Osteochondroma is a type of benign tumor that consists of cartilage and bone.and it is a benign capped-cartilage outgrowth, connected to bone by a stalk.

It is the most frequently observed neoplasm of the skeleton. It is also called a “bone spur”.

They often occur at joints, most commonly the shoulder or the knee.

On most occasions the tumors grow outward from the legs or arms. However, very few cases have been reported with the bone spur growing inward. One such occasion was in Oct 2004, in which a patient was diagnosed with an osteochondroma growning from the rib inward. Puncturing the diaphragm wall and requiring immediate surgery to remove the seventh rib. This allowed the surgeons to alleviate pressure and the chance to remove the large mass of coagulated blood from around the heart. The surgery was performed by Dr. Goerstky at the Children’s Hospital of the King’s Daughters, in Norfolk,VA.

Osteochondroma is a benign tumor that contains both bone and cartilage and usually occurs near the end of a long bone. This tumor, one of the most common benign bone tumors, takes the form of a cartilage-capped bony spur or outgrowth on the surface of the bone. It is sometimes referred to as osteocartilaginous exostosis.

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Osteochondritis dissecans (pronounced /??stio?k?n’dra?t?s ‘d?s??kænz/, often abbreviated to OCD) is a form of osteochondritis affecting the subchondral bone of joints, with harmful side effects on articular cartilage.[1] Physical trauma, avascular necrosis and other stresses may affect the subchondral bone, causing loss of support for adjacent cartilaginous structures.[2] This can lead to separation of a joint fragment from the underlying bone (hence the label dissecans which here means disintegrate), sometimes with formation of loose bodies.[3][4]

Skeletally immature adolescents (whose growth plates have not closed) are more likely to have OCD, which occurs in 15 to 30 people per 100,000 annually.[5] OCD usually causes pain and swelling of the affected joint, catching and locking on movement and a restriction in the range of motion. However, these symptoms characterize many knee conditions and may have many other causes, making OCD relatively hard to diagnose clinically.[6] A diagnosis can be confirmed by X-rays, CT or magnetic resonance imaging (MRI) scans.[7] OCD is classified via diagnostic imaging showing disease progression in stages (I, II, III or IV).[8] After diagnosis the lesion may be treated, depending on its stage, with a form of articular cartilage repair.[9][10]

König[11] coined the term osteochondritis dissecans in 1887, describing it as an inflammation of the bone-cartilage interface.[12] Many other conditions used to be confused with OCD, 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.[13] OCD has been studied in other species of animals; dogs, especially the German Shepherd, are the most commonly affected.[14]

OCD is classified by the progression of the disease in stages. There are two main staging classifications used; one is determined by MRI diagnostic imaging while the other is determined arthroscopically. Regardless of the representation used, this staging represents the pathological conditions associated with the natural progression of osteochondritis dissecans.[15]

While the arthroscopic classification of osteochondral lesions is considered standard, the Anderson MRI staging is the main form of staging used in this article.[8] Stages I and II are stable lesions. Stages III and IV describe unstable lesions in which not only the cartilage is breached, but synovial fluid exists between the fragment and underlying bone.

In osteochondritis dissecans, fragments of cartilage or bone have become loose within a joint, leading to pain and inflammation. These fragments are sometimes referred to as “joint mice”[18] due to a squeaking sound produced by bending the joint. Specifically, 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, though it can also affect other joints such as the ankle or the elbow.[19]

Patients with OCD complain of activity-related pain that develops gradually. Individual complaints usually consist of mechanical symptoms, including pain, swelling, catching, locking, and “giving way”; the primary presenting symptom may be a restriction in the range of movement.[15] Symptoms typically present themselves within the initial weeks of stage I; however, the onset of stage II occurs within months and offers little time for diagnosis. Just as unfortunate is the rapid progression of the disease beyond stage II, as OCD lesions quickly move from stable cysts or fissures to unstable fragments. This progression is compounded when non-specific symptoms (caused by similar injuries such as sprains and strains) lead to a delayed definitive diagnosis.[6]

Physical examination typically reveals an effusion, tenderness, and crepitus. The tenderness may diffuse initially, but often changes 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 of 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.[13]

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Osteoarthritis (OA, also known as degenerative arthritis, degenerative joint disease), is a clinical syndrome in which low-grade inflammation results in pain in the joints, caused by abnormal wearing of the cartilage that covers and acts as a cushion inside joints and destruction or decrease of synovial fluid that lubricates those joints. As the bone surfaces become less well protected by cartilage, sub-chondral bone can eventually be exposed leading to a proliferation of ivory-like, dense, reactive bone in central areas of cartilage loss, a process called eburnation.[1] The patient increasingly experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax.[2] OA is the most common form of arthritis,[2] and the leading cause of chronic disability in the United States.[3]

“Osteoarthritis” is derived from the Greek word “osteo”, meaning “of the bone”, “arthro”, meaning “joint”, and “itis”, meaning inflammation, although many sufferers have little or no inflammation. A common misconception is that OA is due solely to wear and tear, since OA typically is not present in younger people. However, while age is correlated with OA incidence, this correlation merely illustrates that OA is a process that takes time to develop. There is usually an underlying cause for OA, in which case it is described as secondary OA. If no underlying cause can be identified it is described as primary OA. “Degenerative arthritis” is often used as a synonym for OA, but the latter involves both degenerative and regenerative changes.

