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.

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%.

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.

Risk factors for developing shin splints include:

- Excessive pronation at subtalar joint

- Excessively tight calf muscles (which can cause excessive pronation)

- Engaging the medial shin muscle in excessive amounts of eccentric muscle activity

- Undertaking high-impact exercises on hard, noncompliant surfaces (ex: running on asphalt or concrete)

- Smoking and low fitness level

While medial tibial stress syndrome is the most common form of shin splints, compartment syndrome and stress fractures are also common forms of shin splints. Females are 1.5 to 3.5 times more likely to progress to stress fractures from shin splints. This is due in part to females having a higher incidence of diminished bone density and osteoporosis.

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.

In most people, ligaments (which are the tissues that connect bones to each other) are naturally tight in such a way that the joints are restricted to 'normal' ranges of motion. This creates normal joint stability. If muscular control does not compensate for ligamentous laxity, joint instability may result. The trait is almost certainly hereditary, and is usually something the affected person would just be aware of, rather than a serious medical condition. However, if there is widespread laxity of other connective tissue, then this may be a sign of Ehlers-Danlos syndrome.

Ligamentous laxity may also result from injury, such as from a vehicle accident. It can result from whiplash and be overlooked for years by doctors who are not looking for it, despite the chronic pain that accompanies the resultant spinal instability. Ligamentous laxity will show up on an upright magnetic resonance imaging (MRI), the only kind of MRI that will show soft tissue damage. It can be seen in standing stress radiographs in flexion, extension, and neutral views as well, and also digital motion X-ray, or DMX.

An advantage to having lax ligaments and joints is the ability to withstand pain from hyperextension; however, this is also a disadvantage as a lack of perceived pain can prevent a person from removing the ligament from insult, leading to ligament damage. This can also lead to death if you tear the wrong ligament. People with hypermobile joints (or "double-jointed" people), almost by definition, have lax ligaments.

Plantar fasciitis is the most common type of plantar fascia injury and is the most common reason for heel pain, responsible for 80% of cases. The condition tends to occur more often in women, military recruits, older athletes, the obese, and young male athletes.

Plantar fasciitis is estimated to affect 1 in 10 people at some point during their lifetime and most commonly affects people between 40–60 years of age. In the United States alone, more than two million people receive treatment for plantar fasciitis. The cost of treating plantar fasciitis in the United States is estimated to be $284 million each year.

Identified risk factors for plantar fasciitis include excessive running, standing on hard surfaces for prolonged periods of time, high arches of the feet, the presence of a leg length inequality, and flat feet. The tendency of flat feet to excessively roll inward during walking or running makes them more susceptible to plantar fasciitis. Obesity is seen in 70% of individuals who present with plantar fasciitis and is an independent risk factor.

Studies have suggested a strong association exists between an increased body mass index and the development of plantar fasciitis in the non-athletic population; this association between weight and plantar fasciitis has not been observed in the athletic population. Achilles tendon tightness and inappropriate footwear have also been identified as significant risk factors.

While the exact cause is unknown, shin splints can be attributed to the overloading of the lower leg due to biomechanical irregularities resulting in an increase in stress exerted on the tibia. A sudden increase in intensity or frequency in activity level fatigues muscles too quickly to properly help absorb shock, forcing the tibia to absorb most of that shock. This stress is associated with the onset of shin splints. Muscle imbalance, including weak core muscles, inflexibility and tightness of lower leg muscles, including the gastrocnemius, soleus, and plantar muscles (commonly the flexor digitorum longus) can increase the possibility of shin splints. The pain associated with shin splints is caused from a disruption of Sharpey's fibres that connect the medial soleus fascia through the periosteum of the tibia where it inserts into the bone. With repetitive stress, the impact forces eccentrically fatigue the soleus and create repeated tibial bending or bowing, contributing to shin splints. The impact is made worse by running uphill, downhill, on uneven terrain, or on hard surfaces. Improper footwear, including worn-out shoes, can also contribute to shin splints.

The healing time for a routine mandible fractures is 4–6 weeks whether MMF or rigid internal fixation (RIF) is used. For comparable fractures, patients who received MMF will lose more weight and take longer to regain mouth opening, whereas, those who receive RIF have higher infection rates.

The most common long-term complications are loss of sensation in the mandibular nerve, malocclusion and loss of teeth in the line of fracture. The more complicated the fracture (infection, comminution, displacement) the higher the risk of fracture.

