Vasodilators improve the blood flow into the vessels of the hoof. Examples include isoxsuprine (currently unavailable in the UK) and pentoxifylline.

Anticoagulants can also improve blood flow. The use of warfarin has been proposed, but the extensive monitoring required makes it unsuitable in most cases.

Anti-inflammatory drugs are used to treat the pain, and can help the lameness resolve sometimes if shoeing and training changes are made. Include Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and other joint medications. The use of intramuscular glycosaminoglycans has been shown to decrease pain in horses with navicular disease, but this effect wanes after discontinuation of therapy. Oral glycosaminoglycans may have a similar effect.

Bisphosphonates can be useful in cases where bone remodeling is causing pain.

Gallium nitrate (GaN) has been hypothesized as a possible treatment for navicular disease, but its benefits have not been confirmed by formal clinical studies. One pilot study examined horses given gallium nitrate in their feed rations. While it was absorbed slowly, it did stay in the animals' system, providing a baseline dosage for future studies.

No single treatment works for all cases, probably because there is no single cause for all cases. The degenerative changes are usually quite advanced by the time the horse is consistently lame, and these changes are believed to be non-reversible. At this time, it is best to manage the condition and focus on alleviating pain and slowing the degeneration.

Aside from surgery, there are a few options for handling an accessory navicular bone that has become symptomatic. This includes immobilization, icing, medicating, physical therapy, and orthotic devices. Immobilizing involves placing the foot and ankle in a cast or removable walking boot. This alleviates stressors on the foot and can decrease inflammation. Icing will help reduce swelling and inflammation. Medication involves usage of nonsteroidal anti-inflammatory drugs, or steroids (taken orally or injected) to decrease inflammation. Physical therapy can be prescribed in order to strengthen the muscles and help decrease inflammation. Physical therapy can also help prevent the symptoms from returning. Orthotic devices (arch support devices that fit in a shoe) can help prevent future symptoms. Occasionally, the orthotic device will dig into the edge of the accessory navicular and cause discomfort. For this reason, the orthotic devices made for the patient should be carefully constructed.

With prompt treatment, particularly open reduction, and early mobilisation the outcome is generally good. High energy injuries and associated fractures worsen the outcome.

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.

Treatment usually involves resting the affected foot, taking pain relievers and trying to avoid putting pressure on the foot. In acute cases, the patient is often fitted with a cast that stops below the knee. The cast is usually worn for 6 to 8 weeks. After the cast is taken off, some patients are prescribed arch support for about 6 months. Also, moderate exercise is often beneficial, and physical therapy may help as well.

Prognosis for children with this disease is very good. It may persist for some time, but most cases are resolved within two years of the initial diagnosis. Although in most cases no permanent damage is done, some will have lasting damage to the foot. Also, later in life, Kohler's disease can spread to the hips.

The goal of non-surgical treatment of tarsal coalition is to relieve the symptoms by reducing the movement of the affected joint. This might include non-steroidal anti-inflammatory drugs (NSAIDs), steroidal anti-inflammatory injection, stabilizing orthotics or immobilization via a leg cast. At times, short term immobilization followed by long term orthotic use may be sufficient to keep the area free of pain.

Surgery is very commonly required. The type and complexity of the surgery will depend on the location of the coalition. Essentially, there are two types of surgery. Wherever possible, the bar will be removed to restore normal motion between the two bones. If this is not possible, it may be necessary to fuse the affected joints together by using screws to connect them solidly. Cutting away the coalition is more likely to succeed the younger the patient. With age comes extra wear in the affected and adjacent joints that makes treatment more difficult.

Diagnosis is made on plain radiograph of the foot, although the extent of injury is often underestimated.

Treatment comprises early reduction of the dislocation, and frequently involves open reduction internal fixation to restore and stabilise the talonavicular joint. Open reduction and fusion of the calcaneocuboid joint is occasionally required.

Throughout history flat feet were seen as a sign of low class and poor health, and high arches were seen as high class and full of vigor. Research has shown that the two distinctions are far from the case. The effects of flat feet fall under two categories, which are asymptotic and symptomatic. Individuals with rigid flat feet tend to exhibit symptoms such as foot and knee tendinitis, and are recommended to consider surgical options when managing symptoms. Individuals with flexible flat generally exhibit asymptotic effects in response to their flat feet.

In fact, according to AAP news and journal gateway, being flexibly flat-footed does not impede athletic performance.

