Avascular necrosis

Avascular necrosis (AVN), also called osteonecrosis or bone infarction, is death of bone tissue due to interruption of the blood supply.[1] Early on, there may be no symptoms.[1] Gradually joint pain may develop which may limit the ability to move.[1] Complications may include collapse of the bone or nearby joint surface.[1]

Risk factors include bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids.[1] The condition may also occur without any clear reason.[1] The most commonly affected bone is the femur.[1] Other relatively common sites include the upper arm bone, knee, shoulder, and ankle.[1] Diagnosis is typically by medical imaging such as X-ray, CT scan, or MRI.[1] Rarely biopsy may be used.[1]

Treatments may include medication, not walking on the affected leg, stretching, and surgery.[1] Most of the time surgery is eventually required and may include core decompression, osteotomy, bone grafts, or joint replacement.[1] About 15,000 cases occur per year in the United States.[4] People 30 to 50 years old are most commonly affected.[3] Males are more commonly affected than females.[4]

Avascular necrosis
Other namesOsteonecrosis,[1] bone infarction,[2] aseptic necrosis,[1] ischemic bone necrosis[1]
Head of femur avascular necrosis
Head of the femur showing a flap of cartilage due to avascular necrosis (osteochondritis dissecans). Specimen removed during total hip replacement surgery.
SpecialtyOrthopedics
SymptomsJoint pain, decreased ability to move[1]
ComplicationsOsteoarthritis[1]
Usual onsetGradual[1]
Risk factorsBone fractures, joint dislocations, alcoholism, high dose steroids[1]
Diagnostic methodMedical imaging, biopsy[1]
Differential diagnosisOsteopetrosis, rheumatoid arthritis, Legg-Calve-Perthes syndrome, sickle cell disease[3]
TreatmentMedication, not walking on the affected leg, stretching, surgery[1]
Frequency~15,000 per year (US)[4]

Signs and symptoms

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.[5] 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),[6][7] knees,[8][9] shoulders,[6][7] ankles and the jaw.[10]

Causes

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high dose steroids.[1] Other risk factors include radiation therapy, chemotherapy, and organ transplantation.[1] Osteonecrosis is also associated with cancer, lupus, sickle cell disease, HIV infection, Gaucher’s disease, and Caisson disease.[1] The condition may also occur without any clear reason.[1]

Bisphosphonates are associated with osteonecrosis of the mandible.[11] Prolonged, repeated exposure to high pressures (as experienced by commercial and military divers) has been linked to AVN, though the relationship is not well understood.

Pathophysiology

The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours.[2] Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days.[2]

Upon reperfusion, repair of bone occurs in 2 phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris.[2] Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts.[2] Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue.[2]

Diagnosis

OCD Knee WalterReed-1
Front X-ray of right knee of an adolescent (epiphyseal plates are open): arrows point to avascular necrosis and developing osteochondritis dissecans in the outer medial condyle of femur

In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools.[12][13]

X-ray images of avascular necrosis in the early stages usually appear normal. In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia.[2] The necrotic bone itself does not show increased radiographic opacity, as dead bone cannot undergo bone resorption which is carried out by living osteoclasts.[2] Late radiographic signs also include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts.

Osteonecrosis humerus 1

Radiography of total avascular necrosis of right humeral head. Woman of 81 years with diabetes of long evolution.

Osteonecrosis femur 1

Radiography of avascular necrosis of left femoral head. Man of 45 years with AIDS.

Osteonecrosis femur 2img

Nuclear magnetic resonance of avascular necrosis of left femoral head. Man of 45 years with AIDS.

Intravertebral vacuum cleft sign

The intravertebral vacuum cleft sign (at white arrow) is a sign of avascular necrosis. Avascular necrosis of a vertebral body after a vertebral compression fracture is called Kümmel's disease.[14]

Types

When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot,/ primarily in children.

Treatment

A variety of methods may be used to treat[5] the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and short life spans (of the hip joints). THRs are an effective means of treatment in the older population; however, in younger people they may wear out before the end of a person's life.

