The cause of spondylolysis remains unknown, however many factors are thought to contribute to its development. The condition is present in up to 6% of the population, majority of which usually present asymptomatically. Research supports that there are hereditary and acquired risk factors that can make one more susceptible to the defect. The disorder is generally more prevalent in males compared to females, and tends to occur earlier in males due to their involvement in more strenuous activities at a younger age. In a young athlete, the spine is still growing which means there are many ossification centers, leaving points of weakness in the spine. This leaves young athletes at increased risk, particularly when involved in repetitive hyperextension and rotation across the lumbar spine. Spondylolysis is a common cause of low back pain in preadolescents and adolescent athletes, as it accounts for about 50% of all low back pain. It is believed that both repetitive trauma and an inherent genetic weakness can make an individual more susceptible to spondylolysis.

Sports involving repetitive or forceful hyperextension of the spine, especially when combined with rotation are the main mechanism of injury for spondylolysis. The stress fracture of the pars interarticularis occurs on the side opposite to activity. For instance, for a right-handed player, the fracture occurs on the left side of the vertebrae.

Spondylolysis has a higher occurrence in the following activities:

- Baseball

- Tennis

- Diving

- Cheerleading

- Gymnastics

- Football

- Soccer

- Wrestling

- Weightlifting

- Roller Derby

- Cricket

- Pole Vault

- Rugby

- Volleyball

- Gym

- Ultimate Frisbee (especially during impact from laying out)

Although this condition can be caused by repetitive trauma to the lumbar spine in strenuous sports, other risk factors can also predispose individuals to spondylolsis. Males are more commonly affected by spondylolysis than females. In one study looking at youth athletes, it was found that the mean age of individuals with spondylolisthesis was 20 years of age. Spondylolysis also runs in families suggesting a hereditary component such as a predisposition to weaker vertebrae.

People vary in their tendency to get MSDs. Gender is a factor with a higher rate in women than men. Obesity is also a factor, with overweight individuals having a higher risk of some MSDs, specifically lower back.

There is a growing consensus that psychosocial factors are another cause of some MSDs. Some theories for this causal relationship found by many researchers include increased muscle tension, increased blood and fluid pressure, reduction of growth functions, pain sensitivity reduction, pupil dilation, body remaining at heightened state of sensitivity. Although research findings are inconsistent at this stage, some of the workplace stressors found to be associated with MSDs in the workplace include high job demands, low social support, and overall job strain. Researchers have consistently identified causal relationships between job dissatisfaction and MSDs. For example, improving job satisfaction can reduce 17-69 per cent of work-related back disorders and improving job control can reduce 37-84 per cent of work-related wrist disorders.

In most people, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary, and is usually something the affected person would just be aware of, rather than a serious medical condition. However, if there is widespread laxity of other connective tissue, then this may be a sign of Ehlers-Danlos syndrome.

Ligamentous laxity may also result from injury, such as from a vehicle accident. It can result from whiplash and be overlooked for years by doctors who are not looking for it, despite the chronic pain that accompanies the resultant spinal instability. Ligamentous laxity will show up on an upright magnetic resonance imaging (MRI), the only kind of MRI that will show soft tissue damage. It can be seen in standing stress radiographs in flexion, extension, and neutral views as well, and also digital motion X-ray, or DMX.

An advantage to having lax ligaments and joints is the ability to withstand pain from hyperextension; however, this is also a disadvantage as a lack of perceived pain can prevent a person from removing the ligament from insult, leading to ligament damage. This can also lead to death if you tear the wrong ligament. People with hypermobile joints (or "double-jointed" people), almost by definition, have lax ligaments.

A neutral spine or good posture refers to the "three natural curves [that] are present in a healthy spine." Looking directly at the front or back of the body, the 33 vertebrae in the spinal column should appear completely vertical. From a side view, the cervical (neck) region of the spine (C1-C7) is bent inward, the thoracic (upper back) region (T1-T12) bends outward, and the lumbar (lower back) region (L1-L5) bends inward. The sacrum (tailbone area) (S1-S5 fused) and coccyx (on average 4 fused) rest between the pelvic bones. A neutral pelvis indicates the anterior superior iliac spines and pubic symphysis fall in the same vertical line.

Those who have loose ligaments in the legs and feet often mistakenly assume that they have flat feet. While their feet have an arch when not supporting weight, when stood upon, the arch will flatten. This is because the loose ligaments cannot support the arch in the way that they should. This can make walking and standing painful and tiring.

