Osteonecrosis: Current perspectives on pathogenesis and treatment

doi:10.1016/S0049-0172(05)80026-5

Seminars in Arthritis and Rheumatism

Volume 23, Issue 1, August 1993, Pages 47-69

https://doi.org/10.1016/S0049-0172(05)80026-5 Get rights and content

Nontraumatic osteonecrosis results from impairment of circulation to the affected bone. The femoral head is affected most frequently. The underlying cause for the circulatory defect in osteonecrosis varies and may involve both local and systemic changes. Steroid use, alcohol consumption, pancreatitis, and lipid disorders appear to lead to bone death either by development of fat emboli in the microcirculature surrounding the affected bone or by fatty infiltration of the marrow. Decompression syndrome results from the presence of gaseous emboli in the microcirculature. In Legg-Calvé-Perthes disease other associated features are present such as short stature, suboptimal growth velocity, and/or hormonal imbalances, and it is likely that osteonecrosis may be secondary to systemic abnormalities, although specific factors have not been identified. Other frequently suggested pathogenic factors that play a role in the development of osteonecrosis include increased intraosseous pressures, the presence of cytotoxic cellular factors, intravascular coagulation, venous stasis, and the hyperviscosity syndrome. Some investigators have attempted, without success, to find a common etiology for all cases of osteonecrosis. In addition, patients have developed osteonecrosis without any known risk factors; this syndrome has been coined idiopathic avascular necrosis. In advanced stages of femoral head osteonecrosis, total hip arthroplasty appears to be the best therapeutic modality, particularly in older individuals.

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Avascular necrosis (AVN) is a devastating complication often necessitating arthroplasty, particularly common in systemic lupus erythematosus (SLE). Limited research exists on arthroplasty trends since new steroid-sparing agents. We analyzed trends and characteristics associated with AVN and AVN-related arthroplasties among SLE and RA hospitalizations using two decades of data from the U.S. National Inpatient Sample (NIS).
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We report a breakpoint in rising SLE-AVN after 2011, which may relate to newer steroid-sparing therapies (i.e., belimumab). AVN-associated arthroplasties decreased in SLE and RA. Fewer AVN-associated arthroplasties were noted for Black patients and those with Medicaid, indicating potential disparities. Further research should examine treatment differences impacting AVN and arthroplasty rates.
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Forty-eight patients with 53 lesions were consecutively treated with femur SBRT from May 2017 to June 2022. The Kaplan-Meier method and Cox proportional hazard models were used to characterize time-to-event endpoints and associations between baseline factors and clinical outcomes, respectively. Local control and locoregional control were defined as the absence of tumor progression within the radiation treatment field or within the treated femur, respectively.
Most patients had Eastern Cooperative Oncology Group performance status 0 to 1 (90%), prostate (52%) or breast/lung (17%) cancer, and 1 to 3 lesions (100%), including 29 proximal and 5 distal. Fifty-seven percent of the lesions were treated with concurrent systemic therapy. Median planning target volume was 49.1 cc (range, 6.6-387 cc). Planning target volume V100 (%) was 99% (range, 90-100). Fractionation included 18 to 20 Gy/1F, 27 to 30 Gy/3F, and 28.5-40 Gy/5F. Forty-two percent had Mirels score ≥7 and most (94%) did not have extraosseous extension. Acute toxicities included grade 1 fatigue (15%), pain flare (7.5%), nausea (3.8%), and decreased blood counts (1.9%). Late toxicities included fracture (1.9%) at 1.5 years and osteonecrosis (4%) from dose of 40 Gy in 5F and 30 Gy in 5F (after prior 30 Gy/10F). One patient (2%) required fixation postradiation for progressive pain. With median follow-up 19.4 months, 1- and 2-year rates of local control were 94% and 89%, locoregional control was 83% and 67%, progression-free survival were 56% and 25%, and overall survival were 91% and 73%. Fifty percent of local regional recurrence events occurred within 5 cm of gross tumor volume.
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Avascular necrosis of the scaphoid, often referred to as Preiser’s disease, is little known despite the scaphoid being the second most frequently involved location in avascular pathology of the carpal bones after the lunate (Kienböck’s disease). Nonetheless, very few cases have been reported in the medical literature over the last century. Its pathophysiology is not completely elucidated although the unique vascularization of the scaphoid and several risk factors seem to be recurrently incriminated. Two new classifications based on modern imaging have appeared in the last decade and are now considered essential supplements to Herbert and Lanzetta’s original radiographic classification. Because of the lack of formal treatment guidelines, a wide range of different treatments have been explored over time, contributing to the confusion around this pathology. Adding to this confusion, are the numerous terms used to designate the condition and lack of knowledge concerning its pathophysiology, risk factors, clinical and radiographic presentation. The aim of this review is therefore to explore and clarify Preiser’s disease in terms of history, terminology, pathophysiology, clinical considerations and imaging and to propose a simple updated treatment algorithm based on the results provided by a thorough review of literature (53 publications, 170 patients) since Georg Preiser’s original and controversial description in 1910.
La nécrose avasculaire du scaphoïde, souvent appelée "maladie de Preiser", est une maladie peu connue bien que le scaphoïde soit le siège le plus fréquemment impliqué dans l’ostéonécrose des os du carpe après le lunatum (maladie de Kienböck). Très peu de cas ont été rapportés dans la littérature médicale. Sa physiopathologie n'est pas complètement élucidée bien que la vascularisation spécifique du scaphoïde et plusieurs facteurs de risque semblent être incriminés de façon récurrente. Deux nouvelles classifications basées sur l'imagerie moderne sont apparues au cours de la dernière décennie et sont désormais considérées comme des compléments essentiels à la classification radiographique originale d'Herbert et Lanzetta. En raison de l'absence de recommandation sur la prise en charge thérapeutique, un large éventail de traitements différents a été exploré et proposé au fil du temps, ce qui a contribué à la confusion qui entoure cette pathologie. Les nombreux termes utilisés pour désigner cette pathologie, le manque de connaissances concernant sa physiopathologie, les facteurs de risque, la présentation clinique et radiographique contribuent à cette confusion. L'objectif de cette revue était donc d'explorer et de clarifier l’entité connue sous le terme de maladie de Preiser (histoire, terminologie, physiopathologie, considérations cliniques, imagerie) et de proposer un algorithme de traitement simple et actualisé basé sur les résultats fournis par une revue approfondie de la littérature (53 publications, 170 patients) depuis la description originale et controversée de Georg Preiser en 1910.

