Chiropractic Vertebral Subluxation
By Mark Studin
William J. Owens
Citation: Studin M., Owens W. (2018) Vertebral Subluxation Complex, American Chiropractor, 40 (7) 12, 14-16, 18, 20, 22, 24, 26-27
A report on the scientific literature
Chiropractic was discovered in 1895 by Daniel David Palmer and further developed by his son, Bartlett James Palmer. Together, they helped coin the phrase “vertebral subluxation,” yet to date, there has been little evidence of it in the literature. When we consider neuro-biomechanical pathological lesions that will degenerate (please refer to Wolff’s Law) based upon homeostatic mechanisms in the human body we will better understand and be able to define the chiropractic vertebral subluxation and more specifically, the chiropractic vertebral subluxation complex (VSC). In addition, the literature has provided us with a vast amount of evidence on both the biomechanical dysfunction of the spine as well as the neurological consequence as sequelae to that biomechanical dysfunction.
Despite over a century of reported and literature-based clinical results, detractors both outside and inside the chiropractic profession argue to limit the scope of these spinal lesions because the literature has not yet caught up to the results. Additionally, the lack of contemporary literature has been reflected in “underperforming” chiropractic utilization in the United States for conditions that have been well-documented as responding successfully in outcome studies with chiropractic care.
Murphy, Justice, Paskowski, Perle and Schneider (2011) reported:
Spine-related disorders (SRDs) are among the most common, costly and disabling problems in Western society. For the purpose of this commentary, we define SRDs as the group of conditions that include back pain, neck pain, many types of headache, radiculopathy, and other symptoms directly related to the spine. Virtually 100% of the population is affected by this group of disorders at some time in life. Low back pain (LBP) in the adult population is estimated to have a point prevalence of 28%-37%, a 1-year prevalence of 76% and a lifetime prevalence of 85%. Up to 85% of these individuals seek care from some type of health professional. Two-thirds of adults will experience neck pain some time in their lives, with 22% having neck pain at any given point in time.
The burden of SRDs on individuals and society is huge. Direct costs in the United States (US) are US$102 billion annually and $14 billion in lost wages were estimated for the years 2002-4. (p. 1)
In 2017, based upon Alioth Education, dollars adjusted for inflation equates to $18,141, 895,182.64 in direct costs for spinal-related conditions that fall within the chiropractic treatment category and have proven to outperform other forms of care. When considering outcome assessments for efficacy of chiropractic in a population-based study, both Cifuentes, Willets and Wasiak (2011) and Blanchette, Rivard, Dionne, Hogg-Johnson, and Steenstra (2017) offered evidence that the results are rooted in a “first healthcare provider” or “primary spine care” solution.
Cifuentes et al. (2011) compared different treatments of recurrent or chronic low back pain. They considered any condition recurrent or chronic if there was a recurrent disability episode after a 15-day absence and return to disability. Anyone with less than a 15-day absence of disability was excluded from the study. Please note that we kept disability outcomes for all reported treatment and did not limit this to physical therapy. However, the statistic for physical therapy was significant.
According to the Cifuentes, Willets and Wasiak (2011) study, chiropractic care during the disability episode resulted in:
Cifuentes et al. (2011) started by stating, “Given that chiropractors are proponents of health maintenance care...patients with work-related LBP [low back pain] who are treated by chiropractors would have a lower risk of recurrent disability because that specific approach would be used” (p. 396). The authors concluded by stating, “After controlling for demographic factors and multiple severity indicators, patients suffering nonspecific work-related LBP who received health services mostly or only from a chiropractor had a lower risk of recurrent disability than the risk of any other provider type” (Cifuentes et al., 2011, p. 404).
Blanchette, Rivard, Dionne, Hogg-Johnson and Steenstra (2017) reported:
The type of first healthcare provider was a significant predictor of the duration of the first episode of compensation only during the first 5 months of compensation. When compared with medical doctors, chiropractors were associated with shorter durations of compensation and physiotherapists with longer ones. Physiotherapists were also associated with higher odds of a second episode of financial compensation. (p. 388)
Despite compelling evidence of chiropractic being the best option for primary spine care treatment of injuries related to disabilities and pain based upon outcomes, the reasons why chiropractic works have been elusive. Despite the lack of literature-based evidence, answers are still being sought because positive results are consistently being realized in clinical chiropractic practices. When Keating et al. (2005) wrote an opinion or debate article, they concluded, “Subluxation syndrome is a legitimate, potentially testable, theoretical construct for which there is little experimental evidence” (p. 13).
This statement is one of the most unifying statements that could serve to reduce pain and opiate utilization, prevent premature degeneration and increase bio-neuromechanical function for our society, while significantly increasing our utilization because chiropractic is part of the answer. However, the simple question is, “Why aren’t we doing this specific research because the pieces of what is considered subluxation have been verified in the literature for quite some time?”
