The mucopolysaccharidoses share many clinical features but have varying degrees of severity. These features may not be apparent at birth but progress as storage of glycosaminoglycans affects bone, skeletal structure, connective tissues, and organs. Neurological complications may include damage to neurons (which send and receive signals throughout the body) as well as pain and impaired motor function. This results from compression of nerves or nerve roots in the spinal cord or in the peripheral nervous system, the part of the nervous system that connects the brain and spinal cord to sensory organs such as the eyes and to other organs, muscles, and tissues throughout the body.

Depending on the mucopolysaccharidosis subtype, affected individuals may have normal intellect or have cognitive impairments, may experience developmental delay, or may have severe behavioral problems. Many individuals have hearing loss, either conductive (in which pressure behind the eardrum causes fluid from the lining of the middle ear to build up and eventually congeal), neurosensory (in which tiny hair cells in the inner ear are damaged), or both. Communicating hydrocephalus—in which the normal reabsorption of cerebrospinal fluid is blocked and causes increased pressure inside the head—is common in some of the mucopolysaccharidoses. Surgically inserting a shunt into the brain can drain fluid. The eye's cornea often becomes cloudy from intracellular storage, and glaucoma and degeneration of the retina also may affect the patient's vision.

Physical symptoms generally include coarse or rough facial features (including a flat nasal bridge, thick lips, and enlarged mouth and tongue), short stature with disproportionately short trunk (dwarfism), dysplasia (abnormal bone size and/or shape) and other skeletal irregularities, thickened skin, enlarged organs such as liver (hepatomegaly) or spleen (splenomegaly), hernias, and excessive body hair growth. Short and often claw-like hands, progressive joint stiffness, and carpal tunnel syndrome can restrict hand mobility and function. Recurring respiratory infections are common, as are obstructive airway disease and obstructive sleep apnea. Many affected individuals also have heart disease, often involving enlarged or diseased heart valves.

Another lysosomal storage disease often confused with the mucopolysaccharidoses is mucolipidosis. In this disorder, excessive amounts of fatty materials known as lipids (another principal component of living cells) are stored, in addition to sugars. Persons with mucolipidosis may share some of the clinical features associated with the mucopolysaccharidoses (certain facial features, bony structure abnormalities, and damage to the brain), and increased amounts of the enzymes needed to break down the lipids are found in the blood.

MPS I is divided into three subtypes based on severity of symptoms. All three types result from an absence of, or insufficient levels of, the enzyme alpha-L-iduronidase. Children born to an MPS I parent carry the defective gene.

- MPS I H (also called Hurler syndrome or α-L-iduronidase deficiency), is the most severe of the MPS I subtypes. Developmental delay is evident by the end of the first year, and patients usually stop developing between ages 2 and 4. This is followed by progressive mental decline and loss of physical skills. Language may be limited due to hearing loss and an enlarged tongue. In time, the clear layers of the cornea become clouded and retinas may begin to degenerate. Carpal tunnel syndrome (or similar compression of nerves elsewhere in the body) and restricted joint movement are common.

- MPS I S, Scheie syndrome, is the mildest form of MPS I. Symptoms generally begin to appear after age 5, with diagnosis most commonly made after age 10. Children with Scheie syndrome have normal intelligence or may have mild learning disabilities; some may have psychiatric problems. Glaucoma, retinal degeneration, and clouded corneas may significantly impair vision. Other problems include carpal tunnel syndrome or other nerve compression, stiff joints, claw hands and deformed feet, a short neck, and aortic valve disease. Some affected individuals also have obstructive airway disease and sleep apnea. Persons with Scheie syndrome can live into adulthood.

- MPS I H-S, Hurler–Scheie syndrome, is less severe than Hurler syndrome alone. Symptoms generally begin between ages 3 and 8. Children may have moderate intellectual disability and learning difficulties. Skeletal and systemic irregularities include short stature, marked smallness in the jaws, progressive joint stiffness, compressed spinal cord, clouded corneas, hearing loss, heart disease, coarse facial features, and umbilical hernia. Respiratory problems, sleep apnea, and heart disease may develop in adolescence. Some persons with MPS I H-S need continuous positive airway pressure during sleep to ease breathing. Life expectancy is generally into the late teens or early twenties.

