Transient Bone Marrow Edema of the Foot and Ankle and its Association with Reduced Systemic Bone Mineral Density

2011 ◽  
Vol 32 (5) ◽  
pp. 508-512 ◽  
Author(s):  
Anna E. Sprinchorn ◽  
Richard O'Sullivan ◽  
Andrew D. Beischer
2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Omar Alsaed ◽  
Mohammad Hammoudeh

Transient bone marrow edema (TBME) is a self-limiting disease characterized by joint pain with localized bone marrow edema by MRI and has been reported in many case series and case reports. It is well known that joints of the lower extremity including hips, knees, ankles, and feet are the classical sites for TBME. Many theories have been proposed for the pathogenesis of TBME. Systemic osteopenia and vitamin D deficiency is one of the theories that have been suggested in the last few years. In this case report, we present a middle-aged male patient, who presented with 4 attacks of TBME in both knees between September 2016 and August 2017. The patient was found to have persistently low vitamin D and osteopenic T score in DXA scan of the lumbar spine and hips. Patients of TBME usually present with joint pain that is provoked by weight-bearing physical activity. The aim of this case report is to raise the awareness that TBME can be the initial presentation of systemic loss of bone mineral density.


2002 ◽  
Vol 402 ◽  
pp. 171-175 ◽  
Author(s):  
Kyung-Hoi Koo ◽  
In-Oak Ahn ◽  
Hae-Ryong Song ◽  
Shin-Yoon Kim ◽  
John Paul Jones

2018 ◽  
Vol 2018 ◽  
pp. 1-10
Author(s):  
Md Mizanur Rahman ◽  
Amina El Jamali ◽  
Ganesh V. Halade ◽  
Allal Ouhtit ◽  
Haissam Abou-Saleh ◽  
...  

Despite increasing evidence suggesting a role for NADPH oxidases (Nox) in bone pathophysiology, whether Nox enzymes contribute to obesity-mediated bone remodeling remains to be clearly elucidated. Nox2 is one of the predominant Nox enzymes expressed in the bone marrow microenvironment and is a major source of ROS generation during inflammatory processes. It is also well recognized that a high-fat diet (HFD) induces obesity, which negatively impacts bone remodeling. In this work, we investigated the effect of Nox2 loss of function on obesity-mediated alteration of bone remodeling using wild-type (WT) and Nox2-knockout (KO) mice fed with a standard lab chow diet (SD) as a control or a HFD as an obesity model. Bone mineral density (BMD) of mice was assessed at the beginning and after 3 months of feeding with SD or HFD. Our results show that HFD increased bone mineral density to a greater extent in KO mice than in WT mice without affecting the total body weight and fat mass. HFD also significantly increased the number of adipocytes in the bone marrow microenvironment of WT mice as compared to KO mice. The bone levels of proinflammatory cytokines and proosteoclastogenic factors were also significantly elevated in WT-HFD mice as compared to KO-HFD mice. Furthermore, the in vitro differentiation of bone marrow cells into osteoclasts was significantly increased when using bone marrow cells from WT-HFD mice as compared to KO-HFD mice. Our data collectively suggest that Nox2 is implicated in HFD-induced deleterious bone remodeling by enhancing bone marrow adipogenesis and osteoclastogenesis.


2011 ◽  
Vol 19 ◽  
pp. S183-S184
Author(s):  
J.B. Driban ◽  
G.H. Lo ◽  
L.L. Price ◽  
T.E. McAlindon

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