VSC starts with spinal biomechanics and when considering a pathological model, we need to define the normal functioning of the spine.
Panjabi (2006) reported:
The spinal column, consisting of ligaments (spinal ligaments, discs annulus and facet capsules) and vertebrae, is one of the three subsystems of the spinal stabilizing system. The other two are the spinal muscles and neuromuscular control unit. The spinal column has two functions: structural and transducer. The structural function provides stiffness to the spine. The transducer function provides the information needed to precisely characterize the spinal posture, vertebral motions, spinal loads etc. to the neuromuscular control unit via innumerable mechanoreceptors present in the spinal column ligaments, facet capsules and the disc annulus. These mechanical transducers provide information to the neuromuscular control unit which helps to generate muscular spinal stability via the spinal muscle system and neuromuscular control unit. The criterion used by the neuromuscular unit is hypothesized to be the need for adequate and overall mechanical stability of the spine. If the structural function is compromised, due to injury or degeneration, then the muscular stability is increased to compensate the loss. (p. 669)
Panjabi (2003) also reported:
It has been conceptualized that the overall mechanical stability of the spinal column, especially in dynamic conditions and under heavy loads, is provided by the spinal column and the precisely coordinated surrounding muscles. As a result, the spinal stabilizing system of the spine was conceptualized by Panjabi to consist of three subsystems: spinal column providing intrinsic stability, spinal muscles, surrounding the spinal column, providing dynamic stability, and neural control unit evaluating and determining the requirements for stability and coordinating the muscle response. (p. 372)
In defining spinal clinical instability, Panjabi (1992) previously reported:
Clinical instability is defined as a significant decrease in the capacity of the stabilizing system of the spine to maintain the intervertebral neutral zones within the physiological limits so that there is no neurological dysfunction, no major deformity, and no incapacitating pain. (p. 394)
Anatomically, we are starting with the vertebrate and more specifically, the articular facets indicating that VSC is a “complex” and not a simple problem as the anatomical pathology occurs in opposing facets. When looking at normal vertebral structures,
Cervical spine meniscoids, also referred to as synovial folds or intra-articular inclusions, are folds of synovium that extend between the articular surfaces of the joints of the cervical spine. These structures have been identified within cervical zygapophyseal, lateral atlantoaxial and atlanto-occipital joints, and have been hypothesised to be of clinical significance in neck pain through their mechanical impingement or displacement, as a result of fibrotic changes, or via injury as a result of trauma to the cervical spine. (p. 939)
An understanding of the basic structure of meniscoids is necessary to assess their potential role in cervical spine pathology. As described above, cervical spine meniscoids are folds of synovium that protrude into a joint from its margins. Meniscoids lie between the articular surfaces at the ventral and dorsal poles of their enclosing joint. Their basic structure includes a base, which attaches to the joint capsule, a middle region and an apex that protrudes approximately 1–5 mm into the joint cavity. In sagittal cross section, these structures are triangular in shape, and when viewed superiorly they often appear crescent-shaped or semi-circular. Cervical spine meniscoids are thought to function to improve the congruence of articular structures, and to ensure the lubrication of articular surfaces with synovial fluid. (p. 940)
Should these synovial folds or “plicas” become trapped or “pinched” as described by Evans (2002), it would be the beginning of a “negative neurological cascade.”
Evans (2002) reported:
Intra-articular formations have been identified throughout the vertebral column. Giles and Taylor demonstrated by light and transmission electron microscopy the presence of nerve fibers (0.6 to 1 mm in diameter) coursing through synovial folds, remote from blood vessels, that were most likely nociceptive. They concluded, “Should the synovial folds become pinched between the articulating facet surfaces of the zygapophyseal joint, the small nerves demonstrated in this study may have clinical importance as a source of low back pain.” (p. 252)
Figure 1: Images of meniscoid entrapment on flexion, on attempted extension, involving flexion and gapping and realigned.