Other techniques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head.[15] Bisphosphonates which reduce the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN.[16]

Core decompression

Other treatments include core decompression, where internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head.[17] A 2016 Cochrane review found no clear improvement between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease.[18]

Progression of the disease could possibly be halted by transplanting nucleated cells from bone marrow into avascular necrosis lesions after core decompression, although much further research is needed to establish this technique.[19][20]

Prognosis

The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding takes place after an injury as well as during normal growth.[15] Normally, bone continuously breaks down and rebuilds—old bone is resorbed and replaced with new bone. The process keeps the skeleton strong and helps it to maintain a balance of minerals.[15] In the course of avascular necrosis, however, the healing process is usually ineffective and the bone tissues break down faster than the body can repair them. If left untreated, the disease progresses, the bone collapses,[21] and the joint surface breaks down, leading to pain and arthritis.[1]

Epidemiology

Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. When it occurs in children at the femoral head, it is known as Legg-Calvé-Perthes syndrome.[22]

Society and culture

David Martin82 Brett Favre4-Edit2
Favre with the Packers in 2007

Cases of avascular necrosis have been identified in a few high profile athletes. It abruptly ended the career of American football running-back Bo Jackson in 1991. Doctors discovered Jackson to have lost all of the cartilage supporting his hip while he was undergoing tests following a hip-injury he had on the field during a 1991 NFL Playoff game.[23] Avascular necrosis of the hip was also identified in a routine medical check-up on quarterback Brett Favre following his trade to the Green Bay Packers in 1991.[24] However, Favre would go on to have a long career at the Packers.

Another high profile athlete was American road racing cyclist Floyd Landis,[25] winner of the 2006 Tour De France, the title being subsequently stripped from his record by cycling's governing bodies after his blood samples tested positive for banned substances.[26] During that tour, Landis was allowed cortisone shots to help manage his ailment, despite cortisone also being a banned substance in professional cycling at the time.[27]

