The outlook for individuals with EDS depends on the type of EDS they have. Symptoms vary in severity, even within one sub-type, and the frequency of complications changes individually. Some people have negligible symptoms while others are severely restricted in their daily life. Extreme joint instability, chronic musculoskeletal pain, degenerative joint disease, frequent injuries, and spinal deformities may limit mobility. Severe spinal deformities may affect breathing. In the case of extreme joint instability, dislocations may result from simple tasks such as rolling over in bed or turning a doorknob. Secondary conditions such as autonomic dysfunction or cardiovascular problems, occurring in any type, can affect prognosis and quality of life. Severe mobility-related disability is seen more often in Hypermobility-type than in Classical-type or Vascular-type.

Although all types are potentially life-threatening, the majority of individuals will have a normal lifespan. However, those with blood vessel fragility have a high risk of fatal complications. Arterial rupture is the most common cause of sudden death in EDS. Spontaneous arterial rupture most often occurs in the second or third decade, but can occur at any time. The median life-expectancy in the population with Vascular EDS is 48 years.

Ehlers–Danlos syndrome is an inherited disorder estimated to occur in about 1 in 5,000 births worldwide. Initially, prevalence estimates ranged from 1 in 250,000 to 1 in 500,000 people, but these estimates were soon found to be vastly inaccurate as the disorder received further study and medical professionals became more adept at accurately diagnosing EDS. In fact, many experts now believe that Ehlers–Danlos syndrome may be far more common than the currently accepted estimate due to the wide range of severities with which the disorder presents.

The prevalence of the 13 types differs dramatically. The most commonly occurring is the Hypermobility type, followed by the Classical type. The other types of Ehlers–Danlos syndrome are very rare. For example, fewer than ten infants and children with the dermatosparaxis type have been described worldwide. Some types of Ehlers–Danlos are more common in Ashkenazi Jews. For example, the chance of being a carrier for type-VIIc Ehlers–Danlos is 1 in 248 in Ashkenazi Jews, whereas the prevalence of this mutation in the general population is 1 in 2,000.

Treatment is symptomatic, often addressing indicators associated with peripheral pulmonary artery stenosis. Laryngotracheal calcification resulting in dyspnea and forceful breathing can be treated with bronchodilators including the short and long-acting β2-agonists, and various anticholinergics. Prognosis is good, yet life expectancy depends on the severity and extent of diffuse pulmonary and arterial calcification.

Sack–Barabas syndrome is rare and has an estimated prevalence of 1 in 100,000 to 200,000.

The initial clinical manifestation of vascular problems in patients with SBS is early, about 25% have their first symptoms at age 20 and more than 80% of patients have had at least one complication by the age of 40.

The median survival for one study of SBS patients was only 48 years.

Keutel syndrome (KS) is a rare autosomal recessive genetic disorder characterized by abnormal diffuse cartilage calcification, hypoplasia of the mid-face, peripheral pulmonary stenosis, hearing loss, short distal phalanges (tips) of the fingers and mild mental retardation. Individuals with KS often present with peripheral pulmonary stenosis, brachytelephalangism, sloping forehead, midface hypoplasia, and receding chin. It is associated with abnormalities in the gene coding for matrix gla protein (MGP). Being an autosomal recessive disorder, it may be inherited from two unaffected, abnormal MGP-carrying parents. Thus, people who inherit two affected MGP genes will likely inherit KS.

It was first identified in 1972 as a novel rare genetic disorder sharing similar symptoms with chondrodysplasia punctata. Multiple forms of chondrodysplasia punctata share symptoms consistent with KS including abnormal cartilage calcification, forceful respiration, brachytelephalangism, hypotonia, psychomotor delay, and conductive deafness, yet peripheral pulmonary stenosis remains unique to KS.

No chromosomal abnormalities are reported in affected individuals, suggesting that familial consanguinity relates to the autosomal recessive mode of inheritance. Also, despite largely abnormal calcification of regions including the larynx, tracheobronchial tree, nose, pinna (anatomy), and epiglottis, patients exhibit normal serum calcium and phosphate levels.

