In osteochondritis dissecans, fragments of cartilage or bone become loose within a joint, leading to pain and inflammation. These fragments are sometimes referred to as joint mice. OCD is a type of osteochondrosis in which a lesion has formed within the cartilage layer itself, giving rise to secondary inflammation. OCD most commonly affects the knee, although it can affect other joints such as the ankle or the elbow.

People with OCD report activity-related pain that develops gradually. Individual complaints usually consist of mechanical symptoms including pain, swelling, catching, locking, popping noises, and buckling / giving way; the primary presenting symptom may be a restriction in the range of movement. Symptoms typically present within the initial weeks of stage I; however, the onset of stage II occurs within months and offers little time for diagnosis. The disease progresses rapidly beyond stage II, as OCD lesions quickly move from stable cysts or fissures to unstable fragments. Non-specific symptoms, caused by similar injuries such as sprains and strains, can delay a definitive diagnosis.

Physical examination typically reveals fluid in the joint, tenderness, and crepitus. The tenderness may initially spread, but often reverts to a well-defined focal point as the lesion progresses. Just as OCD shares symptoms with common maladies, acute osteochondral fracture has a similar presentation with tenderness in the affected joint, but is usually associated with a fatty hemarthrosis. Although there is no significant pathologic gait or characteristic alignment abnormality associated with OCD, the patient may walk with the involved leg externally rotated in an attempt to avoid tibial spine impingement on the lateral aspect of the medial condyle of the femur.

Elbow dysplasia is a condition involving multiple developmental abnormalities of the elbow-joint in the dog, specifically the growth of cartilage or the structures surrounding it. These abnormalities, known as 'primary lesions', give rise to osteoarthritic processes. Elbow dysplasia is a common condition of certain breeds of dogs.

Most primary lesions are related to osteochondrosis, which is a disease of the joint cartilage and specifically Osteochondritis dissecans (OCD or OD), the separation of a flap of cartilage on the joint surface. Other common causes of elbow dysplasia included ununited anconeal process (UAP) and fragmented or ununited medial coronoid process (FCP or FMCP).

Osteochondritis dissecans is difficult to diagnose clinically as the animal may only exhibit an unusual gait. Consequently, OCD may be masked by, or misdiagnosed as, other skeletal and joint conditions such as hip dysplasia. The problem develops in puppyhood although often subclinically, and there may be pain or stiffness, discomfort on extension, or other compensating characteristics. Diagnosis generally depends on X-rays, arthroscopy, or MRI scans. While cases of OCD of the stifle go undetected and heal spontaneously, others are exhibited in acute lameness. Surgery is recommended once the animal has been deemed lame, before then non-surgical control is usually used.

Children with autosomal dominant MED experience joint pain and fatigue after exercising. Their x-rays show small and irregular ossifications centers, most apparent in the hips and knees. A waddling gait may develop. Flat feet are very common.

The spine is normal but may have a few irregularities, such as scoliosis. There are very small capital femoral epiphyses and hypoplastic, poorly formed acetabular roofs. Knees have metaphyseal widening and irregularity while hands have brachydactyly (short fingers) and proximal metacarpal rounding. By adulthood, people with MED are of short stature or in the low range of normal and have short limbs relative to their trunks. Frequently, movement becomes limited at the major joints, especially at the elbows and hips. However, loose knee and finger joints can occur. Signs of osteoarthritis usually begin in early adulthood.

Children with recessive MED experience joint pain, particularly of the hips and knees, and commonly have deformities of the hands, feet, knees, or vertebral column (like scoliosis). Approximately 50% of affected children have abnormal findings at birth (such as club foot or twisted metatarsals, cleft palate, inward curving fingers due to underdeveloped bones and brachydactyly, or ear swelling caused by injury during birth). Height is in the normal range before puberty. As adults, people with recessive MED are only slightly more diminished in stature, but within the normal range. Lateral knee radiography can show multi-layered patellae.

Hip dysplasia can range from barely detectable to severely malformed or dislocated.

The congenital form, teratologic or non-reducible dislocation occurs as part of more complex conditions.

The condition can be bilateral or unilateral:

- If both hip joints are affected one speaks of "bilateral" dysplasia. In this case some diagnostic indicators like asymmetric folds and leg-length inequality do not apply.

- In unilateral dysplasia only one joint shows deformity, the contralateral side may show resulting effects. In the majority of unilateral cases the left hip has the dysplasia.