Condylar fractures have higher rates of malocclusion which in turn are dependent on the degree of displacement and/or dislocation. When the fracture is intracapsular there is a higher rate of late-term osteoarthritis and the potential for ankylosis although the later is a rare complication as long as mobilization is early. Pediatric condylar fractures have higher rates of ankylosis and the potential for growth disturbance.

Rarely, mandibular fracture can lead to Frey's syndrome.

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.

Mandible fracture causes vary by the time period and the region studied. In North America, blunt force trauma (a punch) is the leading cause of mandible fracture whereas in India, motor vehicle collisions are now a leading cause. On battle grounds, it is more likely to be high velocity injuries (bullets and shrapnel). Prior to the routine use of seat belts, airbags and modern safety measures, motor vehicle collisions were a leading cause of facial trauma. The relationship to blunt force trauma explains why 80% of all mandible fractures occur in males. Mandibular fracture is a rare complication of third molar removal, and may occur during the procedure or afterwards. With respect to trauma patients, roughly 10% have some sort of facial fracture, the majority of which come from motor vehicle collisions. When the person is unrestrained in a car, the risk of fracture rises 50% and when an unhelmeted motorcyclist the risk rises 4-fold.

Although the precise mechanism of injury is unclear, the injury occurs in children who have fallen heavily with their arm trapped under the body. In his original description of the injury, Hume suggested that the injury occurred as a result of hyperextension of the elbow leading to fracture of the olecranon, with pronation of the forearm leading to the radial head dislocation.

Those who have loose ligaments in the legs and feet often mistakenly assume that they have flat feet. While their feet have an arch when not supporting weight, when stood upon, the arch will flatten. This is because the loose ligaments cannot support the arch in the way that they should. This can make walking and standing painful and tiring.

Pain will usually occur in the feet and lower legs, but can also spread to the back due to abnormal standing and walking habits. Wearing shoes that have good arch support can help minimize the discomfort. The underlying problem, however, is not solved by wearing shoes with arch supports or worsened by wearing shoes without arch support. There is currently no cure for the condition.

In addition, people with ligamentous laxity often have clumsy or deliberate gaits, owing to the body having to overcompensate for the greater amount of energy required to offset the weakened ligaments. The feet may be spread apart at a wide angle, and the knees may flex backwards slightly after each stride.

Those who have this disease may experience sprained ankles more frequently than other people.

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 Geist classification divides the accessory navicular bones into three types.

- Type 1: An os tibiale externum is a 2–3 mm sesamoid bone in the distal posterior tibialis tendon. Usually asymptomatic.

- Type 2: Triangular or heart-shaped ossicle measuring up to 12 mm, which represents a secondary ossification center connected to the navicular tuberosity by a 1–2 mm layer of fibrocartilage or hyaline cartilage. Portions of the posterior tibialis tendon sometimes insert onto the accessory ossicle, which can cause dysfunction, and therefore, symptoms.

- Type 3: A cornuate navicular bone represents an enlarged navicular tuberosity, which may represent a fused Type 2 accessory bone. Occasionally symptomatic due to bunion formation.

Morton's neuroma (also known as Morton neuroma, Morton's metatarsalgia, Intermetatarsal neuroma and Intermetatarsal space neuroma.) is a benign neuroma of an intermetatarsal plantar nerve, most commonly of the second and third intermetatarsal spaces (between 2nd−3rd and 3rd−4th metatarsal heads), which results in the entrapment of the affected nerve. The main symptoms are pain and/or numbness, sometimes relieved by removing narrow or high-heeled footwear. Sometimes symptoms are relieved by wearing non-constricting footwear.

Some sources claim that entrapment of the plantar nerve because of compression between the metatarsal heads, as originally proposed by Morton, is highly unlikely, because the plantar nerve is on the plantar side of the transverse metatarsal ligament and thus does not come in contact with the metatarsal heads. It is more likely that the transverse metatarsal ligament is the cause of the entrapment.

Despite the name, the condition was first correctly described by a chiropodist named Durlacher, and although it is labeled a "neuroma", many sources do not consider it a true tumor, but rather a perineural fibroma (fibrous tissue formation around nerve tissue).

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.

Jefferson fracture is often caused by an impact or load on the back of the head, and are frequently associated with diving into shallow water, impact against the roof of a vehicle and falls, and in children may occur due to falls from playground equipment. Less frequently, strong rotation of the head may also result in Jefferson fractures.

Jefferson fractures are extremely rare in children, but recovery is usually complete without surgery.

