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.

Oligodactyly (from the Ancient Greek "oligos" meaning "few" and δάκτυλος "daktylos" meaning "finger") is the presence of fewer than five fingers or toes on a hand or foot.

It is quite often incorrectly called "hypodactyly", but the Greek prefixes and are used for scales (e.g. in hypoglycaemia and hypercholesterolemia). This as opposed to or scales, where and should be used (e.g. in oligarchy and polygamy). Oligodactyly is therefore the opposite of polydactyly. Very rare, this medical condition usually has a genetic or familial cause.

Oligodactyly is sometimes a sign or symptom of several syndromes including Poland syndrome and Weyer Ulnar Ray Syndrome. It is a type of Dysmelia.

Ectrodactyly is an extreme instance of oligodactyly, involving the absence of one or more central digits of the hand or foot and is also known as split hand/split foot malformation (SHFM). The hands and feet of people with ectrodactyly are often described as "claw-like" and may include only the thumb and one finger (usually either the little finger, ring finger, or a syndactyly of the two) with similar abnormalities of the feet.

People with oligodactyly often have full use of the remaining digits and adapt well to their condition. They are not greatly hindered in their daily activities, if at all. Even those with the most extreme forms are known to engage in tasks that require fine control, such as writing and bootmaking as well as working as a cab driver.

Vadoma people of Zimbabwe have a high frequency of oligodactyly.

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.

Rocker bottom foot, also known as congenital vertical talus, is an anomaly of the foot. It is characterized by a prominent calcaneus (heel bone) and a convex rounded bottom of the foot. It gets its name from the foot's resemblance to the bottom of a rocking chair.

It can be associated with Edwards' syndrome (trisomy 18), Patau syndrome (trisomy 13), Trisomy 9 and mutation in the gene HOXD10.

It can also be associated with Charcots foot.

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.

A foot deformity is a disorder of the foot that can be congenital or acquired.

Such deformities can include hammer toe, club foot, flat feet, pes cavus, etc.

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".

Type II should be managed conservatively whereas type I and Ia requires to be treated surgically. Surgery involves four major steps:

- Development of the calcaneal part of the foot

- Repositioning of the navicular bone

- New adjustment of the ankle, and

- Various stabilization measures including the Grice operation and transposition of various tendons.

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%.

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.

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.

Morton's Toe is a minority variant of foot shape. Its recorded prevalence varies in different populations, with estimates from 2.95% to 22%.

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.

Pes cavus may be hereditary or acquired, and the underlying cause may be neurological, orthopedic, or neuromuscular. Pes cavus is sometimes—but not always—connected through Hereditary Motor and Sensory Neuropathy Type 1 (Charcot-Marie-Tooth disease) and Friedreich's Ataxia; many other cases of pes cavus are natural.

The cause and deforming mechanism underlying pes cavus is complex and not well understood. Factors considered influential in the development of pes cavus include muscle weakness and imbalance in neuromuscular disease, residual effects of congenital clubfoot, post-traumatic bone malformation, contracture of the plantar fascia, and shortening of the Achilles tendon.

Among the cases of neuromuscular pes cavus, 50% have been attributed to Charcot-Marie-Tooth disease, which is the most common type of inherited neuropathy with an incidence of 1 per 2,500 persons affected. Also known as Hereditary Motor and Sensory Neuropathy (HMSN), it is genetically heterogeneous and usually presents in the first decade of life with delayed motor milestones, distal muscle weakness, clumsiness, and frequent falls. By adulthood, Charcot-Marie-Tooth disease can cause painful foot deformities such as pes cavus. Although it is a relatively common disorder affecting the foot and ankle, little is known about the distribution of muscle weakness, severity of orthopaedic deformities, or types of foot pain experienced. There are no cures or effective courses of treatment to halt the progression of any form of Charcot-Marie-Tooth disease.

