Is avascular necrosis of the femoral head the result of inhibition of angiogenesis?

Smith, Donna M.

doi:10.1016/s0306-9877(97)90067-0

Cited by 50 publications

(33 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition to affecting healing, nicotine in smoking may cause increased vasoconstriction in bone, leading to ischemic states that may underlie the pathophysiology of osteonecrosis. [23][24][25] Obesity was also found associated with ONJ risk in this group of cancer patients. While it is currently unclear what is the pathway that might cause an obese person to develop ONJ, several hypotheses can be proposed.…”

Section: Discussionmentioning

confidence: 59%

Zoledronate, Smoking, and Obesity Are Strong Risk Factors for Osteonecrosis of the Jaw: A Case-Control Study

Wessel

Dodson

Zavras

2008

Journal of Oral and Maxillofacial Surgery

175

121

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 59%

Zoledronate, Smoking, and Obesity Are Strong Risk Factors for Osteonecrosis of the Jaw: A Case-Control Study

Wessel

Dodson

Zavras

2008

Journal of Oral and Maxillofacial Surgery

175

121

View full text Add to dashboard Cite

show abstract

“…The aetiology of ON in SLE patients is probably multifactorial with several risk factors having been implicated [3][4][5][6][7]. Sella et al [22] found that digital vasculitis was a risk factor for the development of ON.…”

Section: Discussionmentioning

confidence: 99%

“…The final common pathway for the development of ON is ischaemia, which may be related to direct blood vessel injury (post-traumatic necrosis), altered fat metabolism and fat emboli, intravascular coagulation, elevated intracortical pressure, inhibition of angiogenesis, intramedullary haemorrhage, mechanical stress or primary cell death [3][4][5][6][7][8][9][10][11].…”

mentioning

confidence: 99%

The use of joint-specific and whole-body MRI in osteonecrosis: a study in patients with juvenile systemic lupus erythematosus

Castro¹,

Lederman²,

Terreri³

et al. 2011

BJR

View full text Add to dashboard Cite

Objective: This study aimed to estimate the prevalence of osteonecrosis (ON) in juvenile systemic lupus erythematosus (SLE) patients using joint-specific and wholebody MRI; to explore risk factors that are associated with the development of ON; and to evaluate prospectively patients 1 year after initial imaging. Method: Within a 2 year period, we studied 40 juvenile SLE patients (aged 8-18 years) with a history of steroid use of more than 3 months duration. Risk factors including disease activity, corticosteroid use, vasculitis, Raynaud's phenomenon and lipid profile were evaluated. All patients underwent MRI of the hips, knees and ankles using jointspecific MRI. Whole-body STIR (short tau inversion recovery) MRI was performed in all patients with ON lesions. Results: Osteonecrosis was identified in 7 patients (17.5 %) upon joint-specific MRI. Whole-body STIR MRI detected ON in 6 of these 7 patients. There was no significant difference between the ON and non-ON groups in the risk factors studied. One patient had pre-existing symptomatic ON. At 1 year follow-up, the ON lesions had resolved in one patient, remained stable in four and decreased in size in two. No asymptomatic patients with ON developed clinical manifestations. Conclusion: Whole-body STIR MRI may be useful in detecting ON lesions in juvenile SLE patients but larger studies are needed to define its role.

show abstract

“…Generalization between four-legged ANFH animal models and the human disease and collapse process must be cautious. Glucocorticoids and interferon(-alpha) could also inhibit the angiogenesis probably by a mechanism involving the reduction of the proteolytic activity with the synthesis of PAI-1 (Smith 1997).…”

Section: Endothelium Dysfunction and Thrombosismentioning

confidence: 99%

Avascular Necrosis of the Femoral Head: Vascular Hypotheses

et al. 2006

View full text Add to dashboard Cite

Vascular hypotheses provide compelling pathogenic mechanisms for the etiology of avascular necrosis of the femoral head (ANFH). A decrease in local blood flow of the femoral head has been postulated to be the cause of the disease. Several studies in human and animal models of ANFH have shown microvascular thrombosis. Endothelial cell damage could be followed by abnormal blood coagulation and thrombus formation with any resulting degeneration distal to the site of vascular occlusion. Other studies suggest that thrombophilia, particularly impaired fibrinolysis, plays a potential role in thrombus formation in ANFH. Reduction in shear stress due to decreased blood flow could lead to apoptosis of endothelial cells, which can ultimately contribute to plaque erosion and thrombus formation. Dysregulation of endothelial cell activating factors and stimulators of angiogenesis or repair processes could also affect the progression and outcome of ANFH. Likewise, regional endothelium dysfunction (RED), referred to as a potential defect in endothelial cells located in the feeding vessels of the femoral head itself, may also have a crucial role in the pathogenesis of ANFH. Molecular gene analysis of regional endothelial cells could also help to determine potential pathways important in the pathogenesis of ANFH.

show abstract

Is avascular necrosis of the femoral head the result of inhibition of angiogenesis?

Cited by 50 publications

References 23 publications

Zoledronate, Smoking, and Obesity Are Strong Risk Factors for Osteonecrosis of the Jaw: A Case-Control Study

Zoledronate, Smoking, and Obesity Are Strong Risk Factors for Osteonecrosis of the Jaw: A Case-Control Study

The use of joint-specific and whole-body MRI in osteonecrosis: a study in patients with juvenile systemic lupus erythematosus

Avascular Necrosis of the Femoral Head: Vascular Hypotheses

Contact Info

Product

Resources

About