References

  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z "Questions and Answers about Osteonecrosis (Avascular Necrosis)". NIAMS. October 2015. Archived from the original on 9 August 2017. This article incorporates text from this source, which is in the public domain.
  2. ^ a b c d e f g h Khan AN, Al-Salman MJ, Chandramohan M, MacDonald S, Hutchinson CE. "Bone Infarct". eMedicine Specialties. Archived from the original on 4 March 2010.
  3. ^ a b "Osteonecrosis". NORD (National Organization for Rare Disorders). 2009. Archived from the original on 19 February 2017. Retrieved 8 August 2017.
  4. ^ a b c Ferri, Fred F. (2017). Ferri's Clinical Advisor 2018 E-Book: 5 Books in 1. Elsevier Health Sciences. p. 166. ISBN 9780323529570. Archived from the original on 9 August 2017.
  5. ^ a b National Institute of Arthritis and Musculoskeletal and Skin Diseases (March 2006). "Osteonecrosis". Food and Drug Administration. Archived from the original on 23 May 2009. Retrieved 25 May 2009.
  6. ^ a b Chapman C, Mattern C, Levine WN (November 2004). "Arthroscopically assisted core decompression of the proximal humerus for avascular necrosis". Arthroscopy. 20 (9): 1003–6. doi:10.1016/j.arthro.2004.07.003. PMID 15525936.
  7. ^ a b Mansat P, Huser L, Mansat M, Bellumore Y, Rongières M, Bonnevialle P (March 2005). "Shoulder arthroplasty for atraumatic avascular necrosis of the humeral head: nineteen shoulders followed up for a mean of seven years". Journal of Shoulder and Elbow Surgery. 14 (2): 114–20. doi:10.1016/j.jse.2004.06.019. PMID 15789002.
  8. ^ Jacobs MA, Loeb PE, Hungerford DS (August 1989). "Core decompression of the distal femur for avascular necrosis of the knee". The Journal of Bone and Joint Surgery. British Volume. 71 (4): 583–7. PMID 2768301.
  9. ^ Bergman NR, Rand JA (December 1991). "Total knee arthroplasty in osteonecrosis" (Free full text). Clinical Orthopaedics and Related Research (273): 77–82. doi:10.1097/00003086-199112000-00011. PMID 1959290.
  10. ^ Baykul T, Aydin MA, Nasir S (November 2004). "Avascular necrosis of the mandibular condyle causing fibrous ankylosis of the temporomandibular joint in sickle cell anemia". The Journal of Craniofacial Surgery. 15 (6): 1052–6. doi:10.1097/00001665-200411000-00035. PMID 15547404.
  11. ^ Dannemann C, Grätz KW, Riener MO, Zwahlen RA (April 2007). "Jaw osteonecrosis related to bisphosphonate therapy: a severe secondary disorder". Bone. 40 (4): 828–34. doi:10.1016/j.bone.2006.11.023. PMID 17236837.
  12. ^ Maillefert JF, Toubeau M, Piroth C, Piroth L, Brunotte F, Tavernier C (June 1997). "Bone scintigraphy equipped with a pinhole collimator for diagnosis of avascular necrosis of the femoral head". Clinical Rheumatology. 16 (4): 372–7. doi:10.1007/BF02242454. PMID 9259251.
  13. ^ Bluemke DA, Zerhouni EA (August 1996). "MRI of avascular necrosis of bone". Topics in Magnetic Resonance Imaging. 8 (4): 231–46. doi:10.1097/00002142-199608000-00003. PMID 8870181.
  14. ^ Freedman BA, Heller JG (2009). "Kummel disease: a not-so-rare complication of osteoporotic vertebral compression fractures". Journal of the American Board of Family Medicine. 22 (1): 75–8. doi:10.3122/jabfm.2009.01.080100. PMID 19124637.
  15. ^ a b c de Bernard B (15 November 1989). "Calcium Metabolism and Bone Mineralization". In Hall BK (ed.). Bone. CRC Press. pp. 74–. ISBN 978-0-936923-24-6.
  16. ^ Agarwala S, Jain D, Joshi VR, Sule A (March 2005). "Efficacy of alendronate, a bisphosphonate, in the treatment of AVN of the hip. A prospective open-label study". Rheumatology. 44 (3): 352–9. doi:10.1093/rheumatology/keh481. PMID 15572396.
  17. ^ Judet H, Gilbert A (May 2001). "Long-term results of free vascularized fibular grafting for femoral head necrosis" (Free full text). Clinical Orthopaedics and Related Research. 386 (386): 114–9. doi:10.1097/00003086-200105000-00015. PMID 11347824.
  18. ^ Martí-Carvajal, Arturo J.; Solà, Ivan; Agreda-Pérez, Luis H. (10 July 2014). "Treatment for avascular necrosis of bone in people with sickle cell disease". The Cochrane Database of Systematic Reviews (7): CD004344. doi:10.1002/14651858.CD004344.pub5. ISSN 1469-493X. PMID 25009086.
  19. ^ Gangji V, Hauzeur JP (March 2005). "Treatment of osteonecrosis of the femoral head with implantation of autologous bone-marrow cells. Surgical technique". The Journal of Bone and Joint Surgery. American Volume. 87 Suppl 1 (Pt 1): 106–12. doi:10.2106/JBJS.D.02662. PMID 15743852. Archived from the original on 14 February 2009. Retrieved 27 April 2010.
  20. ^ Lieberman JR, Conduah A, Urist MR (December 2004). "Treatment of osteonecrosis of the femoral head with core decompression and human bone morphogenetic protein". Clinical Orthopaedics and Related Research. 429 (429): 139–45. doi:10.1097/01.blo.0000150312.53937.6f. PMID 15577478.
  21. ^ DiGiovanni CW, Patel A, Calfee R, Nickisch F (April 2007). "Osteonecrosis in the foot". The Journal of the American Academy of Orthopaedic Surgeons. 15 (4): 208–17. doi:10.5435/00124635-200704000-00004. PMID 17426292.
  22. ^ Gross GW, Articolo GA, Bowen JR (1999). "Legg-Calve-Perthes Disease: Imaging Evaluation and Management". Seminars in Musculoskeletal Radiology. 3 (4): 379–391. doi:10.1055/s-2008-1080081. PMID 11388931.
  23. ^ Altman LK. "Jackson's Case Is Dividing The Doctors". The New York Times.
  24. ^ "What, his hip? Favre reveals he has avascular necrosis". JS Online. 27 September 2006. Archived from the original on 27 September 2006.
  25. ^ "What He's Been Pedaling". The New York Times. 16 July 2006.
  26. ^ "Landis Tests Positive; Title is a total complete loss". Chicago Tribune. 5 August 2006.
  27. ^ Fotheringham A (24 July 2006). "Cycling: Landis the Tour king celebrates a triumph of survival". The Independent. London. Archived from the original on 6 August 2006. Retrieved 28 July 2006. (subscription required)

