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.

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.

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%.

The most common cause of foot pain is wearing ill fitting shoes. Women often wear tight shoes that are narrow and constrictive, and thus are most prone to foot problems. Tight shoes often cause overcrowding of toes and result in a variety of structural defects. The next most common cause of foot disease is overuse or traumatic injuries.

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

Steps to prevent diabetic foot ulcers include frequent review by a foot specialist, good foot hygiene, diabetic socks and shoes, as well as avoiding injury.

- Foot-care education combined with increased surveillance can reduce the incidence of serious foot lesions.

Trench foot can be prevented by keeping the feet clean, warm, and dry. It was also discovered in World War I that a key preventive measure was regular foot inspections; soldiers would be paired and each made responsible for the feet of the other, and they would generally apply whale oil to prevent trench foot. If left to their own devices, soldiers might neglect to take off their own boots and socks to dry their feet each day, but if it were the responsibility of another, this became less likely. Later on in the war, instances of trench foot began to decrease, probably as a result of the introduction of the aforementioned measures; of wooden duckboards to cover the muddy, wet, cold ground of the trenches; and of the increased practice of troop rotation, which kept soldiers from prolonged time at the front.

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.

Unlike frostbite, trench foot does not require freezing temperatures; it can occur in temperatures up to 16° Celsius (about 60° Fahrenheit) and within as little as 13 hours. Exposure to these environmental conditions causes deterioration and destruction of the capillaries and leads to morbidity of the surrounding flesh. Excessive sweating (hyperhidrosis) has long been regarded as a contributory cause; unsanitary, cold, and wet conditions can also cause trench foot.

Approximately 15 percent of people with diabetes experience foot ulcers. And approximately 84 percent of lower limb amputations have a history of ulceration with only approximately half of amputees surviving for more than 2 years. 56 percent of individuals with foot ulcers who do not have an amputations survive for 5 years. Foot ulcers and amputations significantly reduce the quality of life. Approximately 8.8 percent of hospital admissions of diabetic patients are for foot related problems, and such hospital admissions are about 13 days longer than for diabetics without foot related admissions. Approximately 35 to 40 percent of ulcers recur within 3 years and up to 70 percent recur within 5 years. Diabetic foot disease is the leading cause of non-traumatic lower limb amputations.

Immersion foot syndromes are a class of foot injury caused by water absorption in the outer layer of skin. There are different subclass names for this condition based on the temperature of the water to which the foot is exposed. These include trench foot, tropical immersion foot, and warm water immersion foot. In one 3-day military study, it was found that submersion in water allowing for a higher skin temperature resulted in worse skin maceration and pain.

"Warm water immersion foot" is a skin condition of the feet that results after exposure to warm, wet conditions for 48 hours or more and is characterized by maceration ("pruning"), blanching, and wrinkling of the soles, padding of toes (especially the big toe) and padding of the sides of the feet.

Foot maceration occur whenever exposed for prolong periods to moist conditions. Large watery blisters appear which are painful when they open and begin to peel away from the foot itself. The heels, sides and bony prominences are left with large areas of extremely sensitive, red tissue, exposed and prone to infection. As the condition worsens, more blisters develop due to prolonged dampness which eventually covers the entire heel and/or other large, padded sections of the foot, especially the undersides as well as toes. Each layer in turn peels away resulting in deep, extremely tender, red ulcerations.

Healing occurs only when the feet are cleansed, dried and exposed to air for weeks. Scarring is permanent with dry, thin skin that appears red for up to a year or more. The padding of the feet returns but healing can be painful as the nerves repair with characteristics of diabetic neuropathy. Antibiotics and/or antifungal are sometimes prescribed.

Foot immersion is a common problem with homeless individuals wearing one pair of socks and shoes for extensive periods of time, especially wet shoes and sneakers from rain and snow. The condition is exacerbated by excessive dampness of the feet for prolonged periods of time. Fungus and bacterial infections prosper in the warm, dark, wet conditions and are characterized by a sickly odor that is distinct to foot immersion.

Besides being exposed to any of the modes of transmission presented above, there are additional risk factors that increase one's chance of contracting athlete's foot. Persons who have had athlete's foot before are more likely to become infected than those who have not. Adults are more likely to catch athlete's foot than children. Men have a higher chance of getting athlete's foot than women. People with diabetes or weakened immune systems are more susceptible to the disease. HIV/AIDS hampers the immune system and increases the risk of acquiring athlete's foot. Hyperhidrosis (abnormally increased sweating) increases the risk of infection and makes treatment more difficult.

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".

Ship Foot or Bruised Toenail is a condition where the toenail becomes bruised, usually as a result of a heavy impact such as from football, being stepped on, or dropping something on the toe.

Yoga foot drop is a kind of drop foot, a gait abnormality. It is caused by a prolonged sitting on heels, a common yoga position of vajrasana. The name was suggested by Joseph Chusid, MD, in 1971, who reported a case of foot drop in a student who complained about increasing difficulty to walk, run, or climb stairs. The cause was thought to be injury to the common peroneal nerve, which is compressed and thereby deprived of blood flow while kneeling.

Yoga foot drop is a potential adverse effect of yoga, allegedly unmentioned by yoga teachers and books.

The term is believed to have originated on warships during the Age of sail, where it was common for sailors to sustain such an injury from the impact of a recoiling cannon. The condition in those days would have often been accompanied by other foot injuries, such as a fractured toe.

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.

According to the National Health Service, "Athlete’s foot is very contagious and can be spread through direct and indirect contact." The disease may spread to others directly when they touch the infection. People can contract the disease indirectly by coming into contact with contaminated items (clothes, towels, etc.) or surfaces (such as bathroom, shower, or locker room floors). The fungi that cause athlete's foot can easily spread to one's environment. Fungi rub off of fingers and bare feet, but also travel on the dead skin cells that continually fall off the body. Athlete's foot fungi and infested skin particles and flakes may spread to socks, shoes, clothes, to other people, pets (via petting), bed sheets, bathtubs, showers, sinks, counters, towels, rugs, floors, and carpets.

When the fungus has spread to pets, it can subsequently spread to the hands and fingers of people who pet them. If a pet frequently gnaws upon itself, it might not be fleas it is reacting to, it may be the insatiable itch of tinea.

One way to contract athlete's foot is to get a fungal infection somewhere else on the body first. The fungi causing athlete's foot may spread from other areas of the body to the feet, usually by touching or scratching the affected area, thereby getting the fungus on the fingers, and then touching or scratching the feet. While the fungus remains the same, the name of the condition changes based on where on the body the infection is located. For example, the infection is known as tinea corporis ("ringworm") when the torso or limbs are affected or tinea cruris (jock itch or dhobi itch) when the groin is affected. Clothes (or shoes), body heat, and sweat can keep the skin warm and moist, just the environment the fungus needs to thrive.

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.

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

Tailor's bunion, or bunionette, is a condition caused as a result of inflammation of the fifth metatarsal bone at the base of the little toe.

It is mostly similar to a bunion (the same type of ailment affecting the big toe). It is called Tailor's Bunion because in past centuries, tailors sat cross-legged, and this was thought to cause this protrusion on the outside aspect of the foot.

It is usually characterized by inflammation, pain and redness of the little toe.

Often a tailor's bunion is caused by a faulty mechanical structure of the foot. The fifth metatarsal bone starts to protrude outward, while the little toe moves inward. This change in alignment creates an enlargement on the outside of the foot.

Tailor's bunion is easily diagnosed because the protrusion is visually apparent. X-rays may be ordered to help the surgeon find out the severity of the deformity.