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.

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.

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.

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

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.

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.

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.

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.

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.

For low-risk stress fractures, rest is the best management option. The amount of recovery time varies greatly depending upon the location and severity of the fracture, and the body's healing response. Complete rest and a stirrup leg brace or walking boot are usually used for a period of four to eight weeks, although periods of rest of twelve weeks or more are not uncommon for more severe stress fractures. After this period, activities may be gradually resumed as long as the activities do not cause pain. While the bone may feel healed and not hurt during daily activity, the process of bone remodeling may take place for many months after the injury feels healed. Incidences of refracturing the bone are still a significant risk. Activities such as running or sports that place additional stress on the bone should only gradually be resumed. Rehabilitation usually includes muscle strength training to help dissipate the forces transmitted to the bones.

With severe stress fractures (see "prognosis"), surgery may be needed for proper healing. The procedure may involve pinning the fracture site, and rehabilitation can take up to six months.

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.

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.

Most flexible flat feet are asymptomatic, and do not cause pain. In these cases, there is usually no cause for concern. Flat feet were formerly a physical-health reason for service-rejection in many militaries. However, three military studies on asymptomatic adults (see section below), suggest that persons with asymptomatic flat feet are at least as tolerant of foot stress as the population with various grades of arch. Asymptomatic flat feet are no longer a service disqualification in the U.S. military.

In a study performed to analyze the activation of the tibialis posterior muscle in adults with pes planus, it was noted that the tendon of this muscle may be dysfunctional and lead to disabling weightbearing symptoms associated with acquired flat foot deformity. The results of the study indicated that while barefoot, subjects activated additional lower-leg muscles to complete an exercise that resisted foot adduction. However, when the same subjects performed the exercise while wearing arch supporting orthotics and shoes, the tibialis posterior was selectively activated. Such discoveries suggest that the use of shoes with properly fitting, arch-supporting orthics will enhance selective activation of the tibialis posterior muscle thus, acting as an adequate treatment for the undesirable symptoms of pes planus.

Rigid flatfoot, a condition where the sole of the foot is rigidly flat even when a person is not standing, often indicates a significant problem in the bones of the affected feet, and can cause pain in about a quarter of those affected. Other flatfoot-related conditions, such as various forms of tarsal coalition (two or more bones in the midfoot or hindfoot abnormally joined) or an accessory navicular (extra bone on the inner side of the foot) should be treated promptly, usually by the very early teen years, before a child's bone structure firms up permanently as a young adult. Both tarsal coalition and an accessory navicular can be confirmed by X-ray. Rheumatoid arthritis can destroy tendons in the foot (or both feet) which can cause this condition, and untreated can result in deformity and early onset of osteoarthritis of the joint. Such a condition can cause severe pain and considerably reduced ability to walk, even with orthoses. Ankle fusion is usually recommended.

Treatment of flat feet may also be appropriate if there is associated foot or lower leg pain, or if the condition affects the knees or the lower back. Treatment may include using orthoses such as an arch support, foot gymnastics or other exercises as recommended by a podiatrist/orthotist or physical therapist. In cases of severe flat feet, orthoses should be used through a gradual process to lessen discomfort. Over several weeks, slightly more material is added to the orthosis to raise the arch. These small changes allow the foot structure to adjust gradually, as well as giving the patient time to acclimatise to the sensation of wearing orthoses. Once prescribed, orthoses are generally worn for the rest of the patient's life. In some cases, surgery can provide lasting relief, and even create an arch where none existed before; it should be considered a last resort, as it is usually very time consuming and costly.

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.

Calcitonin, also called calcitonin-salmon, is a synthetic copy of a polypeptide hormone secreted by the ultimobranchial gland of salmon. Miacalcin is administered by injection, three times per week or daily, for 6–18 months. Repeat courses can be given after brief rest periods. Miacalcin may be appropriate for certain patients, but is seldom used. Calcitonin is also linked to increased chance of cancer. Due to the increased risk of cancer, the European Medicines Agency (EMA) recommended that calcitonin be used only on a short-term basis for 3 conditions for which it had previously been approved in the European Union: Paget's disease, acute bone loss resulting from sudden immobilization, and hypercalcemia caused by cancer.