It is generally assumed by running professionals (primarily including some physical trainers, podiatrists, and shoe manufacturers) that a person with flat feet tends to overpronate in the running form. However, some also assert that persons with flat feet may have an underpronating if they are not a neutral gait. With standard running shoes, these professionals claim, a person who overpronates in his or her running form may be more susceptible to shin splints, back problems, and tendonitis in the knee. Running in shoes with extra medial support or using special shoe inserts, orthoses, may help correct one's running form by reducing pronation and may reduce risk of injury.

An accessory navicular bone is an accessory bone of the foot that occasionally develops abnormally in front of the ankle towards the inside of the foot. This bone may be present in approximately 2-21% of the general population and is usually asymptomatic. When it is symptomatic, surgery may be necessary.

Surgery can be performed at any age because it does not alter any other bones.

Symptoms of an accessory navicular bone may include plantar fasciitis, bunions and heel spurs.

Appropriate treatment for lameness depends on the condition diagnosed, but at a minimum it usually includes rest or decreased activity and anti-inflammatory medications. Other treatment options, such as corrective shoeing, joint injections, and regenerative therapies, are pursued based on the cause of lameness and the financial limits of the owner. Consultation with a veterinarian is generally recommended, even for mild cases, as some types of lameness may worsen if not properly diagnosed and treated.

Options include operative or non-operative treatment. If the dislocation is less than 2 mm, the fracture can be managed with casting for six weeks. The patient's injured limb cannot bear weight during this period. For severe Lisfranc injuries, open reduction with internal fixation (ORIF) and temporary screw or Kirschner wire (K-wire) fixation is the treatment of choice. The foot cannot be allowed to bear weight for a minimum of six weeks. Partial weight-bearing may then begin, with full weight bearing after an additional several weeks, depending on the specific injury. K-wires are typically removed after six weeks, before weight bearing, while screws are often removed after 12 weeks.

When a Lisfranc injury is characterized by significant displacement of the tarsometatarsal joint(s), nonoperative treatment often leads to severe loss of function and long-term disability secondary to chronic pain and sometimes to a planovalgus deformity. In cases with severe pain, loss of function, or progressive deformity that has failed to respond to nonoperative treatment, mid-tarsal and tarsometatarsal arthrodesis (operative fusion of the bones) may be indicated.

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.

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.

Altering the biomechanics of training and training schedules may reduce the prevalence of stress fractures. Orthotic insoles have been found to decrease the rate of stress fractures in military recruits, but it is unclear whether this can be extrapolated to the general population or athletes. On the other hand, some athletes have argued that cushioning in shoes actually causes more stress by reducing the body's natural shock-absorbing action, thus increasing the frequency of running injuries. During exercise that applies more stress to the bones, it may help to increase daily calcium (2,000mg) and vitamin D (800 IU) intake, depending on the individual.

A detailed history is the first step of a lameness exam.

1. Age: Foals are more likely to have infectious causes of lameness (septic arthritis). Horses just starting training may be lame due to a developmental orthopedic disease, such as osteochondrosis. Older animals are more likely to experience osteoarthritis.

2. Breed: Breed-specific diseases, such as HYPP, can be ruled out. Additionally, some breeds or types are more prone to certain types of lameness.

3. Discipline: Certain lamenesses are associated with certain uses. For example, racehorses are more likely to have fatigue-related injuries such as stress fractures and injury to the flexor tendons, while western show horses are more likely to suffer from navicular syndrome and English sport horses are more likely to have osteoarthritis or injury to the suspensory ligament.

4. Past history of lameness: An old injury may be re-injured. In the case of progressive disease, such as osteoarthritis, a horse will often experience recurrent lameness that must be managed. Shifting lameness may suggest a bilateral injury or infectious cause of lameness.

5. Duration and progression the lameness: Acute injury is more common with soft tissue injury. Chronic, progressive disease is more common in cases such as osteoarthritis and navicular disease.

6. Recent changes in management: such as turn-out, exercise level, diet, or shoeing.

7. Effect of exercise on degree of lameness.

8. Any treatment implemented, including rest.

Köhler disease (also spelled "Kohler" and referred to in some texts as Kohler disease I) is a rare bone disorder of the foot found in children between six and nine years of age. The disease typically affects boys, but it can also affect girls. It was first described in 1908 by Alban Köhler (1874–1947), a German radiologist.

It is caused when the navicular bone temporarily loses its blood supply. As a result, tissue in the bone dies and the bone collapses. When treated, it causes no long term problems in most cases although rarely can return in adults. As the navicular bone gets back to normal, symptoms typically abate.

In February 2010, the "Journal of the American Medical Association" reported that the 19-year-old king Tutankhamun may well have died of complications from malaria combined with Köhler disease II.