Although no studies have been done to determine the frequency of MPS I in the United States, studies in British Columbia estimate that 1 in 100,000 babies born has Hurler syndrome. The estimate for Scheie syndrome is one in 500,000 births and for Hurler-Scheie syndrome it is one in 115,000 births.

MPS III is characterized by severe deterioration of the central nervous system, resulting in a variety of symptoms. Individuals with Sanfilippo syndrome usually start to show the symptoms between the age of 2 to 6. Speech problems, hyperactivity, aggressive behavior, developmental delays, hirsutism, sleep disturbances, seizures are the common manifestation of the syndrome at the initial stage. After the age of 10, patients start to experience increasingly severe symptoms including loss of motor and cognitive skills and somatic diseases. Patients later enter vegetative state, eventually leading to death in their 30s.

Individuals with MPS III tend to have mild skeletal abnormalities; osteonecrosis of the femoral head may be present in patients with the severe form. Optical nerve atrophy, deafness, otitis can be seen in moderate to severe individuals. Other characteristics include coarse facial features, thick lips, synophrys, and stiff joints. Chronic diarrhea, enlarged liver and spleen are also common.

It is difficult to clinically distinguish differences among the four types of Sanflippo syndrome. However, MPS IIIA is usually the most severe subtype, characterized by earliest onset, rapid clinical progression with severe symptoms, and short survival.

Symptoms of ML III are often not noticed until the child is 3–5 years of age. Patients with ML III are generally of normal intelligence (trait) or have only mild mental retardation. These patients usually have skeletal abnormalities, coarse facial features, short height, corneal clouding, carpal tunnel syndrome, aortic valve disease and mild enlargement of organs. Some children with severe forms of this disease do not live beyond childhood. However, there is a great variability among patients - there are diagnosed individuals with ML III living in their sixties.

The condition is marked by progressive deterioration, hepatosplenomegaly, dwarfism, and unique facial features. A progressive mental retardation occurs, with death frequently occurring by the age of 10 years.

Developmental delay is evident by the end of the first year, and patients usually stop developing between ages 2 and 4. This is followed by progressive mental decline and loss of physical skills. Language may be limited due to hearing loss and an enlarged tongue. In time, the clear layers of the cornea become clouded and retinas may begin to degenerate. Carpal tunnel syndrome (or similar compression of nerves elsewhere in the body) and restricted joint movement are common.

Affected children may be large at birth and appear normal, but may have inguinal (in the groin) or umbilical (where the umbilical cord passes through the abdomen) hernias. Growth in height may be initially faster than normal, then begins to slow before the end of the first year and often ends around age 3. Many children develop a short body trunk and a maximum stature less than 4 feet. Distinct facial features (including flat face, depressed nasal bridge, and bulging forehead) become more evident in the second year. By age 2, the ribs have widened and are oar-shaped. The liver, spleen, and heart are often enlarged. Children may experience noisy breathing and recurring upper respiratory-tract and ear infections. Feeding may be difficult for some children, and many experience periodic bowel problems. Children with Hurler syndrome often die before age 10 from obstructive airway disease, respiratory infections, or cardiac complications.

Sanfilippo syndrome, or mucopolysaccharidosis III (MPS-III) is a rare autosomal recessive lysosomal storage disease. It is caused by a deficiency in one of the enzymes needed to break down the glycosaminoglycan heparan sulfate (which is found in the extra-cellular matrix and on cell surface glycoproteins).

Although undegraded heparan sulfate is the primary stored substrate, glycolipids such as gangliosides are also stored despite no genetic defect in the enzymes associated with their breakdown.

The condition is named for Sylvester Sanfilippo, the pediatrician who first described the disease.

The symptoms of Sly syndrome are similar to those of Hurler syndrome (MPS I). The symptoms include:

- in the head, neck, and face: coarse (Hurler-like) facies and macrocephaly, frontal prominence, premature closure of sagittal lambdoid sutures, and J-shaped sella turcica

- in the eyes: corneal opacity and iris coloboma

- in the nose: anteverted nostrils and a depressed nostril bridge

- in the mouth and oral areas: prominent alveolar processes and cleft palate

- in the thorax: usually pectus carinatum or exacavatum and oar-shaped ribs; also a protruding abdomen and inguinal or umbilical hernia

- in the extremities: talipes, an underdeveloped ilium, aseptic necrosis of femoral head, and shortness of tubular bones occurs

- in the spine: kyphosis or scoliosis and hook-like deformities in thoracic and lumbar vertebrate

- in the bones: dysostosis multiplex

In addition recurrent pulmonary infections occur. Hepatomegaly occurs in the gastrointestinal system. Splenomegaly occurs in the hematopoietic system. Inborn mucopolysaccharide metabolic disorders due to β-glucuronidase deficiency with granular inclusions in granulocytes occurs in the biochemical and metabolic systems. Growth and motor skills are affected, and mental retardation also occurs.