If the joint is fully dislocated a false acetabulum often forms (often higher up on the pelvis) opposite the dislocated femoral head position.

In acetabular dysplasia the acetabulum (socket) is too shallow or deformed. The center-edge angle is measured as described by Wiberg. Two forms of femoral dysplasia are coxa vara, in which the femur head grows at too narrow an angle to the shaft, and coxa valga, in which the angle is too wide.

A rare type, the "Beukes familial hip dysplasia" is found among Afrikaners that are members of the Beukes family. The femur head is flat and irregular. People develop osteoarthritis at an early age.

Petplan Australia reported that signs of arthritis in dogs and cats include stiffness, difficulty moving, lethargy, irritability, and cat or dog may lick, chew or bite at sore joints.

Dogs might exhibit signs of stiffness or soreness after rising from rest, reluctance to exercise, bunny-hopping or other abnormal gait (legs move more together when running rather than swinging alternately), lameness, pain, reluctance to stand on rear legs, jump up, or climb stairs, subluxation or dislocation of the hip joint, or wasting away of the muscle mass in the hip area. Radiographs (X-rays) often confirm the presence of hip dysplasia, but radiographic features may not be present until two years of age in some dogs. Moreover, many affected dogs do not show clinical signs, but some dogs manifest the problem before seven months of age, while others do not show it until well into adulthood.

In part this is because the underlying hip problem may be mild or severe, may be worsening or stable, and the body may be more or less able to keep the joint in repair well enough to cope. Also, different animals have different pain tolerances and different weights, and use their bodies differently, so a light dog who only walks, will have a different joint use than a more heavy or very active dog. Some dogs will have a problem early on, others may never have a real problem at all.

Elbow Dysplasia is a significant genetically determined problem in many breeds of dog, often manifesting from puppyhood and continuing for life. In elbow dysplasia, the complex elbow joint suffers from a structural defect, often related to its cartilage. This initial condition, known as a "primary lesion", causes an abnormal level of wear and tear and gradual degradation of the joint, at times disabling or with chronic pain. Secondary processes such as inflammation and osteoarthritis can arise from this damage which increase the problem and add further problems of their own.

In many cases there is pain and discomfort in a joint which increases over time. While it can affect any bone, about half of cases show multiple sites of damage. Avascular necrosis primarily affects the joints at the shoulder, knee, and hip. The classical sites are: head of femur, neck of talus and waist of the scaphoid.

Avascular necrosis most commonly affects the ends of long bones such as the femur (the bone extending from the knee joint to the hip joint). Other common sites include the humerus (the bone of the upper arm), knees, shoulders, ankles and the jaw.

Common symptoms include hip, knee (hip pathology can refer pain to a normal knee), or groin pain, exacerbated by hip or leg movement, especially internal hip rotation (with the knee flexed 90°, twisting the lower leg away from the center of the body). The range of motion is reduced, particularly in abduction and internal rotation, and the patient presents with a limp. Pain is usually mild. Atrophy of thigh muscles may occur from disuse and an inequality of leg length. In some cases, some activity can cause severe irritation or inflammation of the damaged area, including standing, walking, running, kneeling, or stooping repeatedly for an extended period of time. In cases exhibiting severe femoral osteonecrosis, pain is usually a chronic, throbbing sensation exacerbated by activity.

The first signs are complaints of soreness from the child, which are often dismissed as growing pains, and limping or other guarding of the joint, particularly when tired. The pain is usually in the hip, but can also be felt in the knee (referred pain). In some cases, pain is felt in the unaffected hip and leg, due to the children favoring their injured side and placing the majority of their weight on their "good" leg. It is predominantly a disease of boys (4:1 ratio). Perthes is generally diagnosed between 5 and 12 years of age, although it has been diagnosed as early as 18 months. Typically, the disease is only seen in one hip, but bilateral Perthes is seen in about 10% of children diagnosed.

Osteochondritis dissecans (OCD or OD) is a joint disorder in which cracks form in the articular cartilage and the underlying subchondral bone. OCD usually causes pain and swelling of the affected joint which catches and locks during movement. Physical examination typically reveals an effusion, tenderness, and a crackling sound with joint movement.