Evans (2002) explained the images above as follows:
Meniscoid entrapment. 1) On flexion, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with It. 2) On attempted extension, the inferior articular process returns toward its neutral position, but instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying "lesion" under the capsule. Pain occurs as a result of capsular tension, and extension is inhibited. 3) Manipulation of the joint involving flexion and gapping, reduces the impaction and opens the joint to encourage re-entry of the meniscoid into the joint space (4) [Realignment of the joint.] (p. 253)
Evans (2002) continued:
Bogduk and Jull reviewed the likelihood of intra-articular entrapments within zygapophyseal joints as potential sources of pain…Fibro-adipose meniscoids have also been identified as structures capable of creating a painful situation. Bogduk and Jull reviewed the possible role of fibro-adipose meniscoids causing pain purely by creating a tractioning effect on the zygapophyseal joint capsule, again after intra-articular pinching of tissue(p. 252)
Evans (2002) also noted:
A large number of type III and type IV nerve fibers (nociceptors) have been observed within capsules of zygapophyseal joints. Pain occurs as distension of the joint capsule provides a sufficient stimulus for these nociceptors to depolarize. Muscle spasm would then occur to prevent impaction of the meniscoid. The patient would tend to be more comfortable with the spine maintained in a flexed position, because this will disengage the meniscoid. Extension would therefore tend to be inhibited. This condition has also been termed a “joint lock” or “facet-lock,” the latter of which indicates the involvement of the zygapophyseal joint…
An HVLAT manipulation [chiropractic spinal adjustment CSA], involving gapping of the zygapophyseal joint, reduces the impaction and opens the joint, so encouraging the meniscoid to return to its normal anatomic position in the joint cavity. This ceases the distension of the joint capsule, thus reducing pain. (p. 252-253)
When considering VSC in its entirety, we must consider the etiology as these forces can lead to complex patho-biomechanical components of the spine and supporting tissues. As a result, a neurological cascade can ensue that would further define VSC beyond the inter-articulation entrapments. Panjabi (2006) reported:
Abnormal mechanics of the spinal column has been hypothesized to lead to back pain via nociceptive sensors. The path from abnormal mechanics to nociceptive sensation may go via inflammation, biochemical and nutritional changes, immunological factors, and changes in the structure and material of the endplates and discs, and neural structures, such as nerve ingrowth into diseased intervertebral disc. The abnormal mechanics of the spine may be due to degenerative changes of the spinal column and/or injury of the ligaments. Most likely, the initiating event is some kind of trauma involving the spine. It may be a single trauma due to an accident or microtrauma caused by repetitive motion over a long time. It is also possible that spinal muscles will fire in an uncoordinated way in response to sudden fear of injury, such as when one misjudges the depth of a step. All these events may cause spinal ligament injury. (p.668-669).
Panjabi (2006) goes on to explain what happens when the spinal column is affected by trauma:
The structural function provides stiffness to the spine. The transducer function provides the information needed to precisely characterize the spinal posture, vertebral motions, spinal loads etc. to the neuromuscular control unit via innumerable mechanoreceptors present in the spinal column ligaments, facet capsules and the disc annulus. These mechanical transducers provide information to the neuromuscular control unit which helps to generate muscular spinal stability via the spinal muscle system and neuromuscular control unit. The criterion used by the neuromuscular unit is hypothesized to be the need for adequate and overall mechanical stability of the spine. If the structural function is compromised, due to injury or degeneration, then the muscular stability is increased to compensate the loss. What happens if the transducer function of the ligaments of the spinal column is compromised? This has not been explored. There is evidence from animal studies that the stimulation of the ligaments of the spine (disc and facets, and ligaments) results in spinal muscle firing. (p. 669).
Panjabi (2006) described the mechanism that, coupled with the inter-articulation nociceptor “firing,” further defines the “negative neurological cascade”:
The hypothesis consists of the following sequential steps:
One hallmark of determining vertebral subluxation complex for the chiropractic profession has been ranges of motion of individual motor units. Both hypo- and hypermobility have been clinically associated with muscle spasticity and have offered a piece of clinical history in the practice setting. NOTE: Ranges of motion, like any other findings, are no more than pieces of evidence, all of which must clinically correlate.
Radziminska, Weber-Rajek, Srączyńska and Zukow (2017) reported:
The definition of the neutral zone explains that it as a small range of motion near the zero position of the joint, where no proprioreceptors are stimulated around the joint and osteoligamentous resistance is minimal (lack of centripetal response and, consequently, lack of central muscle stimulation).