Pain will usually occur in the feet and lower legs, but can also spread to the back due to abnormal standing and walking habits. Wearing shoes that have good arch support can help minimize the discomfort. The underlying problem, however, is not solved by wearing shoes with arch supports or worsened by wearing shoes without arch support. There is currently no cure for the condition.

In addition, people with ligamentous laxity often have clumsy or deliberate gaits, owing to the body having to overcompensate for the greater amount of energy required to offset the weakened ligaments. The feet may be spread apart at a wide angle, and the knees may flex backwards slightly after each stride.

Those who have this disease may experience sprained ankles more frequently than other people.

The cause is not currently known, and the condition appears to be multifactorial. Several candidate genes (such as FBN1, which has been associated with Marfan) have been proposed and excluded.

Scoliosis affects 2–3% of the United States population, which is equivalent to about 5 to 9 million cases. A scoliosis spinal column's curve of 10° or less affects 1.5% to 3% of individuals. The age of onset is usually between 10 years and 15 years (can occur at a younger age) in children and adolescents, making up to 85% of those diagnosed. This is seen to be due to rapid growth spurts occurring at puberty when spinal development is most relenting to genetic and environmental influences. Because female adolescents undergo growth spurts before postural musculoskeletal maturity, scoliosis is more prevalent among females. Although fewer cases are present today using Cobb angle analysis for diagnosis, scoliosis remains a prevailing condition, appearing in otherwise healthy children. Incidence of idiopathic scoliosis (IS) stops after puberty when skeletal maturity is reached, however, further curvature may proceed during late adulthood due to vertebral osteoporosis and weakened musculature.

Anterolisthesis location includes which vertebrae are involved, and may also specify which parts of the vertebrae are affected.

"Isthmic" anterolisthesis is where there is a defect in the pars interarticularis. It is the most common form of spondylolisthesis; also called spondylolytic spondylolisthesis, it occurs with a reported prevalence of 5–7 percent in the US population. A slip or fracture of the intravertebral joint is usually acquired between the ages of 6 and 16 years, but remains unnoticed until adulthood. Roughly 90 percent of these isthmic slips are low-grade (less than 50 percent slip) and 10 percent are high-grade (greater than 50 percent slip). It is divided into three subtypes:

- A: pars fatigue fracture

- B: pars elongation due to multiple healed stress effects

- C: pars acute fracture

55% of facet syndrome cases occur in cervical vertebrae, and 31% in lumbar. Facet syndrome can progress to spinal osteoarthritis, which is known as spondylosis. Pathology of the C1-C2 (atlantoaxial) joint, the most mobile of all vertebral segments, accounts for 4% of all spondylosis.

Like many other joints throughout the human body, facets can experience natural degeneration from constant use. Over time, the cartilage within the joints can naturally begin to wear out, allowing it to become thin or disappear entirely which, in turn, allows the conjoining vertebrae to rub directly against one another with little or no lubricant or separation. A result of this rubbing is often swelling, inflammation or other painful symptoms.

Over time, the body will naturally respond to the instability within the spine by developing bone spurs, thickened ligaments or even cysts that can press up against or pinch the sensitive nerve roots exiting the spinal column.

While primarily caused through natural wear and tear, advanced facet syndrome can also occur as a result of injury to the spine, degenerative disease or lifestyle choices. These causes can include:

- An unexpected, traumatic event such as a car accident, significant fall or high impact sports injury.

- Osteoarthritis

- Spondylolisthesis

- Obesity

- Smoking

- Malnutrition

- Lack of physical exercise or daily activity

The injury is immediately fatal in 70% of cases, with an additional 15% surviving to the emergency room, but perishing during their hospital stay. A basion-dental interval of 16mm or greater is associated with mortality. In those with neurologic deficits, survival is unlikely.

Possible causes that lead to the condition of Lumbar hyperlordosis are the following:

- Spines – Natural factors of how spines are formed greatly increase certain individuals' likelihood to experience a strain or sprain in their back or neck. Factors such as having more lumbar vertebrae allowing for too much flexibility, and then in cases of less lumbar the individual not reaching their necessity for flexibility and then pushing their bodies to injury.

- Legs – Another odd body formation is when an individual has a leg shorter than the other, which can be immediate cause for imbalance of hips then putting strain on the posture of the back which an individual has to adjust into vulnerable positions to meet aesthetic appearances. This can lead to permanent damage in the back. Genu recurvatum (sway back knees) is also a factor that forces a dancer to adjust into unstable postures.