View all citing articles on Scopus

^*: Supported in part by NIH grant AR36867.

^**: Reprints not available.

¹: From the Division of Rheumatology, Allergy, and Clinical Immunology, University of California, Davis, Davis, CA, and the Department of Radiology, University of California, Sacramento, Medical Center, Sacramento, CA.

²: Christopher C. Chang, MD: Assistant Clinical Professor, Division of Rheumatology, Allergy, Clinical Immunology, Univesity of California, Davis.

³: Adam Greenspan, MD: Professor of Radiology, Department of Radiology, University of California, Sacramento, Medical Center

⁴: M. Eric Gershwin, MD: Professor of Medicine and Chief, Division of Rheumatology, Allergy, and Clinical Immunology, University of California, Davis.

View full text

Osteonecrosis: Current perspectives on pathogenesis and treatment*,**

J Hand Surg

J Oral Maxillofac Surg

Semin Arthritis Rheum

Am J Med

Am J Med

Orthop Clin North Am

Orthop Clin North

Avascular necrosis of bone

Curr Opin Rheumatol

Osteonecrosis

Curr Opin Rheumatol

Notraumatic necrosis of bone

N Engl J Med

Avascular necrosis and related conditions

Top Magnetic Res Imag

Osteonecrosis

Aseptic necrosis of bone. A historical perspective

Clin Orthop

Avascular necrosis of bone: A review

J R Soc Med

Changes in the bones of the extremities amputated because of arteriovascular disease

Arch Surg

Osteonecrosis of the femoral head

Orthop Rev

Osteonecrosis of the humeral head

Clin Rheumatol

Subcapital fractures of the femur

J Bone Joint Surg

Arthropathy associated with steroid therapy

Ann Intern Med

Steroid-related osteonecrosis of the knee. Two case reports and a literature review

Clin Orthop

Osteonecrosis of the knee

J Bone Joint Surg

Articular manifestations of systemic lupus erythematosus

Ann Intern Med

Osteonecrosis in the foot

J Foot Surg

Corticosteroid-induced avascular necrosis of the talus

J Foot Surg

Small bone changes secondary to systemic lupus erythematosus

Radiology

Osteonecrosis

Spinal cord compression secondary to vertebral aseptic osteonecrosis

Spine

Avascular necrosis of the mandibular condyle: A literature review

Todays FDA

Neuralgia-inducing cavitational osteonecrosis (NICO). Osteomyelitis in 224 jawbone samples from patients with facial neuralgia

Oral Surg Oral Med Pathol

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Can Med Assoc J

Aseptic necrosis of bone in systemic lupus erythematosus. Relationship to corticosteroid therapy

Ann Intern Med

Avascular necrosis in SLE

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J Rheumatol

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J Bone Joint Surg

Steroid arthropathy of the hip

Clin Orthop

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J R Coll Surg Edinburgh

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Lancet

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Netherlands J Med

Steroid treatment and aseptic necrosis of the femoral head in renal transplant recipients

Transplant Proc

Glucocorticoids and avascular bone necrosis in renal transplantation

Adv Exp Med Biol

Glucocorticoids and renal transplant osteonecrosis

Adv Exp Med Biol

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Ann Rheum Dis

Osteonecrosis in patients receiving dialysis: Report of two cases and review of the literature

J Rheumatol