc, and 6.5 g-force and 8 g-force impacts would cause disc damage posteriorly where the neurological elements are.

A spinal biomechanical expert can then look for conclusive evidence by age-dating disc and joint pathology, based on two phenomena. First, it is well known that the body is electric. When an electromyography exam (EMG) is performed, we are measuring electrical activity along nerves to diagnose radiculopathy, which is nerve damage. Second, there are also normal bioelectrical fields in all tissue, known aspiezoelectricity. When an injury occurs, this normal electrical field is disrupted, and as previously stated, in the case of spinal joints, calcium is drawn into the damaged tissue creating bone spurs.  Issacson and Bloebaum (2010) reported, “The specific loading pattern of bone has been documented as an important piezoelectric parameter since potential differences in bone have been known to be caused by charge displacement during the deformation period” (p. 1271).  Fortunately for the patient, we are able to tell how much of this process has occurred either before or after their crash, specifically when we take into account the soft tissue damage seen and evidence of bone/calcium deposition.

Additionally, the body begins a healing process that includes regeneration and remodeling of both soft and hard tissue as reported by Issacson and Bloebaum (2010).  Spinal vertebrae have a unique structure of bone that allows it to adapt to abnormal mobility and stability (injury) by changing shape, which can be seen on radiographs or MRIs.  Furthermore, the bone will change shape according to predictable patterns based on the increased pressure or load that it undergoes post-injury. Issacson and Bloebaum stated that, “Physical forces exerted on a bone alter bone architecture and is a well-established principle…” (p. 1271).  This again is known as Wolff’s Law, first established in the 1800s.  Since we know what “normal” is, when we see “abnormal” findings due to mechanical stress we can broach the topic of an acute injury versus a degenerative process causing the abnormality and make specific medical predictions accordingly.

He and Xinghua (2006) studied the predictability of this bone-remodeling process and were able to make predictions of pathological changes that will occur in bone, specifically the osteophyte (bone spur) on the edge of a bone structure.  Significantly, they noted their findings “confirmed that osteophyte formation was an adaptive process in response to the change of mechanical environment.”  They noted that mechanical factors are crucial to the morphology of bones, notably load-bearing bones such as the femur and vertebrae.

For readers familiar with current medical and academic accepted nomenclature for disc damage, recognized by the combined task forces of the North American Spine Society (NASS), the American Society of Spine Radiology (ASSR) and the American Society of Neuroradiology (ASNR), disc herniations must have a directional component. When this occurs, the abnormal and additional pressure at the level of the disc damage matched with the direction of the herniation will cause only that part of the vertebrae to remodel.

Thus, if there is a C5/6 right-sided herniation (protrusion/extrusion) secondary to a cervical acceleration/deceleration injury, then only that side of the vertebrae will change shape, creating an osteophyte.  This compounded loading on the facet joint additionally causes facet arthritis. This process is similar to the formation of a callous on your hand or foot: The callous is a known and expected tissue response to increased load/friction exposure. Similarly, an osteophyte is a known and expected bone response to an increase in load/friction exposure.

At a basic level, the body has an electrical and mechanical response to injury resulting in additional stress that causes calcium (bone) to flow into the area of injury to further support the joint. The joint then abnormally grows, creating a pathology called hypertrophy, degeneration, disc osteophyte complex, or arthritis/arthropathy, common terms seen in radiology and doctor’s reports.

Everyone is subject to these morphological (structural) changes, which are always and predictably dependent on mechanical imbalances in the spine. Remember from the previous discussion, He and Xinghua (2006) concluded that, “…it will actually take about more than half a year to observe the bone morphological changes…” (p. 101). This indicates that it takes approximately six months for an osteophyte (bone spur) to be demonstrable post-mechanical failure or imbalance. This again provides a time frame to better understand if pathology of the intervertebral disc has been present for a long period of time (pre-existing) or has been produced as the direct result of the specific traumatic event by lack of the existence of an osteophyte, meaning the disc pathology is less than 6 months old, dependent on location and direction of the pathology.

