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.

Depending on the severity of the deformities, the treatment may include the amputation of the foot or part of the leg, lengthening of the femur, extension prosthesis, or custom shoe lifts. Amputation usually requires the use of prosthesis. Another alternative is a rotationplasty procedure, also known as Van Ness surgery. In this situation the foot and ankle are surgically removed, then attached to the femur. This creates a functional "knee joint". This allows the patient to be fit with a below knee prosthesis vs a traditional above knee prosthesis.

In less severe cases, the use of an Ilizarov apparatus can be successful in conjunction with hip and knee surgeries (depending on the status of the femoral head/kneecap) to extend the femur length to normal ranges. This method of treatment can be problematic in that the Ilizarov might need to be applied both during early childhood (to keep the femur from being extremely short at the onset of growth) and after puberty (to match leg lengths after growth has ended). The clear benefit of this approach, however, is that no prosthetics are needed and at the conclusion of surgical procedures the patient will not be biologically or anatomically different from a person born without PFFD.

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.

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.

There is no known specific treatment for this condition. Management is supportive.

Weismann-Netter-Stuhl syndrome, also known as Weismann-Netter Syndrome or more technically by the term tibioperoneal diaphyseal toxopachyosteosis, is a rare disorder characterized by bowing of the lower legs and an abnormal thickening of thinner bone in the leg.

The main sign is anterior bowing and posterior cortical thickening of the diaphyses of both the tibiae and fibulae. It is thought to be inherited in an autosomal dominant fashion, and is most often bilateral and symmetric in nature. Associated features include dwarfism and mild intellectual disability, as well as a process known as tibialization of the fibulae, which involves thickening and enlargement of these bones to an extent resembling the tibiae. The combination of the presence of tibialization of the fibulae, which is highly specific for the disorder, and the absence of laboratory abnormalities ruling out alternative diagnoses including rickets, essentially confirms the diagnosis.

The most prominent and extensively documented findings of Weismann-Netter-Stuhl syndrome are on plain radiographs of the bones. Findings include bilateral and symmetric anterior bowing of both tibiae and fibulae, lateral bowing of the tibiae, femoral bowing, and squaring of iliac and pelvis bones.

Wearing shoes to protect barefoot trauma has shown decrease in incidence in ainhum. Congenital pseudoainhum cannot be prevented and can lead to serious birth defects.

While genu valgum is often a symptom of genetic disorders it can be caused by poor nutrition. A major contributor to genu valgum is obesity, and far less commonly calcium and vitamin d deficiencies.

Persons with knock knees often have collapsed inner arches of their feet, and their inner ankle bones are generally lower than their outer ankle bones. Adults with uncorrected genu valgum are typically prone to injury and chronic knee problems such as chondromalacia and osteoarthritis. These in turn can cause severe pain and problems in walking.

It is normal for children to have knock knees between the ages of two and five years of age, and almost all of them resolve as the child grows older. If symptoms are prolonged and pronounced or hereditary, doctors often use orthotic shoes or leg braces at night to gently move a child's leg back into position. If the condition persists and worsens later in life, surgery may be required to relieve pain and complications resulting from severe or hereditary genu valgum. Available surgical procedures include adjustments to the lower femur and total knee replacement (TKR).

Weight loss and substitution of high-impact for low-impact exercise can help slow progression of the condition. With every step, the patient's weight places a distortion on the knee toward a knocked knee position, and the effect is increased with increased angle or increased weight. Even in the normal knee position, the femurs function at an angle because they connect to the hip girdle at points much further apart than they connect at the knees.

Physical therapy is generally of benefit to people with knock knees. To correct knock knees, the entire leg must be treated, especially:

1. Activating and developing the arches of the feet,

2. Waking up the outer leg muscles (abductors), and

3. Learning how to move the inner ankle bone inwards towards the outer ankle bone, and upwards towards the knee.

Working with a physical medicine specialist such as a physiatrist, or a physiotherapist may assist a patient learning how to improve outcomes and use the leg muscles properly to support the bone structures. Alternative or complementary treatments may include certain procedures from Iyengar Yoga or the Feldenkrais Method.

Rarely, the bone malformation underlying knock knees can be traced to a lack of nutrition necessary for bone growth, which can cause conditions such as rickets (lack of bone nutrients, especially dietary vitamin D and calcium), or scurvy (lack of vitamin C). The correction of the underlying vitamin deficiency may restore a more normal progression of bone growth.

Treatment consist of a long leg orthopedic cast for several weeks.

Most of these conditions are self-correcting during childhood. In the worst cases, surgery may be needed. Most of the time, this involves lengthening the Achilles tendon. Less severe treatment options for pigeon toe include keeping a child from crossing his or her legs, use of corrective shoes, and casting of the foot and lower legs, which is normally done before the child reaches 12 months of age or older.

If the pigeon toe is mild and close to the center, treatment may not be necessary.

Ballet has been used as a treatment for mild cases. Dance exercises can help to bend the legs outward.