External links

External resources
AVN

AVN may refer to:

AVN (magazine), Adult Video News, a trade magazine for the pornographic industry

AVN Award, award issued by AVN magazine

AVN Adult Entertainment Expo, AVN magazine annual convention

AVN (Albania), a television network

Australian Vaccination Network (now Australian Vaccination-risks Network), an Australian anti-vaccination lobby group

Avascular necrosis, a medical condition

Atrioventricular node, a special region of conducting tissue in the heart

AVN, ICAO code for Air Vanuatu

AVN, National Rail code for Avonmouth railway station, UK

FK AVN, former name of FK ASK (1923-1970), a former Latvian football club

Audio-Visual Navigation, a feature of some motor vehicles

An abbreviation for aviation

Alien vs Ninja (2010), a Japanese film

Agencia Venezolana de Noticias, Venezuelan state news agency

Avination, a virtual world simulation game modeled after Second Life.

Crescent sign

In radiology, the crescent sign is a finding on conventional radiographs that is associated with avascular necrosis. It usually occurs later in the disease, in stage III of the four-stage Ficat classification system. It appears as a curved subchondral radiolucent line that is often found on the proximal femoral or humeral head. Usually, this sign indicates a high likelihood of collapse of the affected bone. The crescent sign may be best seen in an abducted (frog-legged) position.The crescent sign is caused by the necrotic and repair processes that occur during avascular necrosis. Osteosclerosis occurs at a margin where new bone is placed over dead trabeculae. When the trabeculae experience stress leading to microfractures and collapse, the crescent sign appears.The crescent sign may be seen with other bone diseases, such as shear fractures.

Dieterich's disease

Dieterich's disease, also known as avascular necrosis of the metacarpal head, is an extremely rare condition characterized by temporary or permanent loss of blood supply to the metacarpal head of the metacarpal bone, resulting in loss of bone tissue. The five metacarpal bones are long bones located between the carpals of the wrist and phalanges of the fingers. Collectively, the metacarpals are referred to as the "metacarpus."

In the case of Dieterich's disease, some but not all metacarpal heads are affected. Onset of this disease can be attributed to steroid usage, systemic lupus erythematosus, or trauma. In some cases, it is randomly-occurring.Dieterich's disease can be diagnosed through medical screening or blood testing. Physicians may also diagnose Dieterich's disease by taking a history of the patient's symptoms.

Some treatment options include medication, surgery, or therapy.

Dysbaric osteonecrosis

Dysbaric osteonecrosis or DON is a form of avascular necrosis where there is death of a portion of the bone that is thought to be caused by nitrogen embolism (blockage of the blood vessels by a bubble of nitrogen coming out of solution) in divers. Although the definitive pathologic process is poorly understood, there are several hypotheses:

Intra- or extravascular nitrogen in bones, "nitrogen embolism".

Osmotic gas effects due to intramedullary pressure effects.

fat embolism

hemoconcentration and increased coagulability.

Freiberg disease

Freiberg disease, also known as a Freiberg infraction, is a form of avascular necrosis in the metatarsal bone of the foot. It generally develops in the second metatarsal, but can occur in any metatarsal. Physical stress causes multiple tiny fractures where the middle of the metatarsal meets the growth plate. These fractures impair blood flow to the end of the metatarsal resulting in the death of bone cells (osteonecrosis). It is an uncommon condition, occurring most often in young women, athletes, and those with abnormally long metatarsals. Approximately 80% of those diagnosed are women.Initial treatment is generally 4–6 weeks of limited activity, often with crutches or orthotics. In rare cases, surgery is necessary to reduce the bone mass of the metatarsal.