The EMA said it based its recommendations on a review of the benefits and risks of calcitonin-containing medicines. Conducted by the agency's Committee for Medicinal Products for Human Use (CHMP), the review encompassed available data from the companies that market these drugs, postmarketing safety data, randomized controlled studies, 2 studies of unlicensed oral calcitonin drugs, and experimental cancer studies, among other sources.

CHMP found that "a higher proportion of patients treated with calcitonin for long periods of time develop cancer of various types, compared with patients taking placebo." The increase in cancer rates ranged from 0.7% for oral formulations to 2.4% for the nasal formulation. CHMP concluded that the benefits of calcitonin for osteoporosis did not exceed the risks. The nasal spray's only indication is for osteoporosis, thus justifying the drug's removal from the market.

As a solution for injection or infusion, calcitonin should be administered for no more than 4 weeks to prevent acute bone loss resulting from sudden immobilization, and normally for no more than 3 months to treat Paget's disease, the EMA said. The agency did not specify a time frame for the short-term use of calcitonin for treating hypercalcemia caused by cancer.

In a case of an adolescent with rear foot pain, the physical exam will reveal that the foot movement is limited. This is both because there is a physical blockade to movement and because the brain will 'turn on' the muscles around the area to stop the joint moving toward the painful 'zone'. X-rays will usually be ordered and, in general, if there is enough toughness to the tissue bridge that pain has begun – there will usually be enough bone laid down to show up in an x-ray.

More high-tech investigations such as CT scan will be required if proceeding to surgery. If the bridge appears to be mostly fibrous tissue, an MRI would be the preferred modality to use.

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.

Nerve blocks involve injecting a small amount of local anesthetic around a nerve or into a synovial structure (such as a joint or tendon sheath) in order to block the perception of pain in a specific area. After the substance is injected, it is given a few minutes to take effect. The block is then tested by pushing a blunt object, such as a ballpoint pen, into the area that is supposed to be desensitized. If the horse does not react to this pressure, the area is desensitized, and the horse is trotted to see if the lameness has improved. Improvement indicates that the cause of lameness was from a structure desensitized by the nerve block.

Nerve blocks are performed in a step-wise fashion, beginning at the most distal (lower) part of the limb and moving upward. This is due to the fact that blocking a nerve higher up will desensitize everything it innervates distal to the blocking location. For example, blocking the leg at the level of the fetlock will also block the entire foot, since the nerve fibers that innervate the foot are inhibited when they travel through the fetlock area. A positive result from this block will not be able to differentiate foot pain from pain in the pastern or fetlock region. More information may be gained from blocking the foot first, then the fetlock, since it allows for greater specificity in determining the cause of lameness.

The duration of the anesthetic varies depending on the substance used. Lidocaine is especially short acting, and is therefore usually not used for lameness evaluations. The longer-acting anesthetic mepivacaine is most-commonly used for nerve blocks, because ideally the block should last throughout the lameness exam to avoid false positives with subsequent blocks as they are performed up the leg. Bupivicaine is very long-lasting (up to 4–6 hours), and is most commonly used for analgesia following surgery rather than for nerve blocks.

Although nerve blocks are very important to the lameness examination, they are not foolproof. Multiple studies have shown that the anesthetic can migrate, especially if the horse is evaluated long after blocking or if a large amount of anesthetic is used. If the anesthetic migrates to the structure that is causing the horse pain, the horse will have a positive block, and the examiner will conclude that the lameness originates in an area that is not actually causing the horse discomfort. False results can also be secondary to practitioner error if the anesthetic is accidentally administered into a location that was unintended, such as a synovial structure rather than around a nerve. Additionally, individual horses have variation in their neural anatomy, and if atypical patterns are present, a given block may block an area unintended by the examiner, leading to false positives. Joints present additional problems. A large volume of anesthetic placed into a joint can diffuse out over time, blocking the surrounding structures. Additionally, there are some cases where joint pain can respond better to perineural blocking rather than blocking of the joint.