Hurler syndrome, also known as mucopolysaccharidosis type I (MPS I), Hurler's disease, also gargoylism, is a genetic disorder that results in the buildup of glycosaminoglycans (formerly known as mucopolysaccharides) due to a deficiency of alpha-L iduronidase, an enzyme responsible for the degradation of mucopolysaccharides in lysosomes. Without this enzyme, a buildup of heparan sulfate and dermatan sulfate occurs in the body. Symptoms appear during childhood and early death can occur due to organ damage.

MPS I is divided into three subtypes based on severity of symptoms. All three types result from an absence of, or insufficient levels of, the enzyme α-L-iduronidase. MPS I H or Hurler syndrome is the most severe of the MPS I subtypes. The other two types are MPS I S or Scheie syndrome and MPS I H-S or Hurler-Scheie syndrome.

Hurler syndrome is often classified as a lysosomal storage disease, and is clinically related to Hunter syndrome, which is X-linked, while Hurler syndrome is autosomal recessive.

It is named for Gertrud Hurler (1889–1965), a German pediatrician.

The symptoms of Hunter syndrome (MPS II) are generally not apparent at birth, but usually start to become noticeable after the first year of life. Often, the first symptoms may include abdominal hernias, ear infections, runny noses, and colds. Since these symptoms are quite common among all infants, they are not likely to lead a doctor to make a diagnosis of Hunter syndrome right away. As the buildup of glycosaminoglycans (GAGs) continues throughout the cells of the body, signs of Hunter syndrome become more visible. Physical appearances of many children with Hunter syndrome include a distinctive coarseness in their facial features, including a prominent forehead, a nose with a flattened bridge, and an enlarged tongue. For this reason, unrelated children with Hunter syndrome often look alike. They may also have a large head, as well as an enlarged abdomen. Many continue to have frequent infections of the ears and respiratory tract.

The continued storage of GAGs in cells can lead to organs being affected in important ways. The thickening of the heart valves along with the walls of the heart can result in progressive decline in cardiac function. The walls of the airway may become thickened, as well, leading to breathing problems while sleeping (obstructive airway disease) and noisy breathing generally. People with Hunter syndrome may also have limited lung capacity due to pulmonary involvement. As the liver and spleen grow larger with time, the belly may become distended, making hernias more noticeable. All major joints (including the wrists, elbows, shoulders, hips, and knees) may be affected by Hunter syndrome, leading to joint stiffness and limited motion. Progressive involvement of the finger and thumb joints results in decreased ability to pick up small objects. The effects on other joints, such as hips and knees, can make walking normally increasingly difficult. If carpal tunnel syndrome develops, a common symptom even in young children with Hunter syndrome, a further decrease in hand function can occur. The bones themselves may be affected, resulting in short stature. In addition, pebbly, ivory-colored skin lesions may be found on the upper arms, legs, and upper back of some people with Hunter syndrome. The presence or absence of the skin lesions is not helpful, however, in predicting clinical severity in Hunter syndrome. Finally, the storage of GAGs in the brain can lead to delayed development with subsequent mental retardation and progressive loss of function. The rate and degree of progression is different for each person with Hunter syndrome.

Although Hunter syndrome is associated with a broad spectrum of clinical severity, two main forms can be recognized - severe and mild/attenuated. The differences between the severe and attenuated forms are due mainly to the progressive development of neurodegeneration in the severe form. Though the terms "attenuated" or "mild" are used by physicians in comparing people with Hunter syndrome, the effects of even mild disease are quite serious. Between the two main forms of disease, and even within them, two of the most significant areas of variability concern the degree of mental retardation and expected lifespan. Some people who have Hunter syndrome experience no mental handicaps and live into their 20s or 30s, with occasional reports of people who have lived into their 50s or 60s. Since the implementation of enzyme replacement therapy for Hunter syndrome, lifespans for those without mental handicaps are expected to lengthen since their physical disease appears to improve or stabilize with such treatment. The quality of life remains high in a large number of people, and many adults are actively employed.