The condition was first described by Dr. Alfred H. Freiberg in 1914. He initially thought the condition was caused by acute physical trauma, which is why it was initially called an infraction.

Georg Axhausen

Georg Axhausen (24 March 1877, in Landsberg an der Warthe – 19 January 1960, in Berlin) was a German oral and maxillofacial surgeon.

He studied medicine at Kaiser-Wilhelms-Akademie (Pépinière) in Berlin, receiving his doctorate in 1901. Later on, he worked in the surgical clinic at Kiel under Heinrich Helferich (1904–06) and in the institute of pathology at Friedrichshain Hospital in Berlin under Ludwig Pick (1907/08). From 1909 to 1924 he worked in the surgical clinic at the Berlin-Charité.In 1908 he obtained his habilitation, and four years later became an associate professor at Berlin. In 1928 he was named a full professor and director of the dental institute at the Charité.He specialized in pathology and surgery of bones and joints, being known for his pioneer studies of bone grafting and necrosis of the epiphysis. He is credited with introducing the term "aseptic necrosis", which is now referred to as avascular necrosis. The eponymous "Axhausen operation" is a procedure for closure of cleft palate.

Hip dislocation

A hip dislocation a disruption of the joint between the femur and pelvis. Specifically it is when the ball–shaped head of the femur comes out of the cup–shaped acetabulum of the pelvis. Symptoms typically include pain and an inability move the hip. Complications may include avascular necrosis of the hip, injury to the sciatic nerve, or arthritis.Dislocations are typically due to significant trauma such as a motor vehicle collision or fall from height. Often there are also other associated injuries. Diagnosis is generally confirmed by plain X-rays. Hip dislocations can also occur follow a hip replacement or from a developmental abnormality known as hip dysplasia.Efforts to prevent the condition include wearing a seat-belt. Emergency treatment generally follows advanced trauma life support. This is generally followed by reduction of the hip carried out under procedural sedation. A CT scan is recommended following reduction to rule out complications. Surgery is required if the joint cannot be reduced otherwise. Often a few months are required for healing to occur.Hip dislocations are uncommon. Males are affected more often than females. Traumatic dislocations occurs most commonly in those 16- to 40-year old. The condition was first described in the medical press in the early 1800s.

Hip pain

Pain in the hip is the experience of pain in the muscles or joints in the hip/ pelvic region, a condition commonly arising from any of a number of factors. Sometimes it is closely associated with lower back pain.

Infarction

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct

(from the Latin infarctus, "stuffed into").

Kienböck's disease

Kienböck's disease is a disorder of the wrist. It is named for Dr. Robert Kienböck, a radiologist in Vienna, Austria who described osteomalacia of the lunate in 1910.It is breakdown of the lunate bone, a carpal bone in the wrist that articulates with the radius in the forearm. Specifically, Kienböck's disease is another name for avascular necrosis (death and fracture of bone tissue due to interruption of blood supply) with fragmentation and collapse of the lunate. This has classically been attributed to arterial disruption, but may also occur after events that produce venous congestion with elevated interosseous pressure.

Legg–Calvé–Perthes disease

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 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. 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. Bilateral Perthes, which means both hips are affected, should always be investigated to rule out multiple epiphyseal dysplasia.

Limb infarction

A limb infarction is an area of tissue death of an arm or leg. It may cause skeletal muscle infarction, avascular necrosis of bones, or necrosis of a part of or an entire limb.

Medial circumflex femoral artery

The medial circumflex femoral artery (internal circumflex artery, medial femoral circumflex artery) is an artery in the upper thigh that helps supply blood to the neck of the femur. Damage to the artery following a femoral neck fracture may lead to avascular necrosis (ischemic) of the femoral neck/head.

Megadeath

Megadeath (or megacorpse) is one million human deaths, usually caused by a nuclear explosion. The term was used by scientists and thinkers who strategized likely outcomes of all-out nuclear warfare.

Osteochondritis dissecans

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.