Traditional analgesics

The pain in Dercum's disease is often reported to be refractory to analgesics and to non-steroidal anti-inflammatory drugs (NSAIDs). However, this has been contradicted by the findings of Herbst et al. They reported that the pain diminished in 89% of patients (n=89) when treated with NSAIDs and in 97% of patients when treated with narcotic analgesics (n=37). The dosage required and the duration of the pain relief are not precisely stated in the article.

Lidocaine

An early report from 1934 showed that intralesional injections of procaine (Novocain®) relieved pain in six cases. More recently, other types of local treatment of painful sites with lidocaine patches (5%) (Lidoderm®) or lidocaine/prilocaine (25 mg/25 mg) cream (EMLA®) have shown a reduction of pain in a few cases.

In the 1980s, treatment with intravenous infusions of lidocaine (Xylocaine®) in varying doses was reported in nine patients. The resulting pain relief lasted from 10 hours to 12 months. In five of the cases, the lidocaine treatment was combined with mexiletine (Mexitil®), which is a class 1B anti-arrhythmic with similar pharmacological properties as lidocaine.

The mechanism by which lidocaine reduces pain in Dercum's disease is unclear. It may block impulse conduction in peripheral nerves, and thereby disconnect abnormal nervous impulse circuits. Nonetheless, it might also depress cerebral activity that could lead to increased pain thresholds. Iwane et al. performed an EEG during the administration of intravenous lidocaine. The EEG showed slow waves appearing 7 minutes after the start of the infusion and disappearing within 20 minutes after the end of the infusion. On the other hand, the pain relief effect was the greatest at about 20 minutes after the end of the infusion.

Based on this, the authors concluded that the effect of lidocaine on peripheral nerves most likely explains why the drug has an effect on pain in Dercum's disease. In contrast, Atkinson et al. have suggested that an effect on the central nervous system is more likely, as lidocaine can depress consciousness and decrease cerebral metabolism. In addition, Skagen et al. demonstrated that a patient with Dercum's disease lacked the vasoconstrictor response to arm and leg lowering, which indicated that the sympathicusmediated local veno-arteriolar reflex was absent. This could suggest increased sympathetic activity. An infusion of lidocaine increased blood flow in subcutaneous tissue and normalised the vasoconstrictor response when the limbs were lowered. The authors suggested that the pain relief was caused by a normalisation of up-regulated sympathetic activity.

Methotrexate and infliximab

One patient's symptoms were improved with methotrexate and infliximab. However, in another patient with Dercum's disease, the effect of methotrexate was discreet. The mechanism of action is unclear. Previously, methotrexate has been shown to reduce neuropathic pain caused by peripheral nerve injury in a study on rats. The mechanism in the rat study case was thought to be a decrease in microglial activation subsequent to nerve injury. Furthermore, a study has shown that infliximab reduces neuropathic pain in patients with central nervous system sarcoidosis. The mechanism is thought to be mediated by tumour necrosis factor inhibition.

Interferon α-2b

Two patients were successfully treated with interferon α-2b. The authors speculated on whether the mechanism could be the antiviral effect of the drug, the production of endogenous substances, such as endorphins, or interference with the production of interleukin-1 and tumour necrosis factor. Interleukin-1 and tumour necrosis factor are involved in cutaneous hyperalgesia.

Corticosteroids

A few patients noted some improvement when treated with systemic corticosteroids (prednisolone), whereas others experienced worsening of the pain. Weinberg et al. treated two patients with juxta-articular Dercum's disease with intralesional injections of methylprednisolone (Depo-Medrol). The patients experienced a dramatic improvement.

The mechanism for the pain-reducing ability of corticosteroids in some conditions is unknown. One theory is that they inhibit the effects of substances, such as histamine, serotonin, bradykinin, and prostaglandins. As the aetiology of Dercum's disease is probably not inflammatory, it is plausible that the improvement some of the patients experience when using corticosteroids is not caused by an anti-inflammatory effect.

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.

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 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.

Surgical excision of fatty tissue deposits around joints (liposuction) has been used in some cases. It may temporarily relieve symptoms although recurrences often develop.

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.