Though articular cartilage damage is not life-threatening, it does strongly affect the quality of life. Articular cartilage damage is often the cause of severe pain, swellings, strong barriers to mobility and severe restrictions to the patient's activities. Over the last decades, however, surgeons and biotech ventures[who?] have elaborated promising procedures[which?] that contribute to articular cartilage repair. These procedures do not, however, treat osteoarthritis.

Increased risk of developing knee and hip osteoarthritis was found in those who:

- work with manual handling (e.g. lifting)

- have physically demanding work

- walk at work

- have climbing tasks at work (e.g. climb stairs or ladders)

Increased risk of developing hip osteoarthritis over time was found among those who work in bent or twisted positions.

Increased risk of knee osteoarthritis was found in those who:

- work in a kneeling or squatting position

- experience heavy lifting in combination with a kneeling or squatting posture

- work standing up

A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis. Although a single factor is not generally sufficient to cause the disease, about half of the variation in susceptibility has been assigned to genetic factors.

As early human ancestors evolved into bipeds, changes occurred in the pelvis, hip joint and spine which increased the risk of osteoarthritis. Additionally genetic variations that increase the risk were likely not selected against because usually problems only occur after reproductive success.

The development of osteoarthritis is correlated with a history of previous joint injury and with obesity, especially with respect to knees. Since the correlation with obesity has been observed not only for knees but also for non-weight bearing joints and the loss of body fat is more closely related to symptom relief than the loss of body weight, it has been suggested that there may be a metabolic link to body fat as opposed to just mechanical loading.

Changes in sex hormone levels may play a role in the development of osteoarthritis as it is more prevalent among post-menopausal women than among men of the same age. A study of mice found natural female hormones to be protective while injections of the male hormone dihydrotestosterone reduced protection.

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.

Despite much research, the causes remain unclear but include repetitive physical trauma, ischemia (restriction of blood flow), hereditary and endocrine factors, avascular necrosis (loss of blood flow), rapid growth, deficiencies and imbalances in the ratio of calcium to phosphorus, and problems of bone formation. Although the name "osteochondritis" implies inflammation, the lack of inflammatory cells in histological examination suggests a non-inflammatory cause. It is thought that repetitive microtrauma, which leads to microfractures and sometimes an interruption of blood supply to the subchondral bone, may cause subsequent localized loss of blood supply or alteration of growth.

Trauma, rather than avascular necrosis, is thought to cause osteochondritis dissecans in juveniles. In adults, trauma is thought to be the main or perhaps the sole cause, and may be endogenous, exogenous or both. The incidence of repetitive strain injury in young athletes is on the rise and accounts for a significant number of visits to primary care; this reinforces the theory that OCD may be associated with increased participation in sports and subsequent trauma. High-impact sports such as gymnastics, soccer, basketball, lacrosse, football, tennis, squash, baseball and weight lifting may put participants at a higher risk of OCD in stressed joints (knees, ankles and elbows).

Recent case reports suggest that some people may be genetically predisposed to OCD. Families with OCD may have mutations in the aggrecan gene. Studies in horses have implicated specific genetic defects.

OCD is a relatively rare disorder, with an estimated incidence of 15 to 30 cases per 100,000 persons per year. Widuchowski W "et al." found OCD to be the cause of articular cartilage defects in 2% of cases in a study of 25,124 knee arthroscopies. Although rare, OCD is noted as an important cause of joint pain in active adolescents. The juvenile form of the disease occurs in children with open growth plates, usually between the ages 5 and 15 years and occurs more commonly in males than females, with a ratio between 2:1 and 3:1. However, OCD has become more common among adolescent females as they become more active in sports. The adult form, which occurs in those who have reached skeletal maturity, is most commonly found in people 16 to 50 years old.

While OCD may affect any joint, the knee—specifically the medial femoral condyle in 75–85% of knee cases—tends to be the most commonly affected, and constitutes 75% of all cases. The elbow (specifically the capitulum of the humerus) is the second most affected joint with 6% of cases; the talar dome of the ankle represents 4% of cases. Less frequent locations include the patella, vertebrae, the femoral head, and the glenoid of the scapula.

A common cause of chondrocalcinosis is calcium pyrophosphate dihydrate crystal deposition disease (CPPD).

Excessive calcium (due to hypomagnesemia) has a potential relationship with chondrocalcinosis, and magnesium supplementation may reduce or alleviate symptoms. In some cases, arthritis from injury can cause chondrocalcinosis.