Preiser disease

Preiser disease, or (idiopathic) avascular necrosis of the scaphoid, is a rare condition where ischemia and necrosis of the scaphoid bone occurs without previous fracture. It is thought to be caused by repetitive microtrauma or side effects of drugs (e.g., steroids or chemotherapy) in conjunction with existing defective vascular supply to the proximal pole of the scaphoid. MRI coupled with CT and X-ray are the methods of choice for diagnosis.

Preiser's disease is initially treated by immobilising the wrist with a cast. However, in most cases the avascular scaphoid will start to collapse leading to degeneration within the wrist joints. This often requires surgical intervention to prevent the progression of arthris. Two commonly performed procedures are:

1. Proximal row carpectomy (PRC), which involves removing the first row of the carpal bones, i.e. the scaphoid, lunate and triquetrum. The wrist is immobilised in a cast for six weeks after the surgery and then physiotherapy is started.

2. Scaphoid excision and 4-corner fusion, which is a procedure consisting of the removal of the scaphoid and fixation of the remaining wrist bones with a plate (called a "spider plate") or wires in order to provide stability. The plate usually is left inside the patient's wrist, while the wires (usually K-wires) have to be removed in a second surgery. This procedure of partial wrist fusion allows for limited wrist movement, whereas total wrist fusion immobilizes the wrist permanently. Following surgery it can take several months for affected patients to regain strength.

Unfortunately both of these operations are salvage procedures and movements in the wrist will be significantly reduced.

Scaphoid fracture

A scaphoid fracture is a break of the scaphoid bone in the wrist. Symptoms generally includes pain at the base of the thumb which is worse with use of the hand. The anatomic snuffbox is generally tender and swelling may occur. Complications may include nonunion of the fracture, avascular necrosis, and arthritis.Scaphoid fractures are most commonly caused by a fall on an outstretched hand. Diagnosis is generally based on examination and medical imaging. Some fractures may not be visible on plain X-rays. In such cases a person may be casted with repeat X-rays in two weeks or an MRI or bone scan may be done.The fracture may be preventable by using wrist guards during certain activities. In those in whom the fracture remains well aligned a cast is generally sufficient. If the fracture is displaced then surgery is generally recommended. Healing may take up to six months. It is the most common wrist bone fracture. Males are affected more often than females.

Steve Arsenault

Stephen Arsenault (born 6 September 1988) is a Canadian ice sledge hockey player.

Arsenault was born in Hamilton, Ontario to Joe and Jill Arsenault. He has avascular necrosis of the femoral head.He began his sledge hockey career in 2004 in Edmonton with the Paralympic Sports Association Dogs. He also played for the Edmonton Impact sledge hockey team. He took a hiatus from sledge hockey from 2007 to 2010, a timespan in which his mother died and his father was seriously injured in a workplace accident which resulted in amputation of a leg.With the Canada men's national ice sledge hockey team, He won a gold medal at the IPC Ice Sledge Hockey World Championships in 2011, 2013, 2017 and a silver in 2012. He also competed in the Sochi 2014 Winter Paralympics with the Canadian national team, winning a bronze in the sledge hockey tournament.He resides in Stony Plain, Alberta. He is also a personal trainer.

The Balance "Ambulance" Tour

The Balance Tour was a concert tour by hard rock band Van Halen promoting their album Balance. It was dubbed the "Ambulance" Tour by Eddie Van Halen due to his hip injury caused by avascular necrosis, and his brother, drummer Alex Van Halen wearing a neck brace for most of the tour, due to rupturing three vertebrae in his neck. Consequently, Eddie was a lot more static on stage. This would be the group's last tour with Sammy Hagar on vocals until 2004, when he briefly rejoined the band for a tour. The opening night in Pensacola, and a combination of footage from the two Toronto shows were broadcast on Pay-Per-View.

The band had not performed any shows as an opening act in over a decade, but on this tour they opened for veteran act Bon Jovi for several sold-out dates at stadiums due to Bon Jovi's huge appeal overseas. Collective Soul, Skid Row, Our Lady Peace, and Brother Cane opened for Van Halen on the North American legs of the tour.

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