OCD is caused by blood deprivation in the subchondral bone. This loss of blood flow causes the subchondral bone to die in a process called avascular necrosis. The bone is then reabsorbed by the body, leaving the articular cartilage it supported prone to damage. The result is fragmentation (dissection) of both cartilage and bone, and the free movement of these bone and cartilage fragments within the joint space, causing pain and further damage. OCD can be difficult to diagnose because these symptoms are found with other diseases. However, the disease can be confirmed by X-rays, computed tomography (CT) or magnetic resonance imaging (MRI) scans.

Non-surgical treatment is rarely an option as the ability for articular cartilage to heal is limited. As a result, even moderate cases require some form of surgery. When possible, non-operative forms of management such as protected reduced or non-weight bearing and immobilization are used. Surgical treatment includes arthroscopic drilling of intact lesions, securing of cartilage flap lesions with pins or screws, drilling and replacement of cartilage plugs, stem cell transplantation, and joint replacement. After surgery rehabilitation is usually a two-stage process of immobilization and physical therapy. Most rehabilitation programs combine efforts to protect the joint with muscle strengthening and range of motion. During the immobilization period, isometric exercises, such as straight leg raises, are commonly used to restore muscle loss without disturbing the cartilage of the affected joint. Once the immobilization period has ended, physical therapy involves continuous passive motion (CPM) and/or low impact activities, such as walking or swimming.

OCD occurs in 15 to 30 people per 100,000 in the general population each year. Although rare, it is an important cause of joint pain in physically active adolescents. Because their bones are still growing, adolescents are more likely than adults to recover from OCD; recovery in adolescents can be attributed to the bone's ability to repair damaged or dead bone tissue and cartilage in a process called bone remodeling. While OCD may affect any joint, the knee tends to be the most commonly affected, and constitutes 75% of all cases. Franz König coined the term osteochondritis dissecans in 1887, describing it as an inflammation of the bone–cartilage interface. Many other conditions were once confused with OCD when attempting to describe how the disease affected the joint, including osteochondral fracture, osteonecrosis, accessory ossification center, osteochondrosis, and hereditary epiphyseal dysplasia. Some authors have used the terms "osteochondrosis dissecans" and "osteochondral fragments" as synonyms for OCD.

In the normal anatomy of the hip joint, the root (the thigh bone) is connected to the pelvis at the hip joint. The almost spherical end of the femur head (the caput, or caput ossis femoris) fits into the acetabulum (a concave socket located in the pelvis). The bony surfaces of the femur head and of the acetabulum are covered by cartilage. While bones provide the strength necessary to support body weight, cartilage ensures a smooth fit and a wide range of motion. Normal hip function can be affected by congenital conditions such as dysplasia, discussed in this article, trauma, and by acquired diseases such as osteoarthritis and rheumatoid arthritis.

Fibrous dysplasia is a mosaic disease that can involve any part or combination of the craniofacial, axillary, and/or appendicular skeleton. The type and severity of the complications therefore depend on the location and extent of the affected skeleton. The clinical spectrum is very broad, ranging from an isolated, asymptomatic monostotic lesion discovered incidentally, to severe disabling disease involving practically the entire skeleton and leading to loss of vision, hearing, and/or mobility.

Individual bone lesions typically manifest during the first few years of life and expand during childhood. The vast majority of clinically significant bone lesions are detectable by age 10 years, with few new and almost no clinically significant bone lesions appearing after age 15 years. Total body scintigraphy is useful to identify and determine the extent of bone lesions, and should be performed in all patients with suspected fibrous dysplasia.

Children with fibrous dysplasia in the appendicular skeleton typically present with limp, pain, and/or pathologic fractures. Frequent fractures and progressive deformity may lead to difficulties with ambulation and impaired mobility. In the craniofacial skeleton, fibrous dysplasia may present as a painless “lump” or facial asymmetry. Expansion of craniofacial lesions may lead to progressive facial deformity. In rare cases patients may develop vision and/or hearing loss due to compromise of the optic nerves and/or auditory canals, which is more common in patients with McCune-Albright syndrome associated growth hormone excess. Fibrous dysplasia commonly involves the spine, and may lead to scoliosis, which in rare instances may be severe. Untreated, progressive scoliosis is one of the few features of fibrous dysplasia that can lead to early fatality.

Bone pain is a common complication of fibrous dysplasia. It may present at any age, but most commonly develops during adolescence and progresses into adulthood.

Bone marrow stromal cells in fibrous dysplasia produce excess amounts of the phosphate-regulating hormone fibroblast growth factor-23 (FGF23), leading to loss of phosphate in the urine. Patients with hypophosphatemia may develop rickets/osteomalacia, increased fractures, and bone pain.