- Hips – Common problems in the hips are tight hip flexors, which causes for poor lifting posture, hip flexion contracture, which means the lack of postural awareness, and thoracic hyperkyphosis, which causes the individual to compensate for limited hip turn out (which is essential to dances such as ballet). Weak psoas (short for iliopsoas-muscle that controls the hip flexor) force the dancer to lift from strength of their back instead of from the hip when lifting their leg into arabesque or attitude. This causes great stress and risk of injury, especially because the dancer will have to compensate to obtain the positions required.

- Muscles – One of the greatest contributors is uneven muscles. Because all muscles have a muscle that works in opposition to it, it is imperative that to keep all muscles protected, the opposite muscle is not stronger than the muscle at risk. In the situation of lumbar lordosis, abdominal muscles are weaker than the muscles in the lumbar spine and the hamstring muscles. The muscular imbalance results in pulling down the pelvis in the front of the body, creating the swayback in the spine.

- Growth spurt – Younger dancers are more at risk for development of lumbar hyperlordosis because the lumbar fascia and hamstrings tighten when a child starts to experience a growth spurt into adolescence.

Technical factors

- Improper lifts – When male dancers are performing dance lifts with another dancer they are extremely prone to lift in the incorrect posture, pushing their arms up to lift the other dancer, while letting their core and spine curve which is easy to then hyperlordosis in a dancer's back.

- Overuse – Over 45% of anatomical sites of injury in dancers are in the lower back. This can be attributed to the strains of repetitive dance training may lead to minor trauma. If the damaged site is not given time to heal the damage of the injury will increase. Abrupt increases in dance intensity or sudden changes in dance choreography do not allow the body to adapt to the new stresses. New styles of dance, returning to dance, or increasing dance time by a great deal will result in exhaustion of the body.

One source of snapping scapula is when the muscles underneath the scapula (the subscapularis muscle) atrophies. This causes the scapula to become very close to the rib cage, eventually causing rubbing or bumping during arm/shoulder movement. Another cause is bursitis, which is when the tissues between the shoulder blade and thoracic wall inflame. Muscle and bone abnormalities in the shoulder area can also contribute to the pain.

A retrolisthesis is a posterior displacement of one vertebral body with respect to the subjacent vertebra to a degree less than a luxation (dislocation). Clinically speaking, retrolisthesis is the opposite of spondylolisthesis (anterior displacement of one vertebral body on the subjacent vertebral body), and is also called retrospondylolisthesis. Retrolistheses are most easily diagnosed on lateral x-ray views of the spine. Views, where care has been taken to expose for a true lateral view without any rotation, offer the best diagnostic quality.

Retrolistheses are found most prominently in the cervical spine and lumbar region but can also be seen in the thoracic area.

There are many causes of scoliosis, including spinal deformities, neuromuscular problems, and inherited diseases or conditions caused by the environment.

An estimated 65% of scoliosis cases are idiopathic, about 15% are congenital and about 10% are secondary to a neuromuscular disease.

Idiopathic scoliosis represents a majority of cases, but its causes are largely unknown. Results of recent studies indicate potential heritability of the disorder. About 38% of variance in scoliosis risk is due to genetic factors, and 62% is due to the environment. The genetics are likely complex however, given the inconsistent inheritance and discordance among monozygotic twins. The specific genes that contribute to development of scoliosis have not been conclusively identified. At least one gene, "CHD7", has been associated with the idiopathic form of scoliosis.

Several candidate gene studies have found associations between idiopathic scoliosis and genes mediating bone formation, bone metabolism, and connective tissue structure. Several genome-wide studies have identified a number of loci as significantly linked to idiopathic scoliosis. In 2006 idiopathic scoliosis was linked with three microsatellite polymorphisms in the MATN1 gene (encoding for "Matrilin 1, cartilage matrix protein"). Fifty-three single nucleotide polymorphism markers in the DNA that are significantly associated with adolescent idiopathic scoliosis were identified through a genome-wide association study.

Adolescent idiopathic scoliosis (AIS) has no clear causal agent, and is generally believed to be multifactorial. The prevalence of scoliosis is 1% to 2% among adolescents, however the likelihood of progression among adolescents with a Cobb angle of less than 20° is about 10% to 20%.