OA affects nearly 21 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will show symptoms.[4] In the United States, hospitalizations for osteoarthritis soared from about 322,000 in 1993 to 735,000 in 2006.[5]

The main symptom is acute pain, causing loss of ability and often stiffness. “Pain” is generally described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called “crepitus”) when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid and cold weather increases the pain in many patients.[6][7]

OA commonly affects the hands, feet, spine, and the large weight bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.

In smaller joints, such as at the fingers, hard bony enlargements, called Heberden’s nodes (on the distal interphalangeal joints) and/or Bouchard’s nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen.

OA is the most common cause of water on the knee, an accumulation of excess fluid in or around the knee joint. [8]

Although it commonly arises from trauma, osteoarthritis often affects multiple members of the same family, suggesting that there is hereditary susceptibility to this condition. A number of studies have shown that there is a greater prevalence of the disease between siblings and especially identical twins, indicating a hereditary basis [9]. Up to 60% of OA cases are thought to result from genetic factors. Researchers are also investigating the possibility of allergies, infections, or fungi as a cause.

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Osgood-Schlatter disease or syndrome (also known as tibial tubercle apophyseal traction injury) is an inflammation of the growth plate at the tibial tuberosity, and is one of a group of conditions collectively called osteochondroses. The condition is named after the American surgeon Robert Bayley Osgood (1873–1956) and the Swiss surgeon Carl Schlatter (1864–1934), who independently described the disease in 1903.[1][2][3]

The condition occurs in active boys and girls aged 11-15[4], coinciding with periods of growth spurts. It occurs more frequently in boys than in girls, with reports of a male-to-female ratio ranging from 3:1 to as high as 7:1. It has been suggested the difference is related to a greater participation by boys in sports and risk activities than by girls.

The condition is usually self-limiting and is caused by stress on the patellar tendon that attaches the quadriceps muscle at the front of the thigh to the tibial tuberosity. Following an adolescent growth spurt, repeated stress from contraction of the quadriceps is transmitted through the patellar tendon to the immature tibial tuberosity. This can cause multiple subacute avulsion fractures along with inflammation of the tendon, leading to excess bone growth in the tuberosity and producing a visible lump.

The syndrome may develop without trauma or other apparent cause. But some studies report up to 50% of patients give a history of precipitating trauma.

In a retrospective study of adolescents, young athletes actively participating in sports showed a frequency of 21% reporting the syndrome compared with only 4.5% of age-matched nonathletic controls.[5]

Sinding–Larsen–Johansson Syndrome is an analogous condition involving the patellar tendon and the lower margin of the patella bone, instead of the upper margin of the tibia.

- Knee pain is usually the presenting symptom that occurs during activities such as running, jumping, squatting, and ascending or descending stairs. The pain can be reproduced by extending the knee against resistance, stressing the quadriceps, or squattin

Diagnosis is made clinically,[7] and treatment is conservative with rest and simple pain reduction measures of ice packs and if required paracetamol (acetaminophen) or ibuprofen. The condition usually resolves in a few months, with a study of young athletes revealing a requirement of complete training cessation for 3 months (on average) and gradual resumption of full training by 7 months.[5]

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Orotic aciduria refers to an excessive excretion of orotic acid in urine.

Its hereditary form, an autosomal recessive disorder,[1] can be caused by a deficiency in the enzyme UMPS,[2] a bifunctional protein that includes the enzyme activities of orotate phosphoribosyltransferase and orotidine 5′-phosphate decarboxylase.

It can also arise secondary to blockage of the urea cycle, particularly ornithine transcarbamylase deficiency.

In addition to the characteristic excessive orotic acid in the urine, patients typically have megaloblastic anemia which cannot be cured by administration of vitamin B12 or folic acid.[3]

It also can cause inhibition of RNA and DNA synthesis and failure to thrive. This can lead to mental and physical retardation.

Administration of cytidine monophosphate and uridine monophosphate reduces urinary orotic acid and the anemia.

Administration of uridine, which is converted to UMP, will bypass the metabolic block and provide the body with a source of pyrimidine.