Increasing the range of motion of the neutral zone is detrimental to the joint - it can lead to its damage. Delayed proprioceptive information about the current joint position that reaches the central system will give a muscle tone response, but it may turn out to be incompatible with external force acting on the joint. The reduced range of motion of the neutral zone is also unfavorable. If the stimulation of proprioreceptors is too early it will result in an increased muscle tension around the joint. The neutral zone is disturbed by traumas, degenerative processes, and muscle stabilization weakness. (p. 72)
With VSC, the joint that has been misplaced creates abnormal biomechanics and abnormal pressure to the joint. This is called Wolff’s Law, formulated and accepted since the 1800’s, and is explained by Kohata, Itoha, Horiuchia, Yoshiokab and Yamashita (2017):
When mechanical stress is impressed upon bone, an electrical potential is induced; the area of bone under compression develops negative potential, whereas that under tension develops positive potential. This phenomenon is generated by collagen piezoelectricity, and the electrical potential generated in bone by collagen displacement has been well documented. (p. 65)
VSC is based upon both the macro- and microtrauma induced motor unit pathology, creating interarticular meniscoid nociceptor entrapment that triggers nociceptors and affects the lateral horn for a local reflex. It then innervates the thalamus through the spinothalamic tracts and periaqueductal grey matter which is then further distributed to various cortical regions to process in the body’s attempt to compensate biomechanically. This, coupled with aberrant motor unit ranges of motion (hypo or hyper), subfailure injuries to the ligaments and the corrupted mechanoreceptors and nociceptor messages that innervate the lateral horn cause a “negative neurological cascade” both reflexively at the cord and the brain. This cascade can cause pain and inflammation and will cause premature degeneration if left uncorrected based upon Wolff’s Law because of improper motor unit biomechanical failure. Should the correction be made after remodelling of the vertebrate, then care changes from corrective to management as the spine can never be perfectly biomechanically balanced as the segments (building blocks for homeostasis) have been permanently remodelled.
The research for VSC exists in its components. However, there needs to be a concise research program that combines all the pieces to further conclude the evidence that exists. Furthermore, we need more conclusive answers as to why chiropractic patients get well, answers that goes beyond pain or aberrant curves.
1. Murphy, D. R., Justice, B. D., Paskowski, I. C., Perle, S. M., & Schneider, M. J. (2011). The establishment of a primary spine care practitioner and its benefits to health care reform in the United States. Chiropractic & manual therapies, 19(1), 17.
2. FinanceRef Inflation Calendar, Alioth Finance. (2017). $14,000,000,000 in 2004 → 2017 | Inflation Calculator. Retrieved from http://www.in2013dollars.com/2004-dollars-in-2017?amount=14000000000
3. Cifuentes, M., Willets, J., & Wasiak, R. (2011). Health maintenance care in work-related low back pain and its association with disability recurrence. Journal of Occupational and Environmental Medicine, 53(4), 396-404.
4. Blanchette, M. A., Rivard, M., Dionne, C. E., Hogg-Johnson, S., & Steenstra, I. (2017). Association between the type of first healthcare provider and the duration of financial compensation for occupational back pain. Journal of occupational rehabilitation, 27(3), 382-392.
5. Keating, J. C., Charlton, K. H., Grod, J. P., Perle, S. M., Sikorski, D., & Winterstein, J. F. (2005). Subluxation: Dogma or science? Chiropractic & Osteopathy, 13(1), 17.
6. Panjabi, M. M. (2006). A hypothesis of chronic back pain: Ligament subfailure injuries lead to muscle control dysfunction. European Spine Journal, 15(5), 668-676.
7. Panjabi, M. M. (1992). The stabilizing system of the spine. Part II. Neutral zone and instability hypothesis. Journal of Spinal Disorders, 5, 390-397
8. Panjabi, M. M. (2003). Clinical spinal instability and low back pain. Journal of Electromyography and Kinesiology, 13(4), 371-379.
9. Farrell, S. F., Osmotherly, P. G., Cornwall, J., Sterling, M., & Rivett, D. A. (2017). Cervical spine meniscoids: an update on their morphological characteristics and potential clinical significance. European Spine Journal, (26) 939-947
10. Evans, D. W. (2002). Mechanisms and effects of spinal high-velocity, low-amplitude thrust manipulation: Previous theories. Journal of Manipulative and Physiological Therapeutics, 25(4), 251-262.
11. Radziminska, A., Weber-Rajek, M., Strączyńska, A., & Zukow, W. (2017). The stabilizing system of the spine. Journal of Education, Health and Sport, 7(11), 67-76.
12. Kohata, K., Itoh, S., Horiuchi, N., Yoshioka, T., & Yamashita, K. (2017). Influences of osteoarthritis and osteoporosis on the electrical properties of human bones as in vivo electrets produced due to Wolff's law. Bio-Medical Materials and Engineering, 28(1), 65-74.
The Mechanism of the Chiropractic
Ligaments and the Bio-Neuro-Mechanical Component
Part 2 of a 5 Part Series
By: Mark Studin
William J. Owens
A report on the scientific literature
Citation: Studin M., Owens W., (2017) The Mechanism of the Chiropractic Spinal Adjustment/Manipulation: Ligaments and the Bio-Neuro-Mechanical Component, Part 2 of 5, American Chiropractor 39 (6), pgs. 22,24-26, 28-31
When we consider the mechanism of the spinal adjustment/manipulation as discussed in part 1 of this series, for clarity for the chiropractic profession, it will be solely referred to as a chiropractic spinal adjustment (CSA) so as not to confuse chiropractic treatment with either physical therapy or osteopathy. In analyzing how the CSA works, we must go beyond the actual adjustment or thrust and look at the tissue and structures that “frame” the actions. Although there are osseous borders and boundaries, there is a significant network of connective tissue that plays a major role in the CSA. We will focus this discussion on the ligaments that both act as restraints to the human skeleton and also function as sensory organs, we will also examine the role of the muscles and tendons that interact with the ligaments. It is critical to realize that muscles act as active and amplified restraints in the spinal system.