Other causes of chondrocalcinosis include:

- Hypercalcaemia, especially when caused by hyperparathyroidism

- Arthritis

- Gout

- Wilson disease

- Hemochromatosis

- Ochronosis

- Hypothyroidism

- Hyperoxalemia

- Acromegaly

- osteoarthritis

Hip dysplasia may be caused by a femur that does not fit correctly into the pelvic socket, or poorly developed muscles in the pelvic area. Large and giant breeds are most susceptible to hip dysplasia (possibly due to the body mass index (BMI) of the individual animal, though, many other breeds can suffer from it. The Orthopedic Foundation for Animals maintains a list of top 100 breeds affected.

To reduce pain, the animal will typically reduce its movement of that hip. This may be visible as "bunny hopping", where both legs move together, or less dynamic movement (running, jumping), or stiffness. Since the hip cannot move fully, the body compensates by adapting its use of the spine, often causing spinal, stifle (a dog's knee joint), or soft tissue problems to arise.

The causes of hip dysplasia are considered heritable, but new research conclusively suggests that environment also plays a role. To what degree the causality is genetic and what portion environmental is a topic of current debate. Neutering a dog, especially before the dog has reached an age of full developmental maturity, has been proven to almost double the chance he or she will develop hip dysplasia versus intact dogs or dogs that were neutered after reaching adulthood Other environmental influences include overweight condition, injury at a young age, overexertion on the hip joint at a young age, ligament tear at a young age, repetitive motion on forming joint (i.e. jogging with puppy under the age of 1 year). As current studies progress, greater information may help provide procedures to effectively reduce the occurrence of this condition.

The problem almost always appears by the time the dog is 18 months old. The defect can be anywhere from mild to severely crippling, and can eventually cause severe osteoarthritis.

It is most common in medium-large pure bred dogs, such as Newfoundlands, German Shepherd Dogs, retrievers (such as Labradors, Tollers, or Goldens), rottweilers and Mastiff, but also occurs in some smaller breeds such as spaniels and pugs.

Osteoarthritis, a common symptom associated with Canine Hip Dysplasia in German Shepherds ultimately results in pain and inflammation. The causes are from bone degradation in which the bone is less rigid, cartilage dissipates and structure of joints becomes weak.

Diet can have a major impact for German Shepherds that are exposed to Canine Hip Dysplasia. Incorporating Omega-3 fatty acids such as Docosahexaenoic acid(DHA) and Eicosapentaenoic acid(EPA) into the diet can result in improved symptoms of the disease. Omega 3 fatty acids can help decrease inflammation that occurs from osteoarthritis, as well as improvement in locomotion of dogs who have the disease. EPA and DHA can be supplemented into the diet through fish oils and in return is beneficial for reducing joint inflammation.

Glucosamine and Chondroitin sulfate are Nutraceuticals that can also be added into the diet to help treat osteoarthritis and its quality of life reducing effects. Both nutraceuticals help with improvement of cartilage, joint health and repairing of tissues. This inclusion will allow for a stronger support and reduced negative effects of osteoarthritis. Another nutrient that can help improve the structural support of the body in German Shepherds is Vitamin C. Vitamin C contributes to the building blocks of collagen that can help to strengthen the joints.

In medicine, chondropathy refers to a disease of the cartilage. It is frequently divided into 5 grades, with 0-2 defined as normal, and 3-4 defined as diseased.

Multiple epiphyseal dysplasia (MED) encompasses a spectrum of skeletal disorders, most of which are inherited in an autosomal dominant form. However, there is an autosomal recessive form.

Associated genes include COL9A1, COL9A2, COL9A3, COMP, and MATN3.

Types include:

Osteochondropathy refers to a disease ("-pathy") of the bone and cartilage.

However, it is more common to refer to these conditions as one of the following:

- chondropathy (disease of the cartilage)

- A bone disease is also called an "osteopathy", but because the term osteopathy is often used to describe a healthcare approach, use of the term can cause some confusion.

In humans, these conditions may be classified into three groups:

1. Spinal: Scheuermann's disease (of the interspinal joints) which is a curve in the thoracic spine.

2. Articular: Legg-Calvé-Perthes disease (or, avascular necrosis of the femoral head in the hip), Köhler's disease (of the tarsal navicular bone of the foot), Panner's disease (of the capitulum of the elbow), and Freiberg's infraction (of the second or third metatarsal of the foot and less frequently the first or fourth; sometimes called Freiberg's Infraction or Freiberg's disease)

3. Non-articular: This group includes Sever's disease (of the calcaneus, or heel), and Kienbock's disease of the hand, and other conditions not completely characteristic of the osteochondrosis, such as Osgood-Schlatter's disease (of the tibial tubercle) and Osteochondritis dissecans.