Congenital scoliosis can be attributed to a malformation of the spine during weeks three to six "in utero" due to a failure of formation, a failure of segmentation, or a combination of stimuli. Incomplete and abnormal segmentation results in an abnormally shaped vertebra, at times fused to a normal vertebra or unilaterally fused vertebrae, leading to the abnormal lateral curvature of the spine.

Many with Scheuermann's disease often have an excessive lordotic curve in the lumbar spine; this is the body's natural way to compensate for the kyphotic curve above. Interestingly, many with Scheuermann's disease have very large lung capacities and males often have broad, barrel chests. Most people have forced vital capacity (FVC) scores above average. It has been proposed that this is the body's natural way to compensate for a loss of breathing depth.

Often patients have tight hamstrings, which, again, is related to the body compensating for excessive spinal curvature, though this is also debated (for example, some suggest the tightness of ligament is the initial cause of the growth abnormality). In addition to the common lordosis, it has been suggested that between 20–30% of patients with Scheuermann's Disease also have scoliosis, though most cases are negligible. In more serious cases, however, the combination is classified as a separate condition known as kyphoscoliosis.

The Jefferson fracture can be associated with this injury, with the C1 ring, or atlas, being fractured in several places, allowing the spine to shift forward relative to the skull base. The Hangman's fracture which is a fracture of the C2 vertebral body or dens of the cervical spine upon which the skull base sits to allow the head to rotate, can also be associated with atlanto-occipital dislocation. Despite its eponym, the fracture is not usually associated with a hanging mechanism of injury.

Doctors often recommend physical therapy in order to strengthen the subscapularis muscle, and prescribe anti-inflammatory medications. For extreme cases, cortisone injections would be utilized.

The salient feature of the disorder is the exuberant osteophytosis that occurs at posterior lumbar spinous processes. Osteophytes are coarse calcifications at the edges of bone that form due to repetitive stress and trauma. There is also atrophy and fatty replacement of paraspinal musculature, which can be detected by CT or MRI.

There are several conditions and syndromes that can affect the cervical spine and they all vary due to the difference in place and type of injury.

- Rheumatoid arthritis Those infected with rheumatoid arthritis in their cervical spine are known to have neurological deficits. It results in occipital pain and myelopathy.

- Occipito-cervical junction This disorder may result from rheumatoid arthritis, causing the hyper-mobility of the connection between the neck and head, resulting in paralysis or pain.

- Cerebrovascular disease Cerebrovascular disease is a type of cervical spine disorder that can cause tetraplegia.

- Subaxial cervical spine

- Atlanto-axial joint

A multitude of conditions may lead to the development of torticollis including: muscular fibrosis, congenital spine abnormalities, or toxic or traumatic brain injury.

A rough categorization discerns between congenital torticollis and acquired torticollis.

Other categories include:

- Osseous

- Traumatic

- CNS/PNS

- Ocular

- Non-muscular soft tissue

- Spasmodic

- Drug induced

A multitude of neurological disorders cause BSS, including motor neuron disease, CNS disorders, and early amyotrophic lateral sclerosis. Usually, the bent spine is caused by dysfunctioning extensor spinal muscles with a neurological cause.

Neurological origin BSS may also result from damage to the basal ganglia nuclei that are a part of the cerebral cortex, which play a major role in bodily positioning. Damage to this part of the brain can inhibit proper flexion and extension in the muscles necessary for maintaining an upright position. Additionally, the neurotransmitter dopamine plays a key role in the operation of basal ganglia. An abnormally low dopamine concentration, such as that associated with Parkinson’s disease, causes dysfunction in the basal ganglia and the associated muscle groups, leading to BSS. Studies have estimated the prevalence of BSS in people affected by Parkinson's to be between 3% and 18%.

The risk of serious complications from spinal fusion surgery for kyphosis is estimated to be 5%, similar to the risks of surgery for scoliosis. Possible complications include inflammation of the soft tissue or deep inflammatory processes, breathing impairments, bleeding, and nerve injuries. According to the latest evidence, the actual rate of complications may be substantially higher. Even among those who do not suffer from serious complications, 5% of patients require reoperation within five years of the procedure, and in general it is not yet clear what one would expect from spine surgery during the long-term. Taking into account that signs and symptoms of spinal deformity cannot be changed by surgical intervention, surgery remains to be a cosmetic indication. Unfortunately, the cosmetic effects of surgery are not necessarily stable.