The neurological innervations of the ligaments play a significant role in influencing the central nervous system, both reflexively and through brain pathways. Those innervations either support homeostasis in a balanced musculoskeletal environment or creates confusion in a system that has been impaired either post-traumatically or systemically. The human body does not discriminate the etiology of biomechanical failure, it only reacts to create a “low energy” or neutral state utilizing the lowest amount of energy to function. This balanced or “low energy state” is considered the most optimal function state as nervous system function is not compromised by aberrant sensory input, this is why a “low energy state” is considered the highest function state.
With understanding the full functional and resultant role of the ligaments and other connective tissues in either macro or repetitive micro traumas, bio-neuro-mechanical failure (something we have historically called vertebral subluxation) occurs. This is the basis for chiropractic care and explains why immediate (pain management), intermediate (corrective) and long-term (wellness or health maintenance) care are necessary to reintegrate the bio-neuro-mechanical system of the human body. Often, the best we can accomplish as practitioners is to support compensation secondary to tissue failure to slow down the resultant joint remodeling and neurological corruption/compromise.
Solomonow (2009) wrote:
The functional complexity of ligaments is amplified when considering their inherent viscoelastic properties such as creep, tension–relaxation, hysteresis and time or frequency-dependent length–tension behavior. As joints go through their range of motion, with or without external load, the ligaments ensure that the bones associated with the joint travel in their prescribed anatomical tracks, keep full and even contact pressure of the articular surfaces, prevent separation of the bones from each other by increasing their tension, as may be necessary, and ensuring stable motion. Joint stability, therefore, is the general role of ligaments without which the joint may subluxate, cause damage to the capsule, cartilage, tendons, nearby nerves and blood vessels, discs (if considering spinal joints) and to the ligaments themselves. Such injury may debilitate the individual by preventing or limiting his/her use of the joint and the loss of function…Dysfunctional or ruptured ligaments, therefore, result in a complex- syndrome, various sensory–motor disorders and other long-term consequences, which impact the individual’s well-being, his athletic activities, employer, skilled work force pool and national medical expenses. (p. 137)
Ligaments are closely packed collagen fibers that are helical at rest in a crimp pattern. This crimp pattern allows the ligament to recruit other fibers when stressed to support the joint and helps prevent ligamentous failure or subfailure (tearing of the ligament). They are comprised of collagen and elastin which give them both tensile strength and elasticity with no two joints being alike in composition. Each joint has a specific biomechanical role and varies depending upon the needs of that joint.
Note. “Ligaments and tendons,” by I. Ziv, (n.d.), [PowerPoint slides]. Retrieved from https://wings.buffalo.edu/eng/mae/courses/417-517/Orthopaedic%20Biomechanics/ Lecture%203u.pdf
Solomonow (2008) continued:
As axial stretching of a ligament is applied, fibers or bundles with a small helical wave appearance straighten first and begin to offer resistance (increased stiffness) to stretch. As the ligament is further elongated, fibers or fiber bundles of progressively larger helical wave straighten and contribute to the overall stiffness. Once all the fibers are straightened, a sharp increase in stiffness is observed. (p. 137)
Solomonow (2008) later stated:
Over all, the mostly collagen (75%), elastin and other substances structure of ligaments is custom tailored by long evolutionary processes to provide various degrees of stiffness at various loads and at various ranges of motion of a joint, while optimally fitting the anatomy inside (inter-capsular) or outside (extra-capsular) a given joint. The various degrees of helical shape of the different fibers allows generation of a wide range of tensile forces by the fiber recruitment process, whereas the overall geometry of the ligament allows selective recruitment of bundles such as to extend function over a wide range of motion. The large content of water (70%) and the cross weave of the long fibers by short fibers provides the necessary lubrication for bundles to slide relative to each other, yet to remain bundled together and generate stiffness in the transverse directions.(p. 137)
Length–tension and recruitment: The general length–tension (or strain–stress) behavior of a ligament is non-linear…The initial [reports] demonstrate rather large strain for very small increase in load. Once all the waves in the collagen fibers of the ligament have been straightened out, and all of the fibers were recruited, additional increase in strain is accompanied with a fast increase in tension…
Creep: When a constant load is applied to a ligament, it first elongates to a given length. If left at the same constant load, it will continue to elongate over time in an exponential fashion up to a finite maximum…
Tension–relaxation:When ligaments are subjected to a stretch and hold over time (or constant elongation) the tension–relaxation phenomena is observed. The tension in the ligament increases immediately upon the elongation to a given value. As time elapses, the tension decreases exponentially to a finite minimum while the length does not change…
Strain rate: The tension developed in a ligament also depends on the rate of elongation or strain rate (Peterson, 1986). In general, slow rates of elongation are associated with the development of relatively low tension, whereas higher rates of elongation result in the development of high tension. Fast stretch of ligaments, such as in high-frequency repetitive motion or in sports activities are known to result in high incidents of ligamentous damage or rupture…Fast rates of stretch, therefore, may exceed the physiological loads that could be sustained by a ligament safely, yet it may still be well within the physiological length range. Development of high tension in the ligaments may result in rupture and permanent sensory–motor deficit to the joint in addition to deficit in its structural functions. (p. 137-139)
Author’s note: A fast strain rate within the physiological limit may also cause ligamentous damage as the ligament hasn’t had enough time to adapt (stretch) to its new tensile demand and this is called a “sub-failure.”
