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Original Article
Quantitative DCE-MRI and QCT were used to evaluate the bone marrow microvascular permeability and trabecular changes in diabetic rabbit models induced by alloxan
CHEN Pianpian  ZHA Yunfei 

Cite this article as: Chen PP, Zha YF. Quantitative DCE-MRI and QCT were used to evaluate the bone marrow microvascular permeability and trabecular changes in diabetic rabbit models induced by alloxan. Chin J Magn Reson Imaging, 2019, 10(7): 540-545. DOI:10.12015/issn.1674-8034.2019.07.012.


[Abstract] Objective: To quantitatively evaluate the bone marrow microvascular permeability and trabecular changes induced by alloxan in diabetic rabbit model via dynamic contrast enhanced MRI (DCE-MRI) and quantitative CT (QCT).Materials and Methods: Eighteen rabbits were randomly divided into the diabetes group (n=14) and the control group (n=10). Fse-T1WI, Fse-T1WI, DCE-MRI examination and CT imaging were performed at each time point (0, 4, 8, 12 and 16 weeks) after the model had been established successfully. DCE-MRI quantitative perfusion parameters of lumbar bone marrow were obtained by fitting the pharmacokinetic model, including volume transfer constant (Ktrans), efflux rate constant (Kep) and extracellular extravascular volume fraction (Ve). QCT software was applied to measure Lumbar vertebral density (BMD). Lumbar vertebral specimens were collected at week 16 for HE staining to calculate the morphometric parameters of bone trabeculae, including the number of bone trabeculae (Tb.N) and the area of bone trabeculae (Tb.Ar).Results: Osmotic parameters Kep and Ve at different time points indicated statistically significant differences in the control group (P<0.001), which was not significant different in the diabetes group (P>0.05). In the control group, the Kep of lumbar spine showed a descending trend from week 4 to week 12, while Ve displayed an rising trend from week 4 to week 12 and declined from week 16. There was no significant difference in BMD between the control group and the diabetes group at different time points (P>0.05).The results of HE staining exhibited that the number and area of bone trabeculae were decreased in the diabetic group at week 16. The trabecular bone area and trabecular bone count was lower than that of the control group (t=12.472, t=4.961, P<0.001). Pearson correlation analysis results showed that there was no correlation between Tb.N and Ktrans, Kep and Ve (r values: 0.135, 0.093 and -0.118), as well as Tb.Ar and Ktrans, Kep and Ve (r values: 0.233, -0.008 and -0.0.095, P>0.05). No significant correlation was observed between BMD with Ktrans, Kep and Ve (r values:0.497, 0.513 and-0.310, P>0.05).Conclusions: The changes of bone marrow microvascular permeability parameters of the lumbar spine in diabetes mellitus rabbits induced by alloxan in the early stage of disease were not correlated with bone mineral density and trabecular morphometrics parameters, and the differences of bone marrow BMD measured by QCT were later than those of bone trabecular morphometrics.
[Keywords] bone marrow;microvessels;diabetes mellitus;lumbar vertebrae;magnetic resonance imaging;tomography, x-ray;animals, laboratory

CHEN Pianpian Department of Radiology, Renmin Hospital of Wuhan University, Wuhan,430060, China

ZHA Yunfei* Department of Radiology, Renmin Hospital of Wuhan University, Wuhan,430060, China; Hubei Key Laboratory of Medical Information Analysis and Tumor Diagnosis & Treatment, wuhan 430060, China

*Correspondence to: Zha YF, Email: zhayunfei999@126.com

Conflicts of interest   None.

ACKNOWLEDGMENTS  The National Natural Science Foundation of China No. 81871332 Hubei Key Laboratory of Medical Information Analysis and Tumor Diagnosis&Treatment No. PJS140011708
Received  2019-01-28
Accepted  2019-05-22
DOI: 10.12015/issn.1674-8034.2019.07.012
Cite this article as: Chen PP, Zha YF. Quantitative DCE-MRI and QCT were used to evaluate the bone marrow microvascular permeability and trabecular changes in diabetic rabbit models induced by alloxan. Chin J Magn Reson Imaging, 2019, 10(7): 540-545. DOI:10.12015/issn.1674-8034.2019.07.012.