Myhre syndrome is a rare genetic disorder inherited in an autosomal dominant fashion. It is caused by mutation in SMAD4 gene.

Respiratory complications are often cause of death in early infancy.

There have been 30 cases of Marden-Walker Syndrome reported since 1966. The first case of this was in 1966 a female infant was diagnosed with blepharophimosis, joint contractures, arachnodactyly and growth development delay. She ended up passing at 3 months due to pneumonia.

Risk factors for osteoporotic fracture can be split between nonmodifiable and (potentially) modifiable. In addition, osteoporosis is a recognized complication of specific diseases and disorders. Medication use is theoretically modifiable, although in many cases, the use of medication that increases osteoporosis risk may be unavoidable.

Caffeine is not a risk factor for osteoporosis.

It is more likely in females than males.

Winchester syndrome is believed to be inherited through autosomal recessive inheritance. For recessive genetic disorders, individuals inherit the mutated gene for the same trait from both parents. It believed that this disease is caused by a nonlysosomal connective-tissue disturbance. The protein inactivation mutation is found on the matrix metalloproteinase 2 gene (MMP2). MM2 is responsible for bone remodeling. Bone remodeling is the process in which old bone is destroyed so that new bone can be created to replace it. This mutation causes a multicentric osteolysis and arthritis syndrome. It is hypothesized that the loss of an upstream MMP-2 protein activator MT1-MMP, results in decreased MMP-2 activity without affecting "MMP2". The inactivating homoallelic mutation of "MT1-MMP" can be seen at the surface of fibroblasts. It was determined that fibroblasts lacking MT1-MMP lack the ability to degrade type I collagen which leads to anomalous function.

The first gene that could cause the syndrome is described recently and is called NF1X (chromosome 19: 19p13.1).

The disorder is progressive, with the ultimate severity of symptoms often depending on age of onset. In severe cases amputation has been performed when conservative measures such as physical therapy and regional anesthetics have been ineffective.

Bruck syndrome is characterized as the combination of arthrogryposis multiplex congenita and osteogenesis imperfecta. Both diseases are uncommon, but concurrence is extremely rare which makes Bruck syndrome very difficult to research. Bruck syndrome is thought to be an atypical variant of osteogenesis imperfecta most resembling type III, if not its own disease. Multiple gene mutations associated with osteogenesis imperfecta are not seen in Bruck syndrome. Many affected individuals are within the same family, and pedigree data supports that the disease is acquired through autosomal recessive inheritance. Bruck syndrome has features of congenital contractures, bone fragility, recurring bone fractures, flexion joint and limb deformities, pterygia, short body height, and progressive kyphoscoliosis. Individuals encounter restricted mobility and pulmonary function. A reduction in bone mineral content and larger hydroxyapatite crystals are also detectable Joint contractures are primarily bilateral and symmetrical, and most prone to ankles. Bruck syndrome has no effect on intelligence, vision, or hearing.

Urban–Rogers–Meyer syndrome, also known as Prader–Willi habitus, osteopenia, and camptodactyly or Urban syndrome, is an extremely rare inherited congenital disorder first described by Urban et al. (1979). It is characterized by genital anomalies, mental retardation, obesity, contractures of fingers, and osteoporosis, though further complications are known.

This is a rare condition with an incidence estimated to be less than 1 in a million live births. About 100 cases have been reported worldwide. The bulk of cases are sporadic but familial forms with autosomal dominant transmission have also been described.

This disorder was first reported in 1981.

It has many similarities to LAPS Syndrome and they both arise from the same mutations in the SMAD4 gene. It is believed that they are the same syndrome.

Weissenbacher-Zweymüller syndrome affects males and females in the same numbers. About 30 cases have been reported in medical literature. This disorder can be underdiagnosed causing no true frequency in the population. Only 30 cases have been reported in medical literature.