In conclusion, that by definition, a disc is a ligament connecting a bone to a bone and it has the structural responsibility to the vertebrae above and below to keep the spinal system in equilibrium. Damage to the disc due to a tear (whether a herniation or an annular fissure) or a bulge will create abnormal load-bearing forces at the injury site.  These present differently depending on [1] if traumatic, as biomechanical failure on the side of the disc lesion, or [2] if age related, as a general complex.  Since other research and human subject crash testing have defined the term “violent trauma” as not being dependent upon the amount of damage done to the vehicle but rather to the forces to which the head and neck are exposed, we can now accurately predict in a demonstrable manner the timing of causality of the disc lesion. This is based upon the symptomatology of the patient and/or the morphology of the vertebral structure and is a subject that can no longer be based upon mere rhetoric or speculation.

References:

Fardon, D. F., & Milette, P. C. (2001). Nomenclature and classification of lumbar disc pathology: Recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 26(5), E93–E113.

Fardon, D. F., Williams, A. L., Dohring, E. J., Murtagh, F. R., Rothman, S. L. G., & Sze, G. K. (2014). Lumbar Disc Nomenclature: Version 2.0: Recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 14(11), 2525-2545.

Brault J. R., Wheeler J. B., Siegmund, G. P., & Brault, E. J. (1998). Clinical response of human subjects to rear-end automobile collisions. Archives of Physical Medicine and Rehabilitation, 79(1), 72-80.

Krafft, M., Kullgren, A., Malm, S., and Ydenius, A. (2002). Influence of crash severity on various whiplash injury symptoms: A study based on real life rear end crashes with recorded crash pulses.  In Proc. 19th Int. Techn. Conf. on ESV, Paper No. 05-0363, 1-7.

Del Grande F., Maus T. P., & Carrino J. A. (2012). Imaging the intervertebral disc: Age-related changes, herniations and radicular pain. Radiological Clinic of North America 50(4), 629-649.

Issacson, B. M., & Bloebaum, R. D. (2010). Bone electricity: What have we learned in the past 160 years? Journal of Biomedical Research, 95A(4), 1270-1279.

Frost, H. M. (1994). Wolff’s Law and bone’s structural adaptations to mechanical usage: an overview for clinicians. The Angle Orthodontist, 64(3), 175-188.

He, G., & Xinghua, Z. (2006). The numerical simulation of osteophyte formation on the edge of the vertebral body using quantitative bone remodeling theory. Joint Bone Spine 73(1), 95-101.

Fardon, D. F., & Milette, P. C. (2001). Nomenclature and classification of lumbar disc pathology: Recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 26(5), E93–E113.

Fardon, D. F., Williams, A. L., Dohring, E. J., Murtagh, F. R., Rothman, S. L. G., & Sze, G. K. (2014). Lumbar Disc Nomenclature: Version 2.0: Recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine, 14(11), 2525-2545.

Krafft, M., Kullgren, A., Malm, S., and Ydenius, A. (2002). Influence of crash severity on various whiplash injury symptoms: A study based on real life rear end crashes with recorded crash pulses.  In Proc. 19th Int. Techn. Conf. on ESV, Paper No. 05-0363, 1-7.

Batterman, S.D., Batterman, S.C. (2002). Delta-V, Spinal Trauma, and the Myth of the Minimal Damage Accident. Journal of Whiplash & Related Disorders, 1:1, 41-64.

Panjabi, M.M. et al. (2004). Injury Mechanisms of the Cervical Intervertebral Disc During Simulated Whiplash. Spine 29 (11): 1217-25.

Issacson, B. M., & Bloebaum, R. D. (2010). Bone electricity: What have we learned in the past 160 years? Journal of Biomedical Research, 95A(4), 1270-1279.

Studin, M., Peyster R., Owens W., Sundby P. (2016) Age dating disc injury: Herniations and bulges, Causally Relating Traumatic Discs.

Frost, H. M. (1994). Wolff’s Law and bone’s structural adaptations to mechanical usage: an overview for clinicians. The Angle Orthodontist, 64(3), 175-188.

He, G., & Xinghua, Z. (2006). The numerical simulation of osteophyte formation on the edge of the vertebral body using quantitative bone remodeling theory. Joint Bone Spine 73(1), 95-101.