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 general, SCFE is caused by increased force applied across the epiphysis, or a decrease in the resistance within the physis to shearing. No single cause accounts for SCFEs, as several factors play a role in the development of a SCFE, particularly mechanical and endocrine (hormone-related) factors. Mechanical risk factors include obesity, coxa profunda, femoral or acetabular retroversion. Obesity is the most significant risk factor. In 65 percent of cases of SCFE, the person is over the 95th percentile for weight. Common misconception is heredity. Majority of cause is due to being overweight. Endocrine diseases also contribute, such as hypothyroidism, hypopituitarism, and renal osteodystrophy.

Chondrocalcinosis is calcification in hyaline and/or fibrocartilage. It can be seen on radiography.

Though articular cartilage damage is not life-threatening, it does strongly affect one's quality of life. Articular cartilage damage is often the cause of severe pain, knee swelling, substantial reduction in mobility and severe restrictions to one's activities. Over the last decades, however, research has focused on regenerating damaged joints.

These regenerative procedures are believed to delay osteoarthritis of injuries on the articular cartilage of the knee, by slowing down the degeneration of the joint compared to untreated damage. According to Mithoefer "et al." (2006), these articular cartilage repair procedures offer the best results when the intervention takes place in the early stages of the cartilage damage.

The most common cause is osteochondrosis, which is a disease of the joint cartilage, and specifically Osteochondritis dissecans (OCD or OD), the separation of a flap of cartilage from the joint surface as a result of avascular necrosis, which in turn arises from failed blood flow in the subchondral bone. Other common causes of elbow dysplasia included ununited anconeal process (UAP) and fractured or ununited medial coronoid process (FCP or FMCP).

In OCD, the normal change of cartilage to bone in the development of the joint fails or is delayed. The cartilage continues to grow and may split or become necrotic. The cause is uncertain, but possibly includes genetics, trauma, and nutrition (including excessive calcium and decreased Vitamin C intake). OCD lesions are found in the elbow at the medial epicondyle of the humerus. Specific conditions related to OCD include fragmentation of the medial coronoid process of the ulna (FMCP) and an ununited anconeal process of the ulna (UAP). All types of OCD of the elbow are most typically found in large breed dogs, with symptoms starting between the ages of 4 to 8 months. Males are affected twice as often as females. The disease often affects both elbows (30 to 70 percent of the time), and symptoms include intermittent lameness, joint swelling, and external rotation and abduction of the paw. Osteoarthritis will develop later in most cases.

UAP is caused by a separation from the ulna of the ossification center of the anconeal process. FMCP is caused by a failure of the coronoid process to unite with the ulna. OCD of the medial epicondyle of the humerus is caused by disturbed endochondral fusion of the epiphysis of the medial epicondyle with the distal end of the humerus, which may in turn be caused by avulsion of the epiphysis.

Eburnation describes a degenerative process of bone commonly found in patients with osteoarthritis or non-union of fractures. It is an ivory-like reaction of bone occurring at the site of cartilage erosion. Osteoarthritis is a degenerative disease of the joints characterized largely by central loss of cartilage and compensatory peripheral bone formation (osteophytes). Over time, as the cartilage wears away, bare, subchondral bone is revealed. Eburnation describes the bony sclerosis which occurs at the areas of cartilage loss.

Osteochondrodysplasia is a general term for a disorder of the development of bone and cartilage.

Pseudoachondroplasia is inherited in an autosomal dominant manner, though one case of a very rare autosomal recessive form has been documented. The offspring of affected individuals are at 50% risk of inheriting the mutant allele. Prenatal testing by molecular genetic examination is available if the disease-causing mutation has been identified in an affected family member (Hecht et al. 1995).

SCFE affects approximately 1-10 per 100,000 children. The incidence varies by geographic location, season of the year, and ethnicity. In eastern Japan, the incidence is 0.2 per 100,000 and in the northeastern U.S. it is about 10 per 100,000. Africans and Polynesians have higher rates of SCFE.

SCFEs are most common in adolescents 11–15 years of age, and affects boys more frequently than girls (male 2:1 female). It is strongly linked to obesity, and weight loss may decrease the risk. Other risk factors include: family history, endocrine disorders, radiation / chemotherapy, and mild trauma.

The left hip is more often affected than the right. Over half of cases may have involvement on both sides (bilateral).

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.

Most reported cases of DEH in the literature have been treated surgically, with excision of the mass, as well as by the correction

of any deformity, while preserving the integrity of the affected joint as much as possible.

Bone disease refers to the medical conditions which affect the bone.