Overall, the prognosis for patients with NOMID is not good, though many (80%) live into adulthood, and a few appear to do relatively well. They are at risk for leukemia, infections, and some develop deposits of protein aggregated called amyloid, which can lead to kidney failure and other problems. The neurologic problems are most troubling. The finding that other diseases are related and a better understanding of where the disease comes from may lead to more effective treatments.

Winchester syndrome is a rare congenital connective tissue disease described in 1969, of which the main characteristics are short stature, marked contractures of joints, opacities in the cornea, coarse facial features, dissolution of the carpal and tarsal bones (in the hands and feet, respectively), and osteoporosis. Winchester syndrome was once considered to be related to a similar condition, multicentric osteolysis, nodulosis, and arthropathy (MONA). However, it was discovered that the two are caused by mutations found in different genes; they are now thought of as two separate disorders. Appearances resemble rheumatoid arthritis. Increased uronic acid is demonstrated in cultured fibroblasts from the skin and to a lesser degree in both parents. Despite initial tests not showing increased mucopolysaccharide excretion, the disease was regarded as a mucopolysaccharidosis. Winchester syndrome is thought to be inherited as an autosomal recessive trait.

Parastremmatic dwarfism is a rare bone disease that features severe dwarfism, thoracic kyphosis (a type of scoliosis that affects the upper back), a distortion and twisting of the limbs, contractures of the large joints, malformations of the vertebrae and pelvis, and incontinence. The disease was first reported in 1970 by Leonard Langer and associates; they used the term "parastremmatic" from the Greek "parastremma", or "distorted limbs", to describe it. On X-rays, the disease is distinguished by a "flocky" or lace-like appearance to the bones. The disease is congenital, which means it is apparent at birth. It is caused by a mutation in the "TRPV4" gene, located on chromosome 12 in humans. The disease is inherited in an autosomal dominant manner.

The genetics of Bruck syndrome differs from osteogenesis imperfecta. Osteogenesis imperfecta involves autosomal dominant mutations to Col 1A2 or Col 1A2 which encode type 1 procollagen. Bruck syndrome is linked to mutations in two genes, and therefore is divided in two types. Bruck syndrome type 1 is caused by a homozygous mutation in the FKBP10 gene. It encodes FKBP65, an endoplasmic reticulum associated peptidyl-prolyl cis/trans isomerase (PPIase) that functions as a chaperone in collagen biosynthesis. Osteoblasts deficient in FKBP65 have a buildup of procollagen aggregates in the endoplasmic reticulum which reduces their ability to form bone. Furthermore, Bruck syndrome type 1 patients have under-hydroxylated lysine residues in the collagen telopeptide and as a result show diminished hydroxylysylpyridinoline cross-links. Type 2 is caused by a homozygous mutation in the PLOD2 gene. It encodes the enzyme, lysyl hydroxylase 2, which catalyzes hydroxylation of lysine residues in collagen cross-links. PLOD2 is most expressed in active osteoblasts since collagen cross-linking is tissue-specific. Mutation in PLOD2 alters the structure of telopeptide lysyl hydroxylase and prevents fibril formation of collagen type 1. Bone analysis shows the lysine residues of telopeptides in collagen type 1 are under-hydroxylated.

Parastremmatic dwarfism is apparent at birth, with affected infants usually being described as "stiff", or as "twisted dwarfs" when the skeletal deformities and appearance of dwarfism further present themselves. Skeletal deformities usually develop in the sixth to twelfth month of an infant's life. The deformities may be attributed to osteomalacia, a lack of bone mineralization.

Many diseases and disorders have been associated with osteoporosis. For some, the underlying mechanism influencing the bone metabolism is straightforward, whereas for others the causes are multiple or unknown.

- In general, immobilization causes bone loss (following the 'use it or lose it' rule). For example, localized osteoporosis can occur after prolonged immobilization of a fractured limb in a cast. This is also more common in active people with a high bone turn-over (for example, athletes). Other examples include bone loss during space flight or in people who are bedridden or use wheelchairs for various reasons.

