All This History  and  it’s Still  a Mystery 

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 

To gain as much experience as possible Monro lodged in the house of an apothecary and visited patients with him, and he also attended lectures by Mr. Whiston and Mr Hawksby on experimental philosophy. He made dissections of the human body and of various animals, though his career was nearly cut short owing to a scratched hand being infected by the suppurated lung of a phthisical subject. Monro took an active part in discussions, and in one of his papers first sketched his “Account of the Bones in General”. Before he left London he sent home to his father some of his anatomical specimens, and received the encouraging reply that on his return to Edinburgh, if he continued as he had begun, Mr Drummond would resign his share of the professorship of anatomy in his favour.


We had 

James Russell

He described osteonecrosis in 1794, 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.

What is Osteonecrosis

Osteonecrosis comes from the Greek words for bone (osteo) and death (necrosis), a concept first put forward by Hippocrates in antiquity. Osteonecrosis term is used to describe cellular death in bone tissue most commonly related to an interruption of its blood supply and the subsequent destruction of its architectural structure. Many different terms have been coined to describe Osteonecrosis, such as avascular necrosis, aseptic necrosis, ischemic necrosis , and osteochondritis dissecans , all of which are commonly used in the medical literature.
In 1794, the first modern-day description of Osteonecrosis disorder was made by James Russell. At that time, infectious etiologies were the primary pathogenic agent. It was only in 1888 that the term aseptic necrosis of the bone was first used to describe what we now know as osteonecrosis.
Most osteonecrosis cases are related to traumatic interruption of the blood supply to the bone; however, nontraumatic cases related to systemic disorders remain a diagnostic challenge, especially in defining the precise cause of bone death.
Different Forms of Osteonecrosis

There seem to be two distinct forms of this condition:
(a) a secondary form, caused by a number of well-recognized risk factors, working alone or in concert, and
(b) an idiopathic, or primary form, for which no identifiable risk factors have been identified
Cause of Osteonecrosis
When osteonecrosis of the femoral head for example,follows a fracture or a dislocation of the hip, there is a clear association between the mechanical interruption of the blood supply and the subsequent development of osteonecrosis.
Vascular Occlusion – Trauma is the most common cause of vascular occlusion with subsequent osteonecrosis, and the likelihood of developing this is directly proportional to the following:
Extent of fracture displacement

Impingement on the vascular supply of the bone

Available collateral circulation of the affected site

Intravascular Coagulation – The intraosseous microcirculation is as susceptible to a prothrombotic state as any other part of the circulation. 
Taking Virchow’s triad as an example, this may be the result of one or a combination of factors, including endothelial damage, circulatory stasis, or a hypercoagulable state. 
Endothelial damage may be related to trauma, atherosclerotic lesions, or autoimmune inflammatory connective tissue disorders that may affect the endothelial lining.
Pregnancy and

Pregnancy and Osteonecrosis

Osteonecrosis of the femoral head is a rare manifestation of pregnancy, especially in healthy women who have no known risk factors for the development of this disorder. The cause of osteonecrosis in these patients is unknown, but different hypotheses have postulated the possibility of amniotic fluid emboli, a relative hypercoagulable state, excessive mechanical strain, and an increase in endogenous steroid production. To date, the largest case series was described by Montell and associates. In this case series, 13 women developed hip pain late in the second or in the third trimester of their pregnancy. In general, these women tended to have a small body habitus, and during their pregnancy, they had gained excessive weight, indicating that this may have a pathogenic role in the development of osteonecrosis. All the affected women had involvement of their left hip, and 4 of them had bilateral involvement. As a rule, a high index of suspicion is required by the clinician to prevent the misdiagnosis or the delayed diagnosis of osteonecrosis in these patients.
Diagnosis of Osteonecrosis

Osteonecrosis following a hip fracture is described as prolonged pain even after the successful surgical treatment of the orthopedic injury. The pain is described as a deep aching or boring pain localized to the groin and at times radiating down the thigh and into the knee region. Radiographs often are normal early, and a high suspicion is required to make the diagnosis by the use of a bone scan or MRI. In patients with atraumatic osteonecrosis of the hip, the earliest stages of the disease process are often asymptomatic.
Treatment and Medical Therapy for osteonecrosis

Therapy for osteonecrosis is based on the stage of the disease as well as the age of the patient. In patients who have, according to the Steinberg classification system, stage I lesions, conservative measures may be undertaken early, such as pain control and limited weight bearing, although the disease itself continues to progress if the lesion is in the weight-bearing portion of the femoral head.

How is it some like myself get it from trauma to knee 

While others get it many joints with no trauma 
Will the mystery ever be solved? 

More on the History later …..Stay Tuned. 

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