Hip dysplasia is an abnormality of the hip joint where the socket portion does not fully cover the ball portion, resulting in an increased risk for joint dislocation. Hip dysplasia may occur at birth or develop in early life. Regardless, it does not typically produce symptoms in babies less than a year old. Occasionally one leg may be shorter than the other. The left hip is more often affected than the right. Complications without treatment can include arthritis, limping, and low back pain.

Risk factors for hip dysplasia include family history, certain swaddling practices, and breech birth. If one identical twin is affected, there is a 40% risk the other will also be affected. Screening all babies for the condition by physical examination is recommended. Ultrasonography may also be useful.

Many of those with mild instability resolve without specific treatment. In more significant cases, if detected early, bracing may be all that is required. In cases that are detected later, surgery and casting may be needed. About 7.5% of hip replacements are done to treat problems which have arisen from hip dysplasia.

About 1 in 1,000 babies have hip dysplasia. Hip instability of meaningful importance occurs in one to two percent of babies born at term. Females are affected more often than males. Hip dysplasia was described at least as early as the 300s BC by Hippocrates.

Disproportionate short stature, deformity of the lower limbs, short fingers, and

ligamentous laxity give pseudoachondroplasia its distinctive features. The average height of adult males with the condition is around 120 centimeters (3 ft, 11 in), while adult females are typically around 116 cm (3ft, 9in). Affected individuals are not noticeably short at birth. Patients with pseudoachondroplasia present with gait abnormalities, lower limb deformity, or a retarded growth rate that characteristically appear at age 2-3 years. Disproportionate short stature is characterized by shortening of proximal limb segments (humeri and femora) also called rhizomelic shortening. Other known clinical features include, genu valgum/varum, brachydactyly (short fingers), supple flexion deformity of the hips, knees, hyperlordosis of lumbar spine, rocker bottom feet and broadening of the metaphyseal ends of long bones especially around the wrists, knees and ankles. Patients with pseudoachondroplasia have normal intelligence and craniofacial features, “Figure 1”, “Figure 2”, “Figure 3”.

Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply. Early on there may be no symptoms. Gradually joint pain may develop which may limit the ability to move. Complication may include collapse of the bone or nearby joint surface.

Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high dose steroids. The condition may also occur without any clear reason. The most commonly affected bone is the femur. Other relatively common sites include the upper arm bone, knee, shoulder, and ankle. Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI. Rarely biopsy may be used.

Treatments may include medication, not walking on the affected leg, stretching, and surgery. Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement. About 15,000 cases occur per year in the United States. People 30 to 50 years old are most commonly affected. Males are more commonly affected than females.

Osteophytes, commonly referred to as bone spurs are bony projections that form along joint margins. They should not be confused with enthesophytes, which are bony projections that form at the attachment of a tendon or ligament. Osteophytes are not always distinguished from exostoses in any definite way, although in many cases there are a number of differences. Osteophytes are typically intra-articular (within the joint capsule).

Osteochondritis is a painful type of osteochondrosis where the cartilage or bone in a joint is inflamed.

It often refers to osteochondritis dissecans (sometimes spelt "dessecans", and abbreviated OCD). The term "dissecans" refers to the "creation of a flap of cartilage that further dissects away from its underlying subchondral attachments (dissecans)".

The other recognized types of osteochondritis are osteochondritis deformans juvenilis (osteochondritis of the capitular head of the epiphysis of the femur) and osteochondritis deformans juvenilis dorsi (osteochondrosis of the spinal vertebrae, also known as Scheuermann's disease).

Osteochondritis, and especially osteochondritis dissecans, can manifest in animals as a primary cause of elbow dysplasia, a chronic condition in some species and breeds.

Osteophyte formation has been classically related to any sequential and consequential changes in bone formation that is due to aging, degeneration, mechanical instability, and disease (such as diffuse idiopathic skeletal hyperostosis). Often osteophytes form in osteoarthritic joints as a result of damage and wear from inflammation. Calcification and new bone formation can also occur in response to mechanical damage in joints.

Fairbank's disease or multiple epiphyseal dysplasia (MED) is a rare genetic disorder (dominant form: 1 in 10,000 births) that affects the growing ends of bones. Long bones normally elongate by expansion of cartilage in the growth plate (epiphyseal plate) near their ends. As it expands outward from the growth plate, the cartilage mineralizes and hardens to become bone (ossification). In MED, this process is defective.

