Bone necrosis

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Classification according to ICD-10
M87 Bone necrosis. V GT
M87.0 Idiopathic aseptic bone necrosis
M87.1 Drug bone necrosis
M87.2 Bone necrosis from previous trauma
M87.3 Other secondary bone necrosis
M87.8 Other bone necrosis (neck, head, ribs, trunk, skull, spine)
M87.9 Bone necrosis, unspecified
M90 * Osteopathies in diseases classified elsewhere
M90.3 * Bone necrosis in caisson disease
M90.4 * Bone necrosis due to hemoglobinopathy
M90.5 * Bone necrosis in other diseases classified elsewhere
ICD-10 online (WHO version 2019)

Bone necrosis or osteonecrosis (abbreviation ON ; English: osteonecrosis ; colloquially: bone infarction ) describes a tissue destruction ( infarction ) of the bone or a section of bone with death ( necrosis ) of the affected bone or section of bone, which is subsequently dismantled or remodeled. This creates a weakened point in the bone structure, whereby the extent of the infarct and the subsequent defect in the bone substance can be different.

All forms are based on an inadequate blood supply to the bone with insufficient supply of oxygen , nutrients and minerals. This is why the term avascular necrosis, English avascular osteonecrosis (AVN), is also in use.

If one only wants to exclude bone necrosis caused by infection, one speaks of aseptic bone necrosis (alternative designation aseptic osteonecrosis ; abbreviation: AON , AKN ; English aseptic osteonecrosis or aseptic bone necrosis ).


The substance defects of the bone can sometimes have no consequences or lead to severe, irreversible damage to joints and bones. The course is variable depending on the localization, the extent, the possibly existing risk factors, the age and the ultimate trigger. Both spontaneous healing and total joint destruction are known. In principle, all bones in the body can be affected. Both unilateral and bilateral (symmetrical) damage are known. Bone necrosis can occur at any age.

to form

Aseptic bone necrosis can be divided into different forms based on several factors. The divisions are made according to

  1. root cause
  2. Affected joint and bones
  3. Expression (severity)
Post-traumatic partial talar necrosis on magnetic resonance imaging. The practically signal-free (dark) zone in the talar roll is easy to recognize as a sign of sclerosis on the one hand and lack of contrast agent absorption / blood flow on the other.

root cause

According to the likely underlying cause of the osteonecrosis, the following types of osteonecrosis can be distinguished:

  • post-traumatic bone necrosis, from an injury.
  • septic bone necrosis, as part of or as a result of an infection .
  • aseptic bone necrosis, not caused by infection.

Risk factors

Certain diseases or external factors promote the occurrence of aseptic bone necrosis. These include:

Sickle cell disease
HbSC disease
Gaucher's disease
Systemic lupus erythematosus (SLE)
Environmental factors
Working in compressed air (tunneling, mining, building bridges in rivers)
Exposure to ionizing radiation . See under osteoradionecrosis .
Chemotherapy for acute leukemia ( ALL , AML ) and lymphoma ( NHL , Hodgkin lymphoma ). Osteochemonecrosis.
Systemic use of corticosteroids
Systemic use of bisphosphonates (only applies to aseptic bone necrosis of the lower jaw)
The medicine sirolimus

Classification according to the affected bone or joint

Table 1. Overview of the forms of aseptic bone necrosis by location
Affected bone section Name of the disease
German name Technical name German name Technical name
Body trunk
Vertebral bodies Vertebra (plana) Vertebral bodies Calvé's disease s. Vertebra plana
Ischium Os ischii Van Neck's disease
Pubic bone Pubis Pierson's disease
Upper extremity
Collarbone Clavicle middle end media end Friedrich's disease
Humerus Humerus (Elbow) Capitulum Panner's disease
Humerus Humerus (Elbow) Trochlea Hegemann's disease
Moon leg (hand) Lunate bone Kienböck's disease
Scaphoid bone (hand) Scaphoid bone Preiser's disease, Preiser's disease
Metacarpal bones Metacarpal bone Brains Dietrich's disease
Phalanx Phalanx medialis Base Thiemann's disease
Lower extremity
Thigh bone Femur Femoral head Head femoris Perthes disease , femoral head necrosis
Thigh bone Femur role Condyle Ahlbäck's disease , Ahlbåck's disease
Kneecap patella top Apex patellae Sinding-Larsen-Johansson disease
Shin Tibia Kneecap tendon attachment hump Tibial tuberosity Osgood-Schlatter disease , Osgood-Schlatter syndrome, Osgood-Schlatter disease
Shin Tibia Medial portion of the proximal epiphysis Blount's disease
Heel bone Calcaneus Apophysis Sever-Haglund disease, Haglund syndrome
Scaphoid bone (foot) in children and adolescents Os naviculare pedis Köhler's disease I, Köhler-Albau 's disease, Köhler's disease
Scaphoid (foot) in the adult Os naviculare pedis Müller-Weiss syndrome
Sesame bone (big toe) Os sesamoide hallucis Renander's disease
Metatarsal bones II – V Metatarsal II – V Brains Caput Köhler-Freiberg 's disease, Köhler's disease II

Severity (stages)

Figure 1a: Coronal MRI (STIR sequence) of an AON of the distal tibia . 13 year old child with ALL . Corresponds to stage ARCO 0-1

The staging of aseptic bone necrosis can be done according to the classification of the Association for Research of Circulation Osseous (ARCO). This combines a Japanese classification, which is based on the location of the necrosis, with a classification from Philadelphia (USA), which is primarily based on the size of the necrosis.