“This phenomenon is associated with repetitive motion when a series of stretch-release cycles are performed over time (Solomnow, 1008, p. 140).
Ligament Reaction to Trauma and Healing
Solomnow (2008) stated:
Ligament Inflammation: Inflammatory response in ligaments is initiated whenever the tissue is subjected to stresses which exceed its routine limits at a given time. For example, a sub-injury/failure load, well within the physiological limits of a ligament when applied to the ligament by an individual who does not do that type of physical activity routinely. The normal homeostatic metabolic, cellular, circulatory and mechanical limits are therefore exceeded by the load, triggering an inflammatory response…
Another case where acute inflammation is present is when physical activities presenting sudden overload/stretch cause a distinct damage to the tissue which is felt immediately. Such cases, as a sudden loss of balance, a fall, collision with another person, exposure to unexpected load, etc., may result in what is called a sprain injury or a partial rupture of the ligament. Acute inflammation sets in within several hours and may last several weeks and up to 12 months. The healing process, however, does not result in full recovery of the functional properties of the tissue. Mostly, only up to 70% of the ligaments original structural and functional characteristics are attained by healing post-injury (Woo et al. 1990)...
Chronic inflammation is an extension of an acute inflammation when the tissue is not allowed to rest, recover and heal. Repetitive exposure to physical activity and reloading of the ligament over prolonged periods without sufficient rest and recovery represent cumulative micro-trauma. The resulting chronic inflammation is associated with atrophy and degeneration of the collagen matrix leaving a permanently damaged, weak and non-functional ligament (Leadbenter, 1990). The dangerous aspect of a chronic inflammation is the fact that it builds up silently over many weeks, months or years (dependent on a presently unknown dose-duration levels of the stressors) and appears one day as a permanent disability associated with pain, limited motion, weakness and other disorders (Safran, 1985). Rest and recovery of as much as 2 years allows only partial resolution of the disability (Woo and Buckwalter, 1988). Full recovery was never reported. (p. 143-144)
Hauser et al. (2013) reported that once a ligament is overloaded in either a failure or subfailure, then the tissue fails which results in partial or complete tears known as a sprain. When this occurs, the body “attempts” to repair the damaged ligament, but cannot completely.
Hauser et al. (2013) wrote:
With time, the tissue matrix starts to resemble normal ligament tissue; however, critical differences in matrix structure and function persist. In fact, evidence suggests that the injured ligament structure is replaced with tissue that is grossly, histologically, biochemically, and biomechanically similar to scar tissue. (p. 6)
Hauser et al. (2013) also stated:
The persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics, depending on the functional demands placed on the tissue. Since remodeled ligament tissue is morphologically and biomechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joint and predisposing other soft tissues in and around the joint to further damage. (p. 7)
Hauser et al. (2013) further said:
In fact, studies of healing ligaments have consistently shown that certain ligaments do not heal independently following rupture, and those that do heal, do so with characteristically inferior compositional properties compared with normal tissue. It is not uncommon for more than one ligament to undergo injury during a single traumatic event. (p. 8)
Author’s note: Ligaments are made with fibroblasts which produce collagen and elastin, and model the ligament throughout puberty. Once puberty is over, the fibroblasts stop producing any ligamentous tissue and remain dormant. Upon injury, the fibroblast activates, but now can only produce collagen, leaving the joint stiffer and in a biomechanically compromised functional environment. The above comment verifies that in the literature.
