Dipygus is caused by genetic, environmental, or teratogenic factors. It occurs early in intrauterine life.

The cause of fibular hemimelia is unclear. Purportedly, there have been some incidents of genetic distribution in a family; however, this does not account for all cases. Maternal viral infections, embryonic trauma, teratogenic environmental exposures or vascular dysgenesis (failure of the embryo to form a satisfactory blood supply) between four and seven weeks gestation are considered possible causes.

In an experimental mouse model, change in the expression of a homeobox gene led to similar, but bilateral, fibular defects.

Beals syndrome (congenital contractural arachnodactyly, Beals–Hecht syndrome) is a rare congenital connective tissue disorder. Beals syndrome has only recently been described as a syndrome distinct from Marfan's syndrome. Ricky Berwick is an internet star with this disease.

It was characterized in 1972.

It is associated with FBN2.

It is caused by a mutation in FBN2 gene on chromosome 5q23. Contractures of varying degrees at birth, mainly involving the large joints, are present in all affected children. Elbows, knees and fingers are most commonly involved. The contractures may be mild and tend to reduce in severity, but residual camptodactyly always remains present. The arm span exceeds body height but the discrepancy may be underestimated due to contractures of elbows and fingers. The same holds for the lower body portion with knee contractures. The most serious complication in CCA is scoliosis and sometimes kyphoscoliosis mandating surgery.

Fibular hemimelia or longitudinal fibular deficiency is "the congenital absence of the fibula and it is the most common congenital absence of long bone of the extremities." It is the shortening of the fibula at birth, or the complete lack thereof. In humans, the disorder can be noted by ultrasound in utero to prepare for amputation after birth or complex bone lengthening surgery. The amputation usually takes place at six months with removal of portions of the legs to prepare them for prosthetic use. The other treatments which include repeated corrective osteotomies and leg-lengthening surgery (Ilizarov apparatus) are costly and associated with residual deformity.

Sufferers usually have long, thin fingers and toes with contractures preventing straightening and limiting movement. Contractures also affect hips, elbows, knees and ankles. They also have unusual external ears that appear crumpled. Contractures may be present from birth and may appear as a club foot. Long bone fractures may also form a part of the syndrome, though the evidence for this is limited to the case report level.

Wearing shoes to protect barefoot trauma has shown decrease in incidence in ainhum. Congenital pseudoainhum cannot be prevented and can lead to serious birth defects.

The condition arises from some factor or set of factors present during approximately the 3rd week to 7th week of fetal development. Formation of the sacrum/lower back and corresponding nervous system is usually nearing completion by the 4th week of development. Due to abnormal gastrulation, the mesoderm migration is disturbed. This disturbance results in symptoms varying from minor lesions of the lower vertebrae to more severe symptoms such as complete fusion of the lower limbs. While the exact cause is unknown, it has been speculated that the condition may be associated with certain dietary deficiencies including a lack or insufficient amounts of folic acid.

Sacral agenesis syndrome (agenesis of the lumbar spine, sacrum, and coccyx, and hypoplasia of the lower extremities) is a well-established congenital anomaly associated with maternal diabetes mellitus (not gestational diabetes). However, other causes are presumably involved, as demonstrated by the rare incidence of caudal regression syndrome (1:60,000) compared to diabetes.

The dominant inherited sacral agenesis (also referred to as Currarino syndrome) is very often correlated with a mutation in the Hb9 (also called HlxB9) gene (shown by Sally Ann Lynch, 1995, Nature Genetics).

It may be the cause of sirenomelia ("Mermaid syndrome").

Caudal regression syndrome or sacral agenesis (or hypoplasia of the sacrum) is a congenital disorder in which there is abnormal fetal development of the lower spine—the caudal partition of the spine.

It occurs at a rate of approximately one per 25,000 live births.

Dipygus manifests as duplicated lower limbs and could include additional organs or bodily structures.

Blount's disease occurs in young children and adolescents. The cause is unknown but is thought to be due to the effects of weight on the growth plate. The inner part of the tibia, just below the knee, fails to develop normally, causing angulation of the bone.

Unlike bowlegs, which tend to straighten as the child develops, Blount's disease is progressive and the condition worsens. It can cause severe bowing of the legs and can affect one or both legs.

This condition is more common among children of African ancestry. It is also associated with obesity, short stature, and early walking. There does not appear to be an obvious genetic factor.

The causes for PWS are either genetic or unknown. Some cases are a direct result of the RASA1 gene mutations. And individuals with RASA1 can be identified because this genetic mutation always causes multiple capillary malformations. PWS displays an autosomal dominant pattern of inheritance. This means that one copy of the damaged or altered gene is sufficient to elicit PWS disorder. In most cases, PWS can occur in people that have no family history of the condition. In such cases the mutation is sporadic. And for patients with PWS with the absence of multiple capillary mutations, the causes are unknown.