The ARCO classification is best investigated for aseptic bone necrosis of the femoral head (femoral head necrosis) and relates primarily to lesions of the epiphysis , i.e. bone sections near the joints that can lead to joint wear when the cartilage breaks into the necrosis area. Bone necrosis of the diaphysis and metaphysis can at best be divided into the ARCO stages.

Image 1b: Sagittal MRI (T1 spin echo sequence) of an AON of the distal tibia. 13 year old child with ALL . Corresponds to stage ARCO 0-1
Stadium ARCO 0

In the initial stage, no pathological changes can be seen in conventional X-rays. In rare cases, a subtle loosening of the fine bone structure ( trabecula ) can be seen in the affected area: however, the extent of this loosening is usually so small that it cannot be reliably recognized. In the magnetic resonance imaging (MRI) is an image at this stage analogous to bone marrow edema (KMÖ, transient osteoporosis , bone marrow edema , BME) to detect. Using the short tau inversion recovery (STIR) recording sequence, a signal hyperintensity (bright flashing in the gray-scale magnetic resonance image) is determined (compare Fig. 1a and 2 light edges). A reliable differentiation between the principally reversible picture of a BME / BME and the stage ARCO I of aseptic bone necrosis is not possible by means of the magnetic resonance tomogram.

ARCO stage 1

Reversible early stage (MRI positive / reactive edge zone)

ARCO stage 2

Irreversible early stage (X-ray positive)

Image 2: Coronal MRI (STIR sequence) of multiple AON in both tibiae and femora . 13 year old child with ALL . Corresponds to stage ARCO 3
ARCO stage 3

Transitional stage (subchondral fractures)

ARCO stage 4

Late stage (calotte impression)

ARCO stage 5

Late stage (secondary osteoarthritis)

ARCO stage 6

Late stage (joint destruction)


None of the symptoms are specific to this disease, as many other diseases could also be responsible for the symptoms. Pain over the section of bone or joint affected by the bone necrosis is common. The pain can appear suddenly. However, it also develops gradually increasing in intensity. Radiation in adjacent unaffected skeletal sections is possible. Typically, the pain occurs at rest and intensifies when the affected bone section or joint is stressed. However, pain can only be present when the affected bone or joint section is stressed, which then also occurs at rest as the disease progresses. The pain can often only appear weeks, sometimes months after the infarction in the bone.

Restrictions in movement of the affected bone or joint are less common than pain. In addition, they typically occur later than the pain in the course of the disease and are usually already signs of advanced damage. But this is not necessarily the case; Restrictions of movement can also occur parallel to pain. In children - especially small children - the sequence of symptoms can sometimes be reversed. The affected toddler is noticed for the first time by limping or lack of movement of the affected leg or arm.



The diagnosis of aseptic bone necrosis includes the physical examination of the likely affected joint section with functional tests of the joints and bones as well as imaging procedures. As a rule, abnormal bone changes are preceded by loads or injuries of various types. This is different with bone necrosis, the symptoms develop gradually. Conventional imaging methods such as x-rays or sonography only provide indications of the diagnosis if the first bone remodeling or bone destruction has occurred. When using magnetic resonance imaging with contrast media, a diagnosis can also be made if there is only typical bone remodeling activity.

Differential diagnosis

Other diseases are to be distinguished from bone necrosis:

Bone cyst
Bone tumor
Inflammation of the bone ( osteitis ) and inflammation of the bone marrow ( osteomyelitis )


Therapy depends on the stage and includes:

  • mechanical relief (e.g. forearm crutches),
  • Femoral head relief bore,
  • Conversion osteotomies and (hip) endoprostheses.
  • In the initial stage, hyperbaric oxygen therapy can be used either alongside or alone. This has a particularly positive effect on the painful bone marrow edema.

The treatment of bone necrosis is also based on the aforementioned prognostic factors: the larger and closer to the joint, the more likely surgical treatment is required. If there is damage to or even destruction of the joint surfaces in the context of bone necrosis close to the joint, an operative intervention can usually not be avoided. Depending on the extent of the bone necrosis, drilling ( Pridie drilling ), bone transplants (with and without cartilage) and, if the severity of the disease is severe, artificial joint replacements ( endoprostheses ) are carried out. Conservative treatment consists of weight relief and rest. However, spontaneous healing has also been described.