In contrast, others with Hunter syndrome develop severe mental impairment and have life expectancies of 15 years or less, often due to neurodegeneration or physical complications from the disease. The age at onset of symptoms and the presence/absence of behavioral disturbances are predictive factors of ultimate disease severity in very young patients. Behavioral disturbances can often mimic combinations of symptoms of attention deficit hyperactivity disorder, autism, obsessive compulsive disorder, and/or sensory processing disorder, although the existence and level of symptoms differ in each affected child. They often also include a lack of an appropriate sense of danger, and aggression. The behavioral symptoms of Hunter syndrome generally precede neurodegeneration and often increase in severity until the mental handicaps become more pronounced.

Pseudo-Hurler polydystrophy, also referred to as mucolipidosis III (ML III), is a lysosomal storage disease closely related to I-cell disease (ML II). This disorder is called Pseudo-Hurler because it resembles a mild form of Hurler syndrome, one of the mucopolysaccharide (MPS) diseases.

Sly syndrome, also called mucopolysaccharidosis type VII (MPS 7), is an autosomal recessive lysosomal storage disease characterized by a deficiency of the enzyme β-glucuronidase, a lysosomal enzyme. Sly syndrome belongs to a group of disorders known as mucopolysaccharidoses, which are lysosomal storage diseases. In Sly syndrome, the deficiency in β-glucuronidase leads to the accumulation of certain complex carbohydrates (mucopolysaccharides) in many tissues and organs of the body.

It was named after its discoverer William S. Sly, an American biochemist who has spent nearly his entire academic career at Saint Louis University.

The following signs are associated with the disease

- Abnormal heart development

- Abnormal skeletal development

- Hypermobile joints

- Large fingers

- Knock-knees

- Widely spaced teeth

- Bell-shaped chest (flared ribs)

- Compression of spinal cord

- Enlarged heart

- Dwarfism

- Heart murmur

- below average height for certain age

Patients with Morquio syndrome appear healthy at birth. They often present with spinal deformity, and there is growth retardation and possibly genu valgum in the second or third year of life. A patient with Morquio's syndrome is likely to die at an early age. Symptoms of the disease may include:

- Short stature and short neck (caused by flat vertebrae)

- Moderate kyphosis or scoliosis

- Mild pectus carinatum ("pigeon chest")

- Cervical spine: odontoid hypoplasia, atlanto-axial instability; may be associated with myelopathy with gradual loss of walking ability

- Joint laxity, mild dysostosis multiplex, dysplastic hips, large unstable knees, large elbows and wrists, and flat feet

- The combined abnormalities usually result in a duck-waddling gait

- Mid-face hypoplasia and mandibular protrusion

- Thin tooth enamel

- Corneal clouding

- Mild hepatosplenomegaly

Regarding the life span of people with Morquio, some can die as early as 2 or 3 years old, and some can live up to 60 or 70 years old. The oldest known person with Morquio syndrome type IV A was Kenneth D. Martin, who was born in Osage City, Kansas, USA and was 81 years old at the time of his death

The symptoms of LSD vary, depending on the particular disorder and other variables such as the age of onset, and can be mild to severe. They can include developmental delay, movement disorders, seizures, dementia, deafness, and/or blindness. Some people with LSDhave enlarged livers (hepatomegaly) and enlarged spleens (splenomegaly), pulmonary and cardiac problems, and bones that grow abnormally.

Children with Maroteaux–Lamy syndrome usually have normal intellectual development but share many of the physical symptoms found in Hurler syndrome. Caused by the deficient enzyme N-acetylgalactosamine 4-sulfatase, Maroteaux–Lamy syndrome has a variable spectrum of severe symptoms. Neurological complications include clouded corneas, deafness, thickening of the dura (the membrane that surrounds and protects the brain and spinal cord), and pain caused by compressed or traumatized nerves and nerve roots.

Signs are revealed early in the affected child's life, with one of the first symptoms often being a significantly prolonged age of learning how to walk. By age 10 children have developed a shortened trunk, crouched stance, and restricted joint movement. In more severe cases, children also develop a protruding abdomen and forward-curving spine. Skeletal changes (particularly in the pelvic region) are progressive and limit movement. Many children also have umbilical hernia or inguinal hernias. Nearly all children have some form of heart disease, usually involving valve dysfunction.

