History of Avascular Necrosis/Osteonecrosis 

All these years over 250 years and still no explanation on Osteonecrosis
Alexander Monro (19 September 1697 – 10 July 1767) was the founder of Edinburgh Medical School. To distinguish him as the first of three generations of physicians of the same name, he is known as primus.

1st described in 1738 by                   Alexander Munro : James Russell first described osteonecrosis in 1794, between 1829 and 1842 Jean Cruveilhier, the noted French anatomist, recorded gross deformation of the femoral head as a late complication of trauma, presumably as a result of vascular damage.Kragelund in 1886 and Konig in 1888 published more comprehensive reports on this subject.
Freund, however, is generally credited with the first detailed description of bilateral idiopathic aseptic necrosis of the femoral heads.The more recent works by Phemister and his associates have become classics on the etiology, pathogenesis, and treatment of this condition.
And a full description of the entity followed in 1930 by Phemister.

Since then many researchers have been trying to determine the pathogenesis of osteonecrosis, but this seems only to have succeeded in creating more questions.
Why does a disease with so many diverse etiologies seem to end in one common pathological entity?
Why do some patients enter this pathway to destruction while others remain unaffected? Is there some genetic predisposition we are yet to discover?
There is no animal model that is suitable for the study of the human form of osteonecrosis.
Many experiments conducted in steroid treated rabbits and rats have produced severe lipidemia, fatty livers, loss of body weight, severe malnutrition, decreased blood flow in the femoral head, fat embolism of multiple organs including bone, but no bone necrosis.
The treatment of osteonecrosis is considerably more successful at early stages of the disease. The early diagnosis of osteonecrosis depends upon the identification of individuals at risk.
Understanding the pathogenic factors leading to osteonecrosis enables the early investigation of at-risk individuals and facilitates prompt diagnosis

A number of hypotheses concerning the pathogenesis of osteonecrosis exist with the most commonly accepted hypothesis by Jones
Osteonecrosis is defined as cell death of bony tissue (marrow and mineralized tissue) due to ischaemia. It represents the final common pathway of several disease entities, which result in impaired blood supply to the bone tissue, causing necrosis of the bone.
Jones has demonstrated the final common pathway for non-traumatic osteonecrosis to be a coagulopathy within the intraosseous microcirculation leading to both intraosseous venous thrombosis and retrograde arterial occlusion. In contrast, a sick cell syndrome hypothesis has been proposed3 suggesting that there is little evidence to support the hypothesis that an interruption of the blood supply to bone is involved directly, rather, the pathologic features may result from a direct metabolic effect on the cells.
Bone as a tissue has a remarkable biological capacity to repair and reconstitute itself. Necrosis of the bony portions of a joint should not in any way affect the normal metabolism and functioning of the articular cartilage. The chondrocytes should initiate a series of cellular responses that ultimately “heal” the dead portion of the bone replacing it with new living bone. Therefore there is no reason to expect that the development of osteonecrosis should result in any discernible biological sequelae or clinical, but it does.
Idiopathic (40% of all reported cases) • Alcoholism (20% of all reported cases)

Antiphospholipid antibody syndrome

Dysbaric disorders
Photo of Alexander Munro

Endotoxic (Schwartzman) reactions secondary to systemic bacteraemia

Gaucher’s disease

Haemoglobinopathies including sickle cell disease

Hypercoagulable states

Protein C and Protein S deficiency

Antiphospholipid antibodies

Lupus anticoagulant


(Cushing’s syndrome)

Exogenous (37% of all reported cases)

Hypersensitivity reactions
Allograft organ rejection

Anaphylactic reactions
Inflammatory conditions
Systemic Lupus Ertythematosus

Inflammatory bowel disease
Metastatic carcinoma

Acute promylelocytic or lymphoid leukaemia

Radiation therapy

Femoral head dislocation

Intracapsular neck of femur fracture
Viral infections






Measles Vascular Anatomy
The circulation and arrangement of blood vessels in long bones have been disputed for many years. The most widely accepted patterns of intraosseous circulation are those proposed by Brooks9 in 1971. Bones have multiple arterial inlets and venous outlets, with long bones having four arterial inputs. The nutrient artery supplies blood to the diaphyseal cortex and marrow, the metaphyseal artery supplies to the metaphyseal cortex and marrow and the epiphyseal artery supplies the epiphysis. The periosteal arteries probably do not provide significant arterial input. Nutrient, metaphyseal and epiphyseal vessels enter the bone through foramina in the cortex and anastamose to supply marrow, cancellous bone, and cortex in a centrifugal direction. The epiphyses of long bones are covered with avascular joint cartilage, as a result, the dual blood supply (periosteal system and the nutrient, metaphyseal and epiphyseal system) does not exist in these areas. Instead, the functional end arteries comprise those ascending in the epiphyseal cancellous bone toward the articular surface. As a result, the epiphysis and the articular surfaces are particularly susceptible to circulatory insufficiency.
Although the role of an impaired blood supply to the femoral head in the pathogenesis of osteonecrosis has not been confirmed, Atsumi and Kuroki10 have found an abnormal blood supply in patients with corticosteroid induced osteonecrosis. They found that in most cases the blood supply of the superior retinacular arteries from the extraosseous site was impaired

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