The Hume fracture is an injury of the elbow comprising a fracture of the olecranon with an associated anterior dislocation of the radial head which occurs in children. It was originally described as an undisplaced olecranon fracture, but more recently includes displaced fractures and can be considered a variant of the Monteggia fracture.

The injury was described in 1957 by A.C. Hume of the orthopaedic surgery department of St. Bartholomew's Hospital, Rochester.

Negative signs include no obvious deformities, erythema, signs of inflammation, or limitation of movement. Direct pressure between the metatarsal heads will replicate the symptoms, as will compression of the forefoot between the finger and thumb so as to compress the transverse arch of the foot. This is referred to as Mulder’s Sign.

There are other causes of pain in the forefoot. Too often all forefoot pain is categorized as neuroma. Other conditions to consider are capsulitis, which is an inflammation of ligaments that surrounds two bones, at the level of the joint. In this case, it would be the ligaments that attach the phalanx (bone of the toe) to the metatarsal bone. Inflammation from this condition will put pressure on an otherwise healthy nerve and give neuroma-type symptoms. Additionally, an intermetatarsal bursitis between the third and fourth metatarsal bones will also give neuroma-type symptoms because it too puts pressure on the nerve. Freiberg's disease, which is an osteochondritis of the metatarsal head, causes pain on weight bearing or compression.

A Le Fort fracture of the skull is a classic transfacial fracture of the midface, involving the maxillary bone and surrounding structures in either a horizontal, pyramidal or transverse direction. The hallmark of Lefort fractures is traumatic "pterygomaxillary separation", which signifies fractures between the pterygoid plates, horseshoe shaped bony protuberances which extend from the inferior margin of the maxilla, and the maxillary sinuses. Continuity of this structure is a keystone for stability of the midface, involvement of which impacts surgical management of trauma victims, as it requires fixation to a horizontal bar of the frontal bone. The pterygoid plates lie posterior to the upper dental row, or alveolar ridge, when viewing the face from an anterior view. The fractures are named after French surgeon René Le Fort (1869–1951), who discovered the fracture patterns by examining crush injuries in cadavers.

In 1997 Morrison et al.

published a study that reviewed the cases of 616 patients (636 shoulders) with impingement syndrome (painful arc of motion) to assess the outcome of non-surgical care. An attempt was made to exclude patients who were suspected of having additional shoulder conditions such as, full-thickness tears of the rotator cuff, degenerative arthritis of the acromioclavicular joint, instability of the glenohumeral joint, or adhesive capsulitis. All patients were managed with anti-inflammatory medication and a specific, supervised physical-therapy regimen. The patients were followed up from six months to over six years. They found that 67% (413 patients) of the patients improved, while 28% did not improve and went to surgical treatment. 5% did not improve and declined further treatment.

Of the 413 patients who improved, 74 had a recurrence of symptoms during the observation period and their symptoms responded to rest or after resumption of the exercise program.

The Morrison study shows that the outcome of impingement symptoms varies with patient characteristics. Younger patients ( 20 years or less) and patients between 41 and 60 years of age, fared better than those who were in the 21 to 40 years age group. This may be related to the peak incidence of work, job requirements, sports and hobby related activities, that may place greater demands on the shoulder. However, patients who were older than sixty years of age had the "poorest results". It is known that the rotator cuff and adjacent structures undergo degenerative changes with ageing.

The authors were unable to posit an explanation for the observation of the bimodal distribution of satisfactory results with regard to age. They concluded that it was "unclear why (those) who were twenty-one to forty years old had less satisfactory results". The poorer outcome for patients over 60 years old was thought to be potentially related to "undiagnosed full-thickness tears of the rotator cuff".

The cause is usually a direct blow to the malar eminence of the cheek during assault. The paired zygomas each have two attachments to the cranium, and two attachments to the maxilla, making up the orbital floors and lateral walls. These complexes are referred to as the zygomaticomaxillary complex. The upper and transverse maxillary bone has the zygomaticomaxillary and zygomaticotemporal sutures, while the lateral and vertical maxillary bone has the zygomaticomaxillary and frontozygomatic sutures.

The formerly used 'tripod fracture' refers to these buttresses, but did not also incorporate the posterior relationship of the zygoma to the sphenoid bone at the zygomaticosphenoid suture.

There is an association of ZMC fractures with naso-orbito-ethmoidal fractures (NOE) on the same side as the injury. Concomitant NOE fractures predict a higher incidence of post operative deformity.