An enzyme replacement therapy, galsulfase (Naglazyme), was tested on patients with Maroteaux–Lamy syndrome and was successful in that it improved growth and joint movement. An experiment was then carried out to see whether an injection of the missing enzyme into the hips would help the range of motion and pain. At a cost of $365,000 a year, Naglazyme is one of the world's most expensive drugs.

Morquio syndrome (referred to as mucopolysaccharidosis IV, MPS IV, Morquio-Brailsford syndrome, or Morquio) is a rare metabolic disorder in which the body cannot process certain types of mucopolysaccharides. This birth defect, which is autosomal recessive, is thus a lysosomal storage disorder that is usually inherited. In the US, the incidence rate for Morquio is estimated at between 1 in 200,000 and 1 in 300,000 live births.

The build-up or elimination of mucopolysaccharides, rather than processing by their usual biochemical pathways, causes various symptoms. These involve accumulation of keratan sulfate.

Hunter syndrome, or mucopolysaccharidosis II (MPS II), is a lysosomal storage disease caused by a deficient (or absent) enzyme, iduronate-2-sulfatase (I2S). The accumulated substrates in Hunter syndrome are heparan sulfate and dermatan sulfate. The syndrome has X-linked recessive inheritance.

Lysosomal storage diseases (LSDs; ) are a group of about 50 rare inherited metabolic disorders that result from defects in lysosomal function. Lysosomes are sacs of enzymes within cells that digest large molecules and pass the fragments on to other parts of the cell for recycling. This process requires several critical enzymes. If one of these enzymes is defective, because of a mutation, the large molecules accumulate within the cell, eventually killing it.

Lysosomal storage disorders are caused by lysosomal dysfunction usually as a consequence of deficiency of a single enzyme required for the metabolism of lipids, glycoproteins (sugar-containing proteins), or so-called mucopolysaccharides. Individually, LSDs occur with incidences of less than 1:100,000; however, as a group, the incidence is about 1:5,000 - 1:10,000. Most of these disorders are autosomal recessively inherited such as Niemann–Pick disease, type C, but a few are X-linked recessively inherited, such as Fabry disease and Hunter syndrome (MPS II).

The lysosome is commonly referred to as the cell's recycling center because it processes unwanted material into substances that the cell can use. Lysosomes break down this unwanted matter by enzymes, highly specialized proteins essential for survival. Lysosomal disorders are usually triggered when a particular enzyme exists in too small an amount or is missing altogether. When this happens, substances accumulate in the cell. In other words, when the lysosome does not function normally, excess products destined for breakdown and recycling are stored in the cell.

Like other genetic disorders, individuals inherit lysosomal storage diseases from their parents. Although each disorder results from different gene mutations that translate into a deficiency in enzyme activity, they all share a common biochemical characteristic – all lysosomal disorders originate from an abnormal accumulation of substances inside the lysosome.

LSDs affect mostly children and they often die at a young and unpredictable age, many within a few months or years of birth. Many other children die of this disease following years of suffering from various symptoms of their particular disorder.

Maroteaux–Lamy syndrome (also known as mucopolysaccharidosis type VI, MPS VI, or polydystrophic dwarfism) is a form of mucopolysaccharidosis caused by a deficiency in arylsulfatase B (ARSB). It is named after Pierre Maroteaux (1926–) and his mentor Maurice Emil Joseph Lamy (1895–1975), both French physicians.

Scheie syndrome (also known as "MPS I-S") is less severe version of Hurler syndrome. It is a condition characterized by corneal clouding, facial dysmorphism, and normal lifespan. People with this condition may have aortic regurgitation.

It is named after Harold Glendon Scheie (1909–1990), an American ophthalmologist.

Usher syndrome is responsible for the majority of deaf-blindness. The word "syndrome" means that multiple symptoms occur together, in this case, deafness and blindness. It occurs in roughly 1 person in 23,000 in the United States, 1 in 28,000 in Norway and 1 in 12,500 in Germany. People with Usher syndrome represent roughly one-sixth of people with retinitis pigmentosa.