The development of the cavus foot structure seen in Charcot-Marie-Tooth disease has been previously linked to an imbalance of muscle strength around the foot and ankle. A hypothetical model proposed by various authors describes a relationship whereby weak evertor muscles are overpowered by stronger invertor muscles, causing an adducted forefoot and inverted rearfoot. Similarly, weak dorsiflexors are overpowered by stronger plantarflexors, causing a plantarflexed first metatarsal and anterior pes cavus.

Pes cavus is also evident in people without neuropathy or other neurological deficit. In the absence of neurological, congenital, or traumatic causes of pes cavus, the remaining cases are classified as being ‘idiopathic’ because their aetiology is unknown.

An equinovalgus is a deformity of the human foot. It may be a flexible deformity or a fixed deformity. Equino- means plantarflexed (as in standing on one's toes), and valgus means that the base of the heel is rotated away from the midline of the foot (eversion) and abduction of foot. This means that the patient is placing his/her weight on the medial border of the foot, and the arch of the foot is absent, which distorts the foot's normal shape.

Equinovalgus mostly occurs due to tightness of plantar flexors (calf muscles) and peroneus group of muscles.

Pigeon toe (also known as metatarsus varus, metatarsus adductus, in-toe gait, intoeing or false clubfoot) is a condition which causes the toes to point inward when walking. It is most common in infants and children under two years of age and, when not the result of simple muscle weakness, normally arises from underlying conditions, such as a twisted shin bone or an excessive anteversion (femoral head is more than 15° from the angle of torsion) resulting in the twisting of the thigh bone when the front part of a person's foot is turned in.

Severe cases are considered a form of clubfoot.

Tarsal coalition is almost exclusively a product of an error during the dividing of embryonic cells in utero. Other causes of synostosis (bone fusion) could include a surgical 'screwing together' of two bones, a very advanced case of arthritis leading to self-fusion of a joint by an internal process within the body or some other very traumatic event. The birth defect responsible for tarsal coalition is thought to often be an autosomal dominant genetic condition. This means that if you have a parent with the disorder it is highly likely to be passed on to offspring.

The affected leg usually has one foot that is in an approximately normal position. The extra foot is composed of at least some metatarsal or tarsal bones and extra digits, though it is usually not complete. The feet can be joined together, so that the limb appears to have one large foot, or the extra foot can be joined to the limb separately, usually above the level of the other foot. Diplopodia affects one or both of the hind limbs.

The accessory nail of the fifth toe is a physical trait of the small toe, where a minuscule "sixth toenail" is present in the outer corner of the nail situated on the smallest toe. It is commonly perceived to be especially prevalent amongst Han Chinese;.

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

Atherosclerotic restriction to the arterial supply in peripheral artery occlusive disease may result in painful arterial ulcers of the ankle and foot, or give rise of gangrene of the toes and foot. Immobility of a person may result in prolonged pressure applied to the heels causing pressure sores.

Impaired venous drainage from the foot in varicose veins may sequentially result in brown haemosiderin discolouration to the ankle and foot, varicose stasis dermatitis and finally venous ulcers.

Other disorders of the foot include osteoarthritis of the joints, peripheral neuropathy and plantar warts.

The most common form of being pigeon toed, when the feet bend inward from the middle part of the foot to the toes.

Asymptomatic anatomical variations in feet generally do not need treatment.

Conservative treatment for foot pain with Morton's toe may involve exercises or placing a flexible pad under the first toe and metatarsal; an early version of the latter treatment was once patented by Dudley Joy Morton. Restoring the Morton’s toe to normal function with proprioceptive orthotics can help alleviate numerous problems of the feet such as metatarsalgia, hammer toes, bunions, Morton's neuroma, plantar fasciitis, and general fatigue of the feet. Rare cases of disabling pain are sometimes treated surgically.

This condition results from denervation of areas exposed to day-to-day friction of bony prominences. The denervation may be result of any of the following diseases:

- Spinal injuries

- Leprosy

- Peripheral nerve injury

- Diabetic neuropathy

- Tabes dorsalis

- Transverse myelitis

- Meningomyelocele