Defects in cortical microarchitecture among African-American women with type 2 diabetes.
CONCLUSIONS
Patients with type 2 diabetes mellitus (DM2) have increased fracture risk. We found that African-American women with DM2 have increased cortical porosity and lower cortical bone density at the radius than non-diabetic controls. These cortical deficits are associated with hyperglycemia and may contribute to skeletal fragility associated with DM2.


BACKGROUND
Fracture risk is increased in patients with type 2 diabetes mellitus (DM2) despite normal areal bone mineral density (aBMD). DM2 is more common in African-Americans than in Caucasians. It is not known whether African-American women with DM2 have deficits in bone microstructure.


METHODS
We measured aBMD at the spine and hip by DXA, and volumetric BMD (vBMD) and microarchitecture at the distal radius and tibia by HR-pQCT in 22 DM2 and 78 non-diabetic African-American women participating in the Study of Women Across the Nation (SWAN). We also measured fasting glucose and HOMA-IR.


RESULTS
Age, weight, and aBMD at all sites were similar in both groups. At the radius, cortical porosity was 26% greater, while cortical vBMD and tissue mineral density were lower in women with DM2 than in controls. There were no differences in radius total vBMD or trabecular vBMD between groups. Despite inferior cortical bone properties at the radius, FEA-estimated failure load was similar between groups. Tibia vBMD and microarchitecture were also similar between groups. There were no significant associations between cortical parameters and duration of DM2 or HOMA-IR. However, among women with DM2, higher fasting glucose levels were associated with lower cortical vBMD (r=-0.54, p=0.018).


CONCLUSIONS
DM2 and higher fasting glucose are associated with unfavorable cortical bone microarchitecture at the distal radius in African-American women. These structural deficits may contribute to the increased fracture risk among women with DM2. Further, our results suggest that hyperglycemia may be involved in mechanisms of skeletal fragility associated with DM2.
Endocrine Unit, Massachusetts General Hospital, 50 Blossom Street, THR-1051, Boston, MA, 02114, USA, ewyu@partners.org.
E W
EW
Yu
M S
MS
Putman
N
N
Derrico
G
G
Abrishamanian-Garcia
J S
JS
Finkelstein
M L
ML
Bouxsein
D015502:Absorptiometry, Photon / Q000379:methods; D001741:Black or African American / Q000706:statistics & numerical data; D001786:Blood Glucose / Q000378:metabolism; D015519:Bone Density / Q000502:physiology; D016022:Case-Control Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000208:ethnology / Q000473:pathology* / Q000503:physiopathology; D005215:Fasting / Q000097:blood; D005260:Female; D006621:Hip Joint / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008159:Lumbar Vertebrae / Q000503:physiopathology; D008875:Middle Aged; D016062:Porosity; D011884:Radius / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D013977:Tibia / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D014057:Tomography, X-Ray Computed / Q000379:methods; D014481:United States / Q000453:epidemiology
D001786:Blood Glucose