- Hypogonadal states can cause secondary osteoporosis. These include Turner syndrome, Klinefelter syndrome, Kallmann syndrome, anorexia nervosa, andropause, hypothalamic amenorrhea or hyperprolactinemia. In females, the effect of hypogonadism is mediated by estrogen deficiency. It can appear as early menopause (1 year). Bilateral oophorectomy (surgical removal of the ovaries) and premature ovarian failure cause deficient estrogen production. In males, testosterone deficiency is the cause (for example, andropause or after surgical removal of the testes).

- Endocrine disorders that can induce bone loss include Cushing's syndrome, hyperparathyroidism, hyperthyroidism, hypothyroidism, diabetes mellitus type 1 and 2, acromegaly, and adrenal insufficiency.

- Malnutrition, parenteral nutrition and malabsorption can lead to osteoporosis. Nutritional and gastrointestinal disorders that can predispose to osteoporosis include undiagnosed and untreated coeliac disease (both symptomatic and asymptomatic people), Crohn's disease, ulcerative colitis, cystic fibrosis, surgery (after gastrectomy, intestinal bypass surgery or bowel resection) and severe liver disease (especially primary biliary cirrhosis). People with lactose intolerance or milk allergy may develop osteoporosis due to restrictions of calcium-containing foods. Individuals with bulimia can also develop osteoporosis. Those with an otherwise adequate calcium intake can develop osteoporosis due to the inability to absorb calcium and/or vitamin D. Other micronutrients such as vitamin K or vitamin B deficiency may also contribute.

- People with rheumatologic disorders such as rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus and polyarticular juvenile idiopathic arthritis are at increased risk of osteoporosis, either as part of their disease or because of other risk factors (notably corticosteroid therapy). Systemic diseases such as amyloidosis and sarcoidosis can also lead to osteoporosis.

- Renal insufficiency can lead to renal osteodystrophy.

- Hematologic disorders linked to osteoporosis are multiple myeloma and other monoclonal gammopathies, lymphoma, leukemia, mastocytosis, hemophilia, sickle-cell disease and thalassemia.

- Several inherited disorders have been linked to osteoporosis. These include osteogenesis imperfecta, Marfan syndrome, hemochromatosis, hypophosphatasia (for which it is often misdiagnosed), glycogen storage diseases, homocystinuria, Ehlers–Danlos syndrome, porphyria, Menkes' syndrome, epidermolysis bullosa and Gaucher's disease.

- People with scoliosis of unknown cause also have a higher risk of osteoporosis. Bone loss can be a feature of complex regional pain syndrome. It is also more frequent in people with Parkinson's disease and chronic obstructive pulmonary disease.

- People with Parkinson's disease have a higher risk of broken bones. This is related to poor balance and poor bone density. In Parkinson’s disease there may be a link between the loss of dopaminergic neurons and altered calcium metabolism (and iron metabolism) causing a stiffening of the skeleton and kyphosis.

The key for managing Sack–Barabas syndrome is for the patient to be aware of their disease. Close follow up and planning of interventions can significantly prolong and maintain the quality of life of a patient with this disease.

Pregnant affected women must take special care due to the increased risk of premature death due to rupture of arteries, bowel or uterine rupture with a reported mortality rate of 50%.

Genetic counselling is recommended for prospective parents with a family history of Ehlers–Danlos syndrome. Affected parents should be aware of the type of Ehlers-Danlos syndrome they have and its mode of inheritance.

Genitopatellar Syndrome is an autosomal dominant inheritance where the mutation in the KAT6B causes the syndrome. The KAT6B gene is responsible for making an enzyme called histone acetyltransferase which functions in regulating and making of histone which are proteins that attach to DNA and give the chromosomes their shape. The function of histone acetyltransferase produced from KAT6B is unknown but it is considered as a regulator of early developments. There is little known about how the mutation in the KAT6B causes the syndrome but researchers suspects that the mutations occur near the end of the KAT6B gene and causes it to produce shortened acetyltransferase enzyme. The shortened enzyme alters the regulation of other genes. On the other hand, the mutation of KAT6B leading to the specific features of genitopatellar syndrome is still not surely proven.