According to Boston’s Children Hospital, no known food, medications or drugs can cause PWS during pregnancy. PWS is not transmitted from person to person. But it can run in families and can be inherited. PWS effects both males and females equally and as of now no racial predominance is found

At the moment, there are no known measures that can be taken in order to prevent the onset of the disorder. But Genetic Testing Registry can be great resource for patients with PWS as it provides information of possible genetic tests that could be done to see if the patient has the necessary mutations. If PWS is sporadic or does not have RASA1 mutation then genetic testing will not work and there is not a way to prevent the onset of PWS.

Ainhum is an acquired and progressive condition, and thus differs from congenital annular constrictions. Ainhum has been much confused with similar constrictions caused by other diseases such as leprosy, diabetic gangrene, syringomyelia, scleroderma or Vohwinkel syndrome. In this case, it is called pseudo-ainhum, treatable with minor surgery or intralesional corticosteroids, as with ainhum. It has even been seen in psoriasis or it is acquired by the wrapping toes, penis or nipple with hairs, threads or fibers. Oral retinoids, such as tretinoin, and antifibrotic agents like tranilast have been tested for pseudo-ainhum. Impending amputation in Vohwinkel syndrome can sometimes be aborted by therapy with oral etretinate. It is rarely seen in the United States but often discussed in the international medical literature.

Diplopodia is a congenital anomaly in tetrapods that involves duplication of elements of the foot on the hind limb. It comes from the Greek roots diplo = "double" and pod = "foot". Diplopodia is often found in conjunction with other structural abnormalities and can be lethal. It is more extreme than polydactyly, the presence of extra digits.

Pathology is insertional tendinopathy of the medius and tendons and enlargement of the associated bursa.

Gluteals remain inactive in a seated position. Movements that require muscles become more difficult; stress is put on the spine.

The cause of PFFD is uncertain. Two hypotheses have been advanced. The theory of sclerotome subtraction posits injury to neural crest cells that are the precursors to sensory nerves at the level of L4 and L5. Histologic studies of a fetus with unilateral PFFD have prompted an alternative hypothesis that PFFD is caused by a defect in maturation of chondrocytes (cartilage cells) at the growth plate. In either hypothesis, the agent causing the injury is usually not known. Thalidomide is known to cause PFFD when the mother is exposed to it in the fifth or sixth week of pregnancy, and it is speculated that exposure to other toxins during pregnancy may also be a cause. Other etiologies that have been suggested, but not proven, include anoxia, ischemia, radiation, infection, hormones, and mechanical force. PFFD occurs sporadically, and does not appear to be hereditary.

There are few good estimates of prevalence for pes cavus in the general community. While pes cavus has been reported in between 2 and 29% of the adult population, there are several limitations of the prevalence data reported in these studies. Population-based studies suggest the prevalence of the cavus foot is approximately 10%.

Weismann-Netter-Stuhl syndrome, also known as Weismann-Netter Syndrome or more technically by the term tibioperoneal diaphyseal toxopachyosteosis, is a rare disorder characterized by bowing of the lower legs and an abnormal thickening of thinner bone in the leg.

The main sign is anterior bowing and posterior cortical thickening of the diaphyses of both the tibiae and fibulae. It is thought to be inherited in an autosomal dominant fashion, and is most often bilateral and symmetric in nature. Associated features include dwarfism and mild intellectual disability, as well as a process known as tibialization of the fibulae, which involves thickening and enlargement of these bones to an extent resembling the tibiae. The combination of the presence of tibialization of the fibulae, which is highly specific for the disorder, and the absence of laboratory abnormalities ruling out alternative diagnoses including rickets, essentially confirms the diagnosis.

In most cases persisting after childhood, there is little or no effect on the ability to walk. Due to uneven stress and wear on the knees, however, even milder manifestations can see an accelerated onset of arthritis.

There are many hypotheses about how clubfoot develops. Some hypothesis include: environmental factors, genetics, or a combination of both. Research has not yet pinpointed the root cause, but many findings agree that "it is likely there is more than one different cause and at least in some cases the phenotype may occur as a result of a threshold effect of different factors acting together."

Some researchers hypothesize, from the early development stages of humans, that clubfoot is formed by a malfunction during gestation. Early amniocentesis (11–13 wks) is believed to increase the rate of clubfoot because there is an increase in potential amniotic leakage from the procedure. Underdevelopment of the bones and muscles of the embryonic foot may be another underlying cause. In the early 1900s it was thought that constriction of the foot by the uterus contributed to the occurrence of clubfoot.