Web links

Commons : Aseptic Bone Necrosis  - Collection of Pictures, Videos and Audio Files

Individual evidence

  1. CM Aguilar, LD Neumayr u. a .: Clinical evaluation of avascular necrosis in patients with sickle cell disease: Children's Hospital Oakland Hip Evaluation Scale - a modification of the Harris Hip Score. In: Archives of physical medicine and rehabilitation. Volume 86, Number 7, July 2005, pp. 1369-1375, ISSN  0003-9993 . PMID 16003666 .
  2. ^ RL Nagel, ME Fabry, MH Steinberg: The paradox of hemoglobin SC disease. In: Blood Reviews . Volume 17, Number 3, September 2003, pp. 167-178, ISSN  0268-960X . PMID 12818227 . (Review).
  3. ^ SW Rodrigue, DI Rosenthal u. a .: Risk factors for osteonecrosis in patients with type 1 Gaucher's disease. In: Clinical Orthopedics and Related Research . Number 362, May 1999, pp. 201-207, ISSN  0009-921X . PMID 10335299 .
  4. SN Oh, WH Jee et al. a .: Osteonecrosis in patients with systemic lupus erythematosus: MR imaging and scintigraphic evaluation. In: Clinical imaging. Volume 28, Number 4, 2004 Jul-Aug, pp. 305-309, ISSN  0899-7071 . doi : 10.1016 / S0899-7071 (03) 00192-X . PMID 15246483 .
  5. EP child Wall, JR Nellen, DR mirror Hoff: Aseptic necrosis in compressed air tunnel workers using current OSHA decompression schedules. In: Journal of occupational medicine. Volume 24, Number 10, October 1982, pp. 741-745, ISSN  0096-1736 . PMID 7143120 .
  6. K. Miyanishi, Y. Kamo et al. a .: Risk factors for dysbaric osteonecrosis. In: Rheumatology . Volume 45, Number 7, July 2006, pp. 855-858, ISSN  1462-0324 . doi: 10.1093 / rheumatology / kel013 . PMID 16436490 .
  7. U. Höller, S. Hoecht u. a .: Osteoradionecrosis after radiation therapy of gynecological tumors. In: Radiation Therapy and Oncology . Volume 177, Number 6, June 2001, pp. 291-295, ISSN  0179-7158 . PMID 11446317 .
  8. EJ Karimova, SN Rai et al. a .: MRI of knee osteonecrosis in children with leukemia and lymphoma: Part 1, observer agreement. In: American Journal of Roentgenology . Volume 186, Number 2, February 2006, pp. 470-476, ISSN  0361-803X . doi: 10.2214 / AJR.04.1598 . PMID 16423955 .
  9. D. van Schaardenburg, HR van den Brink, HJ Wieringa: Short-term steroid therapy, sometimes with long-term sequelae. In: Nederlands tijdschrift voor geneeskunde. Volume 145, Number 37, September 2001, pp. 1769-1773, ISSN  0028-2162 . PMID 11582637 . (Review).
  10. J. Steinhagen, W. Rüther: Aseptic bone necrosis after steroid therapy. In: Journal of Rheumatology. Volume 63, Number 3, June 2004, pp. 242-243, ISSN  0340-1855 . doi: 10.1007 / s00393-004-0556-9 . PMID 15224230 .
  11. ^ TJ O'Brien, GR Mack: Multifocal osteonecrosis after short-term high-dose corticosteroid therapy. A case report. In: Clinical orthopedics and related research. Number 279, June 1992, pp. 176-179, ISSN  0009-921X . PMID 1600653 .
  12. E. Merigo, M. Manfredi u. a .: Jaw bone necrosis without previous dental extractions associated with the use of bisphosphonates (pamidronate and zoledronate): a four-case report. In: Journal of Oral Pathology & Medicine . Volume 34, Number 10, November 2005, pp. 613-617, ISSN  0904-2512 . doi: 10.1111 / j.1600-0714.2005.00351.x . PMID 16202082 .
  13. S. Bhandari, J. Eris: Drug points: Premature osteonecrosis and sirolimus treatment in renal transplantation. In: BMJ. Volume 323, Number 7314, September 2001, p. 665, ISSN  0959-8138 . PMID 11566830 . PMC 55926 (free full text).
  14. P. Ueblacker, AB Imhoff: Overview osteonecroses. In: Arthroscopy. May 2003; 16, pp. 102-103.
  15. KM Baumgarten, MA Mont u. a .: Atraumatic osteonecrosis of the patella. In: Clinical orthopedics and related research. Number 383, February 2001, pp. 191-196, ISSN  0009-921X . PMID 11210953 .
  16. a b J. Reumont et al.: HBO therapy for aseptic knee joint bone necrosis . In: Trauma and Occupational Disease . tape 6 , no. 1 , April 1, 2004, p. 35-40 , doi : 10.1007 / s10039-003-0826-9 .