Hauser et al. (2013) explained:
Osteoarthritis [OA] or joint degeneration is one of the most common consequences of ligament laxity. Traditionally, the pathophysiology of OA was thought to be due to aging and wear and tear on a joint, but more recent studies have shown that ligaments play a crucial role in the development of OA. OA begins when one or more ligaments become unstable or lax, and the bones begin to track improperly and put pressure on different areas, resulting in the rubbing of bone on cartilage. This causes the breakdown of cartilage and ultimately leads to deterioration, whereby the joint is reduced to bone on bone, a mechanical problem of the joint that leads to abnormality of the joint’s mechanics.
Hypermobility and ligament laxity have become clear risk factors for the prevalence of OA. The results of spinal ligament injury show that over time the inability of the ligaments to heal causes an increase in the degeneration of disc and facet joints, which eventually leads to osteochondral degeneration. (p. 9)
Ligaments as Sensory Organs
Spinal pain and the effects of the chiropractic spinal adjustment is both central and peripheral in etiology. According to Studin and Owens (2016), the CSA also affects the central nervous system with systemic sequelae verifying that chiropractic supports systemic changes and is not comprised solely of “back pain providers.” Although chiropractic is not limited to pain, chiropractors do treat back pain, inclusive of all spinal regions. Regarding pain, much of the pain generators originate in the ligaments.
Solomonow (2009) wrote:While ligaments are primarily known for mechanical support for joint stability, they have equally important sensory functions. Anatomical studies demonstrate that ligaments in the extremity joints and the spine are endowed with mechanoreceptors consisting of: Pacinian, Golgi, Ruffini and bare nerve endings. (Burgess and Clark, 1969; Freeman and Wyke, 1967a,b; Gardner, 1944; Guanche et al., 1995; Halata et al., 1985; Jackson et al., 1966; Mountcastle, 1974; Petrie et al., 1988, Schulz et al. 1984, Sjölander, 1989; Skoglund, 1956; Solomonow et al., 1996; Wyke, 1981; Yahia and Newman, 1991; Zimney and Wink, 1991). The presence of such afferents in the ligaments confirms that they contribute to proprioception and kinesthesia and may also have a distinct role in reflex activation or inhibition of muscular activities.(p. 144)
Dougherty (n.d.) reported:
Pacinian corpusclesare found in subcutaneous tissue beneath the dermis…and in the connective tissues of bone [ligaments and tendons], the body wall and body cavity. Therefore, they can be cutaneous, proprioceptive or visceral receptors, depending on their location…
When a force is applied to the tissue overlying the Pacinian corpuscle…its outer laminar cells, which contain fluid, are displaced and distort the axon terminal membrane. If the pressure is sustained on the corpuscle, the fluid is displaced, which dissipates the applied force on the axon terminal. Consequently, a sustained force on the Pacinian corpuscle is transformed into a transient force on its axon terminal. The Pacinian corpuscle 1° afferent axon response is rapidly adapting and action potentials are only generated when the force is first applied. (http://neuroscience.uth.tmc.edu/ s2/chapter02.html)
Dougherty (n.d.) stated:
TheRuffini corpusclesare found deep in the skin…as well as in joint ligaments and joint capsules and can function as cutaneous or proprioceptive receptors depending on their location. The Ruffini corpuscle…is cigar-shaped, encapsulated, and contains longitudinal strands of collagenous fibers that are continuous with the connective tissue of the skin or joint. Within the capsule, the 1° afferent fiber branches repeatedly and its branches are intertwined with the encapsulated collagenous fibers. (http://neuroscience.uth.tmc. edu/s2/chapter02.html) “Ruffini corpuscles in skin are considered to be skin stretch sensitive receptors of the discriminative touch system. They also work with the proprioceptors in joints and muscles to indicate the position and movement of body parts” (Dougherty, http://neuroscience.uth.tmc.edu/s2/chapter02.html).
Dougherty (n.d.) stated:
Golgi tendon organsare found in the tendons of striated extrafusal muscles near the muscle-tendon junction…Golgi tendon organs resemble Ruffini corpuscles. For example, they are encapsulated and contain intertwining collagen bundles, which are continuous with the muscle tendon, and fine branches of afferent fibers that weave between the collagen bundles…They are functionally "in series" with striated muscle. (http://neuroscience.uth.tmc.edu/s2/ chapter02.html)
“TheGolgi tendon organis a proprioceptor that monitors and signals muscle contraction against a force (muscle tension), whereas the muscle spindle is a proprioceptor that monitors and signals muscle stretch (muscle length)” (Dougherty, http://neuroscience.uth.tmc.edu/ s2/chapter02.html).
Dougherty (n.d.) stated:
…free nerve endings of 1° afferents are abundant in muscles, tendons, joints, and ligaments. These free nerve endings are considered to be the somatosensory receptors for pain resulting from muscle, tendon, joint, or ligament damage and are not considered to be part of the proprioceptive system. [These free nerve endings are called nociceptors.]