Usher syndrome is inherited in an autosomal recessive pattern. "Recessive" means both parents must contribute an appropriate gene for the syndrome to appear, and "autosomal" means the gene is not carried on one of the sex chromosomes (X or Y), but rather on one of the 22 other pairs. (See the article on human genetics for more details.)

The progressive blindness of Usher syndrome results from retinitis pigmentosa. The photoreceptor cells usually start to degenerate from the outer to the center of the retina, including the macula. The degeneration is usually first noticed as night blindness (nyctalopia); peripheral vision is gradually lost, restricting the visual field (tunnel vision), which generally progresses to complete blindness. The qualifier 'pigmentosa' reflects the fact that clumps of pigment may be visible by an ophthalmoscope in advanced stages of degeneration.

Although Usher syndrome has been classified clinically in several ways, the prevailing approach is to classify it into three clinical sub-types called Usher I, II and III in order of decreasing severity of deafness. Usher I and II are the more common forms; the fraction of people with Usher III is significant only in a few specific areas, such as Finland and Birmingham. As described below, these clinical subtypes may be further subdivided by the particular gene mutated; people with Usher I and II may have any one of six and three genes mutated, respectively, whereas only one gene has been associated with Usher III. The function of these genes is still poorly understood. The hearing impairment associated with Usher syndrome is better understood: damaged hair cells in the cochlea of the inner ear inhibit electrical impulses from reaching the brain.

Usher syndrome, also known as Hallgren syndrome, Usher-Hallgren syndrome, retinitis pigmentosa-dysacusis syndrome, or dystrophia retinae dysacusis syndrome, is an extremely rare genetic disorder caused by a mutation in any one of at least 11 genes resulting in a combination of hearing loss and visual impairment. It is a leading cause of deafblindness and is at present incurable.

Usher syndrome is classed into three subtypes according to onset and severity of symptoms. All three subtypes are caused by mutations in genes involved in the function of the inner ear and retina. These mutations are inherited in an autosomal recessive pattern.

Myofascial pain is pain in muscles or fascia (a type of connective tissue that surrounds muscles). It can occur in distinct, isolated areas of the body. Because any muscle or fascia in the body may be affected, this may cause a variety of localized symptoms.

Generally speaking, the muscular pain is steady, aching, and deep. Depending on the case and location the intensity can range from mild discomfort to excruciating and "lightning-like".

LA SKIN'S DIAGNOSTIC CRITERIA:

- Unilateral pain

- Muscle tenderness

- Clicking sound

- Limitations in jaw function

Knots may be visible or felt beneath the skin. The pain does not resolve on its own, even after typical first-aid self-care such as ice, heat, and rest.

Myofascial pain syndrome (MPS), also known as chronic myofascial pain (CMP), is a syndrome characterized by chronic pain in multiple myofascial trigger points ("knots") and fascial (connective tissue) constrictions. It can appear in any body part.

Characteristic features of a myofascial trigger points include: focal point tenderness, reproduction of pain upon trigger point palpation, hardening of the muscle upon trigger point palpation, pseudo-weakness of the involved muscle, referred pain, and limited range of motion following approximately 5 seconds of sustained trigger point pressure.

Gibbus deformity is a form of structural kyphosis typically found in the upper lumbar and lower thoracic vertebrae, where one or more adjacent vertebrae become wedged. Gibbus deformity most often develops in young children as a result of spinal tuberculosis and is the result of collapse of vertebral bodies. This can in turn lead to spinal cord compression causing paraplegia.

In addition to tuberculosis, other possible causes of gibbus deformity include pathological diseases, hereditary and congenital conditions, and physical trauma to the spine that results in injury. Gibbus deformity may result from the sail vertebrae associated with cretinism (the childhood form of hypothyroidism), mucopolysaccharidosis (MPS), and certain congenital syndromes, including achondroplasia. Because most children with MPS I (Hurler Syndrome) also exhibit symptoms of a gibbus deformity, the latter can possibly be used to identify the former.

Gibbus deformity is included in a subset of structural kyphosis that is distinguished by a higher-degree angle in the spinal curve that is specific to these forms of kyphosis. Other conditions within this subset include Pott’s disease and Scheuermann kyphosis, but gibbus deformity is marked by an especially sharp angle. Viewed from behind, the resulting hunchback is more easily seen when bending forward. A kyphosis of >70° can be an indication of the need for surgery and these surgeries can be necessary for children as young as two years old, with a reported average of 8 years of age.