Avascular Necrosis and the Blood Supply of the Femoral Head

Spencer, J. D.; Brookes, Murray

doi:10.1007/978-3-642-73644-5_19

Cited by 15 publications

(8 citation statements)

References 6 publications

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“…This view was later supported by Spencer following histological analysis of steroid-induced osteonecrosis of the femoral head. 23,24 Our study supports the views of these authors and suggests that the process of cell death may involve the activation of iNOS. This leads to locally toxic levels of NO in osteoblasts and osteocytes with death of these cells, further activation of inflammatory mediators and continuing damage to bone.…”

Section: Discussionsupporting

confidence: 89%

Apoptosis – a significant cause of bone cell death in osteonecrosis of the femoral head

Calder

Buttery

Revell

et al. 2004

The Journal of Bone and Joint Surgery. British volume

162

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Osteonecrosis of the femoral head usually affects young individuals and is responsible for up to 12% of total hip arthroplasties. The underlying pathophysiology of the death of the bone cells remains uncertain. We have investigated nitric oxide mediated apoptosis as a potential mechanism and found that steroid- and alcohol-induced osteonecrosis is accompanied by widespread apoptosis of osteoblasts and osteocytes. Certain drugs or their metabolites may have a direct cytotoxic effect on cancellous bone of the femoral head leading to apoptosis rather than purely necrosis.

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Section: Discussionsupporting

confidence: 89%

Apoptosis – a significant cause of bone cell death in osteonecrosis of the femoral head

Calder

Buttery

Revell

et al. 2004

The Journal of Bone and Joint Surgery. British volume

162

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“…It has long been known from studies on adults and children that systemic administration of corticosteroids can lead to FHN (5, 25). Possible causes include changes in vessel walls with a subsequent decrease in blood circulation, particularly in bones (26, 27).…”

Section: Discussionmentioning

confidence: 99%

The efficacy and safety of intraarticular corticosteroid therapy for coxitis in juvenile rheumatoid arthritis

Neidel¹,

Boehnke²,

Küster³

2002

Arthritis & Rheumatism

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Objective. To study the efficacy and safety of intraarticular triamcinolone hexacetonide (IATH) for the treatment of coxitis in patients with juvenile rheumatoid arthritis (JRA).Methods. Fifty consecutive patients with JRA and coxitis were studied prospectively. Forty-eight children received IATH in 67 arthritic hips. The remaining 2 children exhibited 3 cases of femoral head necrosis (FHN) at the initial assessment and were only followed up; both were receiving long-term systemic steroids. After a minimum of 2 years, the study was concluded with a final evaluation that included magnetic resonance imaging.Results. In 39 of 67 hip joints (58%), remission of the coxitis for a period of 2 years was obtained through a single administration of IATH, while another 12 hip joints showed remission of coxitis after repeated TH injections (total remission rate 76%). We observed 2 patients with FHN following IATH. Both of these children were receiving long-term systemic steroids. During the period between onset of JRA and screening assessment for this study, the children exhibited 2.4 cases of FHN per 100 patient-years, while 1.5 cases of FHN per 100 patient-years were observed between IATH treatment and final followup. All 5 observed cases of FHN occurred among the 20 children who received long-term systemic steroids, while no necrosis occurred in the 30 children who did not receive systemic corticosteroids (P ‫؍‬ 0.009 by Fisher's exact test).Conclusion. IATH for juvenile rheumatoid coxitis was an effective treatment that did not increase the rate of FHN. Systemic steroids, however (or their covariable, severity of JRA), may increase the risk of FHN in JRA.

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“…Intravascular occlusion by fibrin thrombi or embolic fat has been found in a large number of specimens of AVN, and microcirculatory thrombosis associated specifically with fat emboli has been described. [44][45][46][47][48] Regardless of the pathogenic mechanisms, ischemic necrosis of various etiologies eventually converges to a common and consistent structural compromise. 43 Osteocyte necrosis occurs after two to three hours of ischemia but histologic signs of osteocyte death are not apparent until 24-72 hours after the ischemic insult.…”

Section: Pathogenesis and Histopathology Of Avnmentioning

confidence: 99%

Corticosteroid‐associated avascular necrosis: dose relationships and early diagnosis

Aaron

Voisinet

Racine

et al. 2011

Annals of the New York Academy of Sciences

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Corticosteroids are the most common etiological factor in nontraumatic avascular necrosis (AVN) of bone, accounting for about 10% of arthroplasties performed annually in the United States. Evidence is conflicting on the relative importance of peak dose, daily dose, or cumulative dose, and most likely all three represent "high dose" corticosteroid administration and play a role in AVN. The etiology may be multifactorial with corticosteroids superimposed on genetic or pathological predispositions. Joint preservation depends upon early diagnosis and treatment before fracture of the subchondral trabeculae and joint incongruity. Early intervention depends upon identifying at-risk patients and quantifying their risk by understanding clinical and pathophysiological contributions to that risk. Our data and that of others suggest that a screening MRI of at-risk populations will permit detection of AVN at a prefracture stage when preservation of the joint is possible.

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Avascular Necrosis and the Blood Supply of the Femoral Head

Cited by 15 publications

References 6 publications

Apoptosis – a significant cause of bone cell death in osteonecrosis of the femoral head

Apoptosis – a significant cause of bone cell death in osteonecrosis of the femoral head

The efficacy and safety of intraarticular corticosteroid therapy for coxitis in juvenile rheumatoid arthritis

Corticosteroid‐associated avascular necrosis: dose relationships and early diagnosis

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