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Optic atrophy is the loss of some or most of the fibers of the optic nerve.[1] In medicine, “atrophy” usually means “shrunken but capable of regrowth”, so some argue that “optic atrophy” as a pathological term is somewhat misleading and use “optic neuropathy” instead.

The optic nerve is part of the brain and has no capability for regeneration. Hence, there can be no recovery from optic atrophy and the term may refer to serious or mild, but always irreversible visual loss due to damage to the optic nerve. Three types of degeneration are seen: transsynaptic, anterograde, and retrograde.

There may be symptoms associated with loss of vision (although there may be a particular difficulty with colour vision).

Bilateral Optic Atrophy: Loss of vision and discoloration of discs in both eyes. This is a genetic form and can be inherited.

Optic atrophy can be congenital or acquired.

If congenital, it is usually hereditary with an onset of deterioration in childhood and may be accompanied by nystagmus. Leber’s Hereditary Optic Neuropathy, (LHON) or Leber Optic Atrophy is hereditary, but typically has its onset in 20-30 year old males. This is due to a mutation of the mitochondrial genome and hence is passed exclusively through the mothers. Dominant optic atrophy or Kjer’s optic neuropathy has autosomal dominant inheritance. It usually presents in early childhood. There are numerous less common genetically related syndromes.[2]

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Ondine’s Curse, also called congenital central hypoventilation syndrome (CCHS) or primary alveolar hypoventilation, is a respiratory disorder that is fatal if untreated. Persons afflicted with Ondine’s curse classically suffer from respiratory arrest during sleep.

Persons who have CCHS get it at birth, or develop it due to severe neurological trauma/damage to the brainstem. The diagnosis may be delayed because of variations in the severity of the manifestations or lack of awareness in the medical community, particularly in milder cases. (Chin, 2006).[1]

This very rare and serious form of central sleep apnea involves an inborn failure of autonomic control of breathing. About 1 in 200,000 live born children have the condition. In 2006, there were only about 200 known cases worldwide. In all cases, episodes of apnea occur in sleep, but in a few patients, at the most severe end of the spectrum, apnea also occurs while awake.

A person’s gender or race is not a determining factor when dealing with susceptibility to CCHS. Males and females are both affected equally and a person’s ethnicity, as of this point, has been not been coincided a variable to the disease.[2]

Ondine’s curse is associated with respiratory arrests during sleep and, with incomplete penetrance, neuroblastoma (tumors of the sympathetic ganglia), Hirschsprung disease (partial agenesis of the enteric nervous system), dysphagia (difficulty swallowing), anomalies of the pupilla, etc.

Ondine’s curse is exhibited typically as a congenital disorder, but in rare circumstances, can also result from severe brain or spinal trauma (such as after an automobile accident, stroke, or as a complication of neurosurgery).

Medical investigation of patients with this syndrome has led to a deeper understanding of how the body and brain regulate breathing on a molecular level. PHOX2B can be associated with this condition.[3][4][5][6] This homeobox gene is important for the normal development of the autonomic nervous system.

The disease used to be classified as a “neurocristopathy”,[7][8] or disease of the neural crest because part of the autonomic nervous system (such as sympathetic ganglia) derives from the neural crest. However, this denomination should be dropped because essential neurons of the autonomic nervous system, including those that underlie the defining symptom of the disease (respiratory arrests), are derived from the neural tube (the medulla), not from the neural crest.

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Olivopontocerebellar atrophy (OPCA) is a term used to define neuronal degeneration in the cerebellum, pontine nuclei, and inferior olivary nucleus. The use of the term has changed considerably in recent years due to the progressing knowledge of the genetic bases of the disease.

The term was originally coined by Joseph Jules Dejerine and André Thomas.[2][3]

The term “olivopontocerebellar atrophy” currently applies only to two hereditary disorders whose genetic basis remains unknown:

In the past, the term “olivopontocerebellar atrophy” extended to both the sporadic (non-hereditary) cases of the disease, which have been currently reclassified as a form of multiple system atrophy[4], as well as to four hereditary types, which have been currently reclassified as four different forms of spinocerebellar ataxia:

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Obesity is a condition in which excess body fat has accumulated to such an extent that health may be negatively affected.[1] It is commonly defined as a body mass index (BMI) of 30 kg/m2 or higher.[1] This distinguishes it from being overweight as defined by a BMI of 25 kg/m2 or higher.[1]

Excessive body weight is associated with various diseases, particularly cardiovascular diseases, diabetes mellitus type 2, obstructive sleep apnea, certain types of cancer, and osteoarthritis.[2][3] As a result, obesity has been found to reduce life expectancy.[3] The primary treatment for obesity is dieting and physical exercise. If this fails, anti-obesity drugs and (in severe cases) bariatric surgery can be tried.[2][4] A combination of excessive caloric intake, lack of physical activity, and genetic susceptibility is thought to explain most cases of obesity, with a limited number of cases due solely to genetics, medical reasons, or psychiatric illness.