Solomonow (2009) commented:
The presence of such afferents in the ligaments confirms that they contribute to proprioception and kinesthesia and may also have a distinct role in reflex activation or inhibition of muscular activities…
Overall, the decrease or loss of function in a ligament due to rupture or damage does not only compromise its mechanical contributions to joint stability, but also sensory loss of proprioceptive and kinesthetic perception and fast reflexive activation of muscles and the forces they generate in order to enforce joint stability…
It was suggested, as far back as the turn of the last century, that a reflex may exist from sensory receptors in the ligaments to muscles that may directly or indirectly modify the load imposed on the ligament (Payr, 1900)…A clear demonstration of a reflex activation of muscles was finally provided in 1987 (Solomonow et al., 1987) and reconfirmed several times since then (beard et al., 1994; Dyhre-Poulsen and Krogsgard, 2000; Raunest et al., 1996; Johansson et al., 1989; Kim et al., 1995). It was further shown that such a ligamento-muscular reflex exists in most extremity joints (Freeman and Wyke, 1967b; Guanche et al., 1995, Knatt et al., 1995; Schaible and Schmidt, 1983; Schaible et al., 1986; Solomonow et al., 1996; Phillips et al., 1997; Solomonow and Lewis, 2002) and in the spine (Indahl et al., 1995, 1997; Stubbs et al., 1998; Solomonow et al., 1998). (p. 144).
“Ligamento-muscular reflexes, therefore, may be inhibitory or excitatory, as may be fit to preserve joint stability; inhibiting muscles that destabilize the joint or increased antagonist co-activation to stabilize the joint” (Solomonow, 2009, p. 145).
Spinal Stabilization and Destabilization
Panjabi (2006) reported:
1. Single trauma or cumulative microtrauma causes subfailure injury of the spinal ligaments and injury to the mechanoreceptors [and nociceptors] embedded in the ligaments.
2. When the injured spine performs a task or it is challenged by an external load, the transducer signals generated by the mechanoreceptors [and nociceptors] are corrupted.
3. Neuromuscular control unit has diﬃculty in interpreting the corrupted transducer signals because there is spatial and temporal mismatch between the normally expected and the corrupted signals received.
4. The muscle response pattern generated by the neuromuscular control unit is corrupted, aﬀecting the spatial and temporal coordination and activation of each spinal muscle.
5. The corrupted muscle response pattern leads to corrupted feedback to the control unit via tendon organs of muscles and injured mechanoreceptors [and nociceptors], further corrupting the muscle response pattern. (p. 669)
The above stabilization-destabilization scenario is the foundation for why a CSA is clinically indicated for short, intermediate and long-term treatment (biomechanical stabilization) as clinically indicated. It also clearly outlines what the goal of the CSA is, to integrate the bio-neuro-mechanical system to bring the human body to utilize its lowest form of energy for homeostasis or as close to normal as tissue pathology allows.
This is part 2 of a 5-part series where part 1 covers the osseous mechanics of the chiropractic spinal adjustment. This part covered the ligamentous involvement from a supportive and neurological perspective. The topic of part 3 will be spinal biomechanics and their neurological components in addition to how the chiropractic spinal adjustment makes changes bio-neuro-mechanically. Part 4 will be an in-depth contemporary comparative analysis of the chiropractic spinal adjustment vs. physical therapy joint mobilization. The final part will be a concise overview of the chiropractic spinal adjustment.
1. Solomonow, M. (2009). Ligaments: A source of musculoskeletal disorders.Journal of Bodywork and Movement Therapies,13(2), 136-154.
2. Ziv, I. (n.d.). Ligaments and tendons [PowerPoint slides]. Retrieved from https://wings.buffalo.edu/eng/mae/courses/417-517/Orthopaedic%20Biomechanics/Lecture%203u.pdf
3. Hauser, R. A., Dolan, E. E., Phillips, H. J., Newlin, A. C., Moore, R. E., & Woldin, B. A. (2013). Ligament injury and healing: A review of current clinical diagnostics and therapeutics.The Open Rehabilitation Journal,6, 1-20.
4. Solomonow, M. (2006). Sensory–motor control of ligaments and associated neuromuscular disorders.Journal of Electromyography and Kinesiology,16(6), 549-567.
5. Studin M., & Owens W. (2016). Chiropractic spinal adjustments and the effects on the neuroendocrine system and the central nervous system connection. The American Chiropractor, 38(1), 46-51.
6. Dougherty, P. (n.d.). Chapter 2: Somatosensory systems. Neuroscience Online. Retrieved from http://neuroscience.uth.tmc.edu/s2/chapter02.html
7. Panjabi, M. M. (2006). A hypothesis of chronic back pain: Ligament subfailure injuries lead to muscle control dysfunction.European Spine Journal,15(5), 668-676.