Underdevelopment of the bones also affects the muscles and tissues of the foot. Abnormality in the connective tissue causes "the presence of increased fibrous tissue in muscles, fascia, ligaments and tendon sheaths".

Training of the feet, utilizing foot gymnastics and going barefoot on varying terrain, can facilitate the formation of arches during childhood, with a developed arch occurring for most by the age of four to six years. Ligament laxity is also among the factors known to be associated with flat feet. One medical study in India with a large sample size of children who had grown up wearing shoes and others going barefoot found that the longitudinal arches of the bare-footers were generally strongest and highest as a group, and that flat feet were less common in children who had grown up wearing sandals or slippers than among those who had worn closed-toe shoes. Focusing on the influence of footwear on the prevalence of pes planus, the cross-sectional study performed on children noted that wearing shoes throughout early childhood can be detrimental to the development of a normal or a high medial longitudinal arch. The vulnerability for flat foot among shoe-wearing children increases if the child has an associated ligament laxity condition. The results of the study suggest that children be encouraged to play barefooted on various surfaces of terrain and that slippers and sandals are less harmful compared to closed-toe shoes. It appeared that closed-toe shoes greatly inhibited the development of the arch of the foot more so than slippers or sandals. This conclusion may be a result of the notion that intrinsic muscle activity of the arch is required to prevent slippers and sandals from falling off the child’s foot.

Flat feet can also develop as an adult ("adult acquired flatfoot") due to injury, illness, unusual or prolonged stress to the foot, faulty biomechanics, or as part of the normal aging process. This is most common in women over 40 years of age. Known risk factors include obesity, hypertension and diabetes. Flat feet can also occur in pregnant women as a result of temporary changes, due to increased elastin (elasticity) during pregnancy. However, if developed by adulthood, flat feet generally remain flat permanently.

If a youth or adult appears flatfooted while standing in a full weight bearing position, but an arch appears when the person plantarflexes, or pulls the toes back with the rest of the foot flat on the floor, this condition is called flexible flatfoot. This is not a true collapsed arch, as the medial longitudinal arch is still present and the windlass mechanism still operates; this presentation is actually due to excessive pronation of the foot (rolling inwards), although the term 'flat foot' is still applicable as it is a somewhat generic term. Muscular training of the feet is helpful and will often result in increased arch height regardless of age.

Clubfoot is a birth defect where one or both feet are rotated inwards and downwards. The affected foot, calf, and leg may be smaller than the other. In about half of those affected, both feet are involved. Most cases are not associated with other problems. Without treatment, people walk on the sides of their feet which causes issues with walking.

The exact cause is usually unclear. A few cases are associated with distal arthrogryposis or myelomeningocele. If one identical twin is affected there is a 33% chance the other one will be as well. Diagnosis may occur at birth or before birth during an ultrasound exam.

Initial treatment is most often with the Ponseti method. This involves moving the foot into an improved position followed by casting, which is repeated at weekly intervals. Once the inward bending is improved, the Achilles tendon is often cut and braces are worn until the age of four. Initially the brace is worn nearly continuously and then just at night. In about 20% of cases further surgery is required.

Clubfoot occurs in about one in 1,000 newborns. The condition is less common among the Chinese and more common among Maori. Males are affected about twice as often as females. Treatment can be carried out by a range of healthcare providers and can generally be achieved in the developing world with few resources.

Spondyloepiphyseal dysplasia congenita (abbreviated to SED more often than SDC) is a rare disorder of bone growth that results in dwarfism, characteristic skeletal abnormalities, and occasionally problems with vision and hearing. The name of the condition indicates that it affects the bones of the spine (spondylo-) and the ends of bones (epiphyses), and that it is present from birth (congenital). The signs and symptoms of spondyloepiphyseal dysplasia congenita are similar to, but milder than, the related skeletal disorders achondrogenesis type 2 and hypochondrogenesis. Spondyloepiphyseal dysplasia congenita is a subtype of collagenopathy, types II and XI.

Prosthetic replacement of missing teeth is possible using dental implant technology or dentures. This treatment can be successful in giving patients with anodontia a more aesthetically pleasing appearance. The use of an implant prosthesis in the lower jaw could be recommended for younger patients as it is shown to significantly improve the craniofacial growth, social development and self-image. The study associated with this evidence worked with individuals who had ectodermal dysplasia of varying age groups of up to 11, 11 to 18 and more than 18 years. It was noted that the risk of implant failure was significantly higher in patients younger than 18 years, but there is significant reason to use this methodology of treatment in those older. Overall the use of an implant-prosthesis has a considerable functional, aesthetic and psychological advantage when compared to a conventional denture, in the patients.

There are typically four classes (or "types") of PFFD, ranging from class A to class D, as detailed by Aitken.