As obesity is one of the leading preventable causes of death worldwide and with rates of adult and childhood obesity increasing, authorities view it as one of the most serious public health problem of the 21st century.[5] Obesity is often stigmatized in the modern Western world. It has, however been perceived as a symbol of wealth and fertility at other times in history and still is in many parts of Africa.[3][6]

Obesity, in absolute terms, is an increase of body adipose tissue (fat tissue) mass. In a practical setting it is difficult to determine this directly. Therefore, obesity is typically assessed by BMI (body mass index) and in terms of its distribution via the waist circumference.[7] In addition, the presence of obesity needs to be evaluated in the context of other risk factors such as medical conditions that could influence the risk of complications.[2]

Body mass index or BMI is a simple and widely used method for estimating body fat mass.[8] BMI was developed in the 19th century by the Belgian statistician and anthropometrist Adolphe Quetelet.[9] BMI is an accurate reflection of body fat percentage in the majority of the adult population. It is less accurate in people such as body builders and pregnant women in whom body composition is affected.[2]

BMI is calculated by dividing the subject’s mass by the square of his or her height, typically expressed either in metric or US “Customary” units:

where lb is the subject’s weight in pounds and in is the subject’s height in inches.

The most commonly used definitions, established by the WHO in 1997 and published in 2000, provide the values listed in the table at right.[1]

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Obsessive-compulsive disorder (OCD) is a mental disorder most commonly characterized by intrusive, repetitive thoughts resulting in compulsive behaviors and mental acts that the person feels driven to perform, according to rules that must be applied rigidly, aimed at preventing some imagined dreaded event; however, these behaviors or mental acts are not connected to the imagined dreaded event.

According to the current epidemiological data, OCD is the fourth most common mental disorder and OCD is considered “nearly as common as asthma and diabetes mellitus.”[1] In the United States, 1 in 50 adults have OCD.[2] In severe cases, it affects a person’s ability to function in everyday activities. The disorder often has a serious impact on the sufferer’s (and his/her family’s) quality of life. Also, the psychological self-awareness of the irrationality of the disorder can be painful. For people with severe OCD, it may take several hours a day to carry out the compulsive acts.

Experts[who?] believe OCD may be related to levels of a normal chemical in the brain called serotonin. When the proper flow of serotonin is blocked, the brain’s “alarm system” overreacts. Danger messages are mistakenly triggered. Instead of the brain filtering out these unnecessary thoughts, the brain dwells on them—and the person repeatedly experiences unrealistic fears and doubts.

The phrase “obsessive-compulsive” has become part of the English lexicon, and is often used in an informal or caricatured manner to describe someone who is meticulous, perfectionistic, absorbed in a cause, or otherwise fixated on something or someone.[3] Although these signs are often present in OCD, a person who exhibits them does not necessarily have OCD, and may instead have obsessive-compulsive personality disorder (OCPD) or some other condition.

To be diagnosed with OCD, a person must have obsessions and/or compulsions, according to the DSM-IV-TR diagnostic criteria. The Quick Reference to the diagnostic criteria from DSM-IV-TR (2000)[4] states six characteristics of obsessions and compulsions:

In addition to these criteria, at some point during the course of the disorder, the individual must realize that his/her obsessions or compulsions are unreasonable or excessive. Moreover, the obsessions or compulsions must be time-consuming (taking up more than one hour per day), cause distress, or cause impairment in social, occupational, or school functioning.[4] OCD often causes feelings similar to those of depression.

OCD manifests in a variety of forms. Studies have placed the prevalence between one and three percent, although the prevalence of clinically recognized OCD is much lower, suggesting that many individuals with the disorder may not be diagnosed.[5] The fact that many individuals do not seek treatment may be due in part to stigma associated with OCD. Another reason for not seeking treatment is that many sufferers of OCD do not realize that they have the condition.

The typical OCD sufferer performs tasks (or compulsions) to seek relief from obsession-related anxiety. To others, these tasks may appear odd and unnecessary. But for the sufferer, such tasks can feel critically important, and must be performed in particular ways to ward off dire consequences and to stop the stress from building up. Examples of these tasks are repeatedly checking that one’s parked car has been locked before leaving it, turning lights on and off a set number of times before exiting a room, repeatedly washing hands at regular intervals throughout the day, touching objects a certain number of times before leaving a room, or walking in a certain routine way. Physical symptoms may include those brought on from anxieties and unwanted thoughts, as well as tics or Parkinson’s disease-like symptoms: rigidity, tremor, jerking arm movements, or involuntary movements of the limbs.

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