Women with type 2 diabetes mellitus have lower cortical porosity of the proximal femoral shaft using low-resolution CT than nondiabetic women, and increasing glucose is associated with reduced cortical porosity.
Increased cortical porosity has been suggested as a possible factor increasing fracture propensity in patients with type 2 diabetes mellitus (T2DM). This is a paradox because cortical porosity is generally associated with high bone turnover, while bone turnover is reduced in patients with T2DM. We therefore wanted to test the hypothesis that women with T2DM have lower bone turnover markers (BTM) and lower cortical porosity than those without diabetes, and that higher serum glucose and body mass index (BMI) are associated with lower BTM, and with lower cortical porosity. This cross-sectional study is based on a prior nested case-control study including 443 postmenopausal women aged 54-94years from the Tromsø Study, 211 with non-vertebral fracture and 232 fracture-free controls. Of those 443 participants, 22 women exhibited T2DM and 421 women did not have diabetes. All had fasting blood samples assayed for procollagen type I N-terminal propeptide (PINP), C-terminal cross-linking telopeptide of type I collagen (CTX) and glucose, and femoral subtrochanteric architecture was quantified using low-resolution clinical CT and StrAx1.0 software. Women with T2DM had higher serum glucose (7.2 vs. 5.3mmol/L), BMI (29.0 vs. 26.4kg/m2), and higher femoral subtrochanteric total volumetric bone mineral density (vBMD) (783 vs. 715mgHA/cm3), but lower cortical porosity (40.9 vs. 42.8%) than nondiabetic women (all p<0.05). Each standard deviation (SD) increment in glucose was associated with 0.10-0.12 SD lower PINP and CTX, and 0.13 SD lower cortical porosity (all p<0.05). Each SD increment in BMI was associated with 0.10-0.18 SD lower serum PINP and CTX, and 0.19 SD thicker cortices (all p<0.05). Increasing glucose and BMI were associated with lower bone turnover suggesting that reduced intracortical and endocortical remodeling leads to reduced porosity and thicker cortices. Using low-resolution clinical CT, cortical porosity was lower in women with T2DM compared to women without diabetes. This indicates that other changes in bone qualities, not increased cortical porosity, are likely to explain the increased fracture propensity in patients with T2DM.
Department of Community Medicine, UiT The Arctic University of Norway, Tromsø, Norway; Department of Orthopaedic Surgery, University Hospital of North Norway, Tromsø, Norway. Electronic address: mos015@uit.no.
Marit
M
Osima
Department of Obstetrics and Gynaecology, University Hospital of North Norway, Tromsø, Norway.
Rita
R
Kral
Department of Rheumatology, Vestre Viken Hospital Trust, Hospital of Drammen, Drammen, Norway.
Tove T
TT
Borgen
Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; Department of Clinical Medicine, University of Oslo, Oslo, Norway.
Ingvild K
IK
Høgestøl
Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway; Department of Medicine, University Hospital of North Norway, Tromsø, Norway.
Ragnar M
RM
Joakimsen
Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, Oslo, Norway; Department of Clinical Medicine, University of Oslo, Oslo, Norway.
Erik F
EF
Eriksen
Department of Obstetrics and Gynaecology, University Hospital of North Norway, Tromsø, Norway; Department of Clinical Medicine, UiT The Arctic University of Norway, Tromsø, Norway.
Åshild
Å
Bjørnerem
D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D016723:Bone Remodeling; D016022:Case-Control Studies; D024042:Collagen Type I / Q000378:metabolism; D000071538:Cortical Bone / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005269:Femur / Q000000981:diagnostic imaging* / Q000473:pathology / Q000503:physiopathology*; D050723:Fractures, Bone / Q000150:complications / Q000473:pathology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007328:Insulin / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D010455:Peptides / Q000378:metabolism; D016062:Porosity; D011347:Procollagen / Q000378:metabolism; D014057:Tomography, X-Ray Computed
D015415:Biomarkers; D001786:Blood Glucose; D024042:Collagen Type I; D007328:Insulin; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide
Bone turnover markers; Cortical porosity; Glucose; Postmenopausal women; Type 2 diabetes mellitus