Legg–Calvé–Perthes disease (LCPD, also known as Perthes disease or Legg–Perthes disease) is a childhood hip disorder initiated by a disruption of blood flow to the head of the femur. Due to the lack of blood flow, the bone dies (osteonecrosis or avascular necrosis) and stops growing. Over time, healing occurs by new blood vessels infiltrating the dead bone and removing the necrotic bone which leads to a loss of bone mass and a weakening of the femoral head. The bone loss leads to some degree of collapse and deformity of the femoral head and sometimes secondary changes to the shape of the hip socket. It is also referred to as idiopathic avascular osteonecrosis of the capital femoral epiphysis of the femoral head since the cause of the interruption of the blood supply of the head of the femur in the hip joint is unknown.

The condition is most commonly found in children between the ages of 4 and 8, but it can occur in children between the ages of 2 and 15. The main long-term problem with this condition is that it can produce a permanent deformity of the femoral head, which increases the risk of developing osteoarthritis in adults. Perthes is a form of osteochondritis which only affects the hip, although other forms of osteochondritis can affect elbows, knees, ankles, and feet. Bilateral Perthes, which means both hips are affected, should always be investigated thoroughly to rule out multiple epiphyseal dysplasia.

Fibrous dysplasia is a disorder where normal bone and marrow is replaced with fibrous tissue, resulting in formation of bone that is weak and prone to expansion. As a result, most complications result from fracture, deformity, functional impairment, and pain. Disease occurs along a broad clinical spectrum ranging from asymptomatic, incidental lesions to severe disabling disease. Disease can affect one bone (monostotic) or multiple (polyostotic), and may occur in isolation or in combination with cafe-au-lait skin macules and hyperfunctioning endocrinopathies, termed McCune-Albright syndrome. More rarely, fibrous dysplasia may be associated with intramuscular myxomas, termed Mazabraud's syndrome. Fibrous dysplasia is very rare, and there is no known cure. Fibrous dysplasia is not a form of cancer.

"Cleidocranial dysostosis" is a general skeletal condition named for the collarbone (cleido-) and cranium deformities which people with it often have. Common features include:

- Partly or completely missing collarbones.

- A soft spot or larger soft area in the top of the head where the fontanelle failed to close.

- Bones and joints are underdeveloped.

- The permanent teeth include supernumerary teeth.

- Permanent teeth not erupting

- Bossing (bulging) of the forehead.

- Hypertelorism

Pseudoachondroplasia is an inherited disorder of bone growth. It is a genetic autosomal dominant disorder. It is generally not discovered until 2-3 years of age, since growth is normal at first. Pseudoachondroplasia is usually first detected by a drop of linear growth in contrast to peers, a curious, waddling gait or arising lower limb deformities.

Pseudoachondroplasia (also known as PSACH, Pseudoachondroplastic dysplasia, and Pseudoachondroplastic spondyloepiphyseal dysplasia syndrome) is an osteochondrodysplasia that results in mild to severely short stature due to the inhibition of skeletal growth primarily in the limbs. Though similarities in nomenclature may cause confusion, Pseudoachondroplasia should not be confused with achondroplasia, which is a clinically and genetically distinct skeletal dysplasia. Pseudoachondroplasia is caused by a heterozygous mutation in the gene encoding cartilage oligomeric matrix protein COMP. Mutation in the COMP gene can also multiple epiphyseal dysplasia. Despite the radioclinical similarities between pseudoachondroplasia and multiple epiphyseal dysplasia, the latter is less severe.132400

"Fibrous dysplasia" causes bone thinning and growths or lesions in one or more bones of the human body.

These lesions are tumor-like growths that consist of replacement of the medullary bone with fibrous tissue, causing the expansion and weakening of the areas of bone involved. Especially when involving the skull or facial bones, the lesions can cause externally visible deformities. The skull is often, but not necessarily, affected, and any other bone(s) can be involved.

In orthopedic medicine, fractures are classified in various ways. Historically they are named after the physician who first described the fracture conditions, however, there are more systematic classifications in place currently.

A bone fracture (sometimes abbreviated FRX or Fx, F, or #) is a medical condition in which there is a damage in the continuity of the bone. A bone fracture may be the result of high force impact or stress, or a minimal trauma injury as a result of certain medical conditions that weaken the bones, such as osteoporosis, bone cancer, or osteogenesis imperfecta, where the fracture is then properly termed a pathologic fracture.