In the US, the annual incidence of stress fractures in athletes and military recruits ranges from 5% to 30%, depending on the sport and other risk factors. Women and highly active individuals are also at a higher risk. The incidence probably also increases with age due to age-related reductions in bone mass density (BMD). Children may also be at risk because their bones have yet to reach full density and strength. The female athlete triad also can put women at risk as disordered eating and osteoporosis can cause the bones to be severely weakened.

Lisfranc injury, also known as Lisfranc fracture, is an injury of the foot in which one or more of the metatarsal bones are displaced from the tarsus. The injury is named after Jacques Lisfranc de St. Martin (2 April 179013 May 1847), a French surgeon and gynecologist who described an amputation of the foot through the tarsometatarsal articulation, in 1815, after the War of the Sixth Coalition.

The ultimate cause for these conditions is unknown, but the most commonly cited cause factors are rapid growth, heredity, trauma (or overuse), anatomic conformation, and dietary imbalances; however, only anatomic conformation and heredity are well supported by scientific literature. The way that the disease is initiated has been debated. Although failure of chondrocyte differentiation, formation of a fragile cartilage, failure of blood supply to the growth cartilage, and bone necrosis all have been proposed as the starting point in the pathogenesis, recent literature strongly supports failure of blood supply to growth cartilage as most likely.

The term osteochondrosis has been used to describe a wide range of lesions among different species. There are different types of the prognosis: latens, which is a lesion restricted to epiphyseal cartilage, manifesta, a lesion paired with a delay in endochondral ossification, and dissecans which is a cleft formation in the articular cartilage.

The prognosis for these conditions is very variable, and depends both on the anatomic site and on the time at which it is detected. In some cases of osteochondrosis, such as Sever's disease and Freiberg's infraction, the involved bone may heal in a relatively normal shape and leave the patient asymptomatic. On the contrary, Legg-Calvé-Perthes disease frequently results in a deformed femoral head that leads to arthritis and the need for joint replacement.

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.

Five bisphosphonates are currently available. In general, the most commonly prescribed are risedronic acid, alendronic acid, and pamidronic acid. Etidronic acid and other bisphosphonates may be appropriate therapies for selected patients but are less commonly used. None of these drugs should be used by people with severe kidney disease.

- Etidronate disodium The approved regimen is once daily for six months; a higher dose is more commonly used. No food, beverage, or medications should be consumed for two hours before and after taking. The course should not exceed six months, but repeat courses can be given after rest periods, preferably of three to six months duration.

- Pamidronate disodium in intravenous form: the approved regimen uses an infusion over four hours on each of three consecutive days, but a more commonly used regimen is over two to four hours for two or more consecutive or nonconsecutive days.

- Alendronate sodium is given as tablets once daily for six months; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).

- Tiludronate disodium are taken once daily for three months; they may be taken any time of day, as long as there is a period of two hours before and after resuming food, beverages, and medications.

- Risedronate sodium tablet taken once daily for 2 months is the prescribed regimen; patients should wait at least 30 minutes after taking before eating any food, drinking anything other than tap water, taking any medication, or lying down (patient may sit).

- Zoledronic acid is given as an intravenous infusion; a single dose is effective for two years. This is recommended for most people at high risk with active disease.

Medical therapy prior to surgery helps to decrease bleeding and other complications. Patients who are having surgery should discuss treatment with their physician. There are generally three major complications of Paget's disease for which surgery may be recommended.

- Fractures — Surgery may allow fractures to heal in a better position.

- Severe degenerative arthritis — If disability is severe and medication and physical therapy are no longer helpful, joint replacement of the hips and knees may be considered.

- Bone deformity — Cutting and realignment of pagetic bone (osteotomy) may help painful weight bearing joints, especially the knees.

Complications resulting from enlargement of the skull or spine may injure the nervous system. However, most neurologic symptoms, even those that are moderately severe, can be treated with medication and do not require neurosurgery.

CVAC sessions

Cyclic Variations in Adaptive Conditioning (CVAC) is a method of touch free cyclic hypobaric pneumatic compression for treatment of tissue edema and, therefore, edema-associated pain. As a pilot study, 10 participants with AD completed pain and quality of life questionnaires before and after 20–40 minutes of CVAC process daily for 5 days. After treatment, there was a significant decrease in pain as measured by the Pain Catastrophizing Scale and the Visual Analogue Scale, but there was no change in pain quality by the McGill Pain Questionnaire. However, there were no changes in the Pain Disability Index or Pittsburgh Sleep Quality Index. This study suggests a potential treatment role for CVAC, and the authors recommended randomized controlled clinical trials.