Presence at birth is extremely rare and associated with other congenital anomalies such as proximal femoral focal deficiency, fibular hemimelia or anomalies in other part of the body such as cleidocranial dyastosis. The femoral deformity is present in the subtrochantric area where the bone is bent. The cortices are thickened and may be associated with overlying skin dimples. External rotation of the femur with valgus deformity of knee may be noted. This condition does not resolve and requires surgical management. Surgical management includes valgus osteotomy to improve hip biomechanics and length and rotational osteotomy to correct retroversion and lengthening.

Hemimelia comprises

- Fibular hemimelia, Congenital longitudinal deficiency of the fibula or Fibular longitudinal meromelia

- Tibial hemimelia, Congenital longitudenal deficiency of the tibia, Congenital aplasia and dysplasia of the tibia with intact fibula, Congenital longitudinal deficiency of the tibia or Tibial longitudinal meromelia

- Radial Hemimelia, Congenital longitudinal deficiency of the radius, Radial clubhand, Radial longitudinal meromelia or Radial ray agenesis

- Ulnar hemimelia, Congenital longitudinal deficiency of the ulna, Ulnar clubhand or Ulnar longitudinal meromelia

Treatment differs depending on the cause. Each cause has a different treatment, and may involve either medical treatment, surgery, or therapy. If serious damage has already been done, then the focus of treatment is upon avoidance of vestibular suppressants and ototoxins. It is recommended that you tell your physicians to avoid drugs that end in mycin ( Azithromycin, Erythromycin ) because of possible reactions which could lead to setbacks. Vestibular rehabilitation is important. Your physician will try to keep the administering of drugs to a minimum.

Coxa vara is a deformity of the hip, whereby the angle between the head and the shaft of the femur is reduced to less than 120 degrees. This results in the leg being shortened, and the development of a limp. It is commonly caused by injury, such as a fracture. It can also occur when the bone tissue in the neck of the femur is softer than normal, causing it to bend under the weight of the body. This may either be congenital or the result of a bone disorder. The most common cause of coxa vara is either congenital or developmental. Other common causes include metabolic bone diseases (e.g. Paget's disease of bone), post-Perthes deformity, osteomyelitis, and post traumatic (due to improper healing of a fracture between the greater and lesser trochanter). Shepherd's Crook deformity is a severe form of coxa vara where the proximal femur is severely deformed with a reduction in the neck shaft angle beyond 90 degrees. It is most commonly a sequela of osteogenesis imperfecta, Pagets disease, osteomyelitis, tumour and tumour-like conditions (e.g. fibrous dysplasia).

Coxa vara can happen in cleidocranial dysostosis.

Ectromelia is a congenital condition where long bones are missing or underdeveloped.

Examples include:

- Amelia

- Hemimelia

- Phocomelia

- Sirenomelia

Bernese periacetabular osteotomy resulted in major nerve deficits in the sciatic or femoral nerves in 2.1% of 1760 patients, of whom approximately half experienced complete recovery within a mean of 5.5 months.

Sciatic nerve exploration can be done by endoscopy in a minimally invasive procedure to assess lesions of the nerve. Endoscopic treatment for sciatic nerve entrapment has been investigated in deep gluteal syndrome; "Patients were treated with sciatic nerve decompression by resection of fibrovascular scar bands, piriformis tendon release, obturator internus, or quadratus femoris or by hamstring tendon scarring."

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.

Incisions across the groove turned out to be ineffective. Excision of the groove followed by z-plasty could relieve pain and prevent autoamputation in Grade I and Grade II lesions. Grade III lesions are treated with disarticulating the metatarsophalangeal joint. This also relieves pain, and all patients have a useful and stable foot. Intralesional injection of corticosteroids is also helpful.

The proposed mechanism involves shear stress and lack of displacement due to the periosteum that is relatively strong compared to the elastic bone in young children.

The cause of this condition is not known. A genetic basis is suspected. More than one case have been reported in three families.

The sciatic nerve (; also called "ischiadic nerve", "ischiatic nerve", "butt nerve") is a large nerve in humans and other animals. It begins in the lower back and runs through the buttock and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect. The sciatic nerve provides the connection to the nervous system for nearly the whole of the skin of the leg, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 to S3. It contains fibers from both the anterior and posterior divisions of the lumbosacral plexus.

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.

The exact cause of Tarsal Tunnel Syndrome (TTS) can vary from patient to patient. However the same end result is true for all patients, the compression of the posterior tibial nerve and it branches as it travels around the medial malleolus causes pain and irritation for the patient. There are many possible causes for compression of the tibial nerve therefore there are a variety of prevention strategies. One being immobilization, by placing the foot in a neutral position with a brace, pressure is relieved from the tibial nerve thus reducing patients pain. Eversion, inversion, and plantarflexion (as seen in figure 1) all can cause compression of the tibial nerve therefore in the neutral position the tibial nerve is less agitated. Typically this is recommended for the patient to do while sleeping(see figure 2). Another common problem is improper footwear, having shoes deforming the foot due to being too tight can lead to increased pressure on the tibial nerve. Having footwear that tightens the foot for extended periods of time even will lead to TTS. Therefore, by simply having properly fitted shoes TTS can be prevented.