[1]
Fadini G, Ferraro F, Quaini F, et al. Concise review: diabetes, the bone marrow niche, and impaired vascular regeneration. Stem Cells Transl Med, 2014, 3(8): 949-957.
[2]
Shanbhogue V, Hansen S, Frost M, et al. Bone disease in diabetes: another manifestation of microvascular disease? Lancet Diabetes Endocrinol, 2017, 5(10): 827-838.
[3]
Hinton P. Role of reduced insulin-stimulated bone blood flow in the pathogenesis of metabolic insulin resistance and diabetic bone fragility. Med Hypotheses, 2016, 93: 81-86.
[4]
Fadini G. Is bone marrow another target of diabetic complications? Eur J Clin Invest, 2011, 41(4): 457-463.
[5]
Bhatwadekar A, Duan Y, Korah M, et al. Hematopoietic stem/progenitor involvement in retinal microvascular repair during diabetes: implications for bone marrow rejuvenation. Vision Res, 2017, 139: 211-220.
[6]
Fajardo R. Is diabetic skeletal fragility associated with microvascular complications in bone? Curr Osteoporos Rep, 2017, 15(1): 1-8.
[7]
Hu L, Zha Y, Wang L, et al. Quantitative evaluation of vertebral microvascular permeability and fat fraction in alloxan-induced diabetic rabbits. Radiology, 2018, 287(1): 128-136.
[8]
程晓光,余卫.定量CT骨密度测量技术的进展与临床应用.中国医学影像学杂志, 2011, 19(12): 881-883.
[9]
Sheu Y, Amati F, Schwartz AV, et al. Vertebral bone marrow fat, bone mineral density and diabetes: the osteoporotic fractures in men (MrOS) study. Bone, 2017, 97: 299-305.
[10]
Napoli N, Chandran M, Pierroz D, et al. Mechanisms of diabetes mellitus-induced bone fragility. Nat Rev Endocrinol, 2017, 13(4): 208-219.
[11]
Liu T, Zhao H, Li J, et al. Rosiglitazone attenuates atrial structural remodeling and atrial fibrillation promotion in alloxan-induced diabetic rabbits. Cardiovasc Ther, 2014, 32(4): 178-183.
[12]
Shanbhogue V, Hansen S, Frost M, et al. Bone disease in diabetes: another manifestation of microvascular disease? Lancet Diabetes Endocrinol, 2017, 5(10): 827-838.
[13]
Oikawa A, Siragusa M, Quaini F, et al. Diabetes mellitus induces bone marrow microangiopathy. Arterioscler Thromb Vasc Biol, 2010, 30(3): 498-508.
[14]
Fadini G. Is bone marrow another target of diabetic complications? Eur J Clin Invest, 2011, 41(4): 457-463.
[15]
Manavalan JS, Cremers S, Dempster DW, et al. Circulating osteogenic precursor cells in type 2 diabetes mellitus. J Clin Endocrinol Metab, 2012, 97(9): 3240-3250.
[16]
Burghardt AJ, Issever AS, Schwartz AV, et al. High-resolution peripheral quantitative computed tomographic imaging of cortical and trabecular bone microarchitecture in patients with type 2 diabetes mellitus. J Clin Endocrinol Metab, 2010, 95(11): 5045-5055.
[17]
Yu EW, Putman MS, Derrico N, et al. Defects in cortical microarchitecture among African-American women with type 2 diabetes. Osteoporos Int, 2015, 26(2): 673-679.
[18]
Shu A, Yin MT, Stein E, et al. Bone structure and turnover in type 2 diabetes mellitus. Osteoporos Int, 2012, 23(2): 635-641.
[19]
Farr JN, Drake MT, Shreyasee A, et al. In vivo assessment of bone quality in postmenopausal women with type 2 diabetes. J Bone Miner Res, 2014, 29(4): 787-795.
[20]
Register TC, Lenchik L, Hsu FC, et al. Type 2 diabetes is not independently associated with spinal trabecular volumetric bone mineral density measured by QCT in the Diabetes Heart Study. Bone, 2006, 39(3): 628-633.
[21]
Rakic V, Davis WA, Chubb SA, et al. Bone mineral density and its determinants in diabetes: the Fremantle Diabetes Study. Diabetologia, 2006, 49(5): 863-871.
[22]
Vestergaard P. Discrepancies in bone mineral density and fracture risk in patients with type 1 and type 2 diabetes: a meta-analysis. Osteoporos Int, 2007, 18(4): 427-444.
[23]
Ramiya VK, Maraist M, Arfors KE, et al. Reversal of insulin-dependent diabetes using islets generated in vitro from pancreatic stem cells. Nat Med, 2000, 6(3): 278-282.
[24]
Listed N. Hypoglycemia in the diabetes control and complications trial. The diabetes control and complications trial research group. Diabetes, 1997, 46(2): 271-286.
[25]
Mattila TK, Anthonius DB. Influence of intensive versus conventional glucose control on microvascular and macrovascular complications in type 1 and 2 diabetes mellitus. Drugs, 2010, 70(17): 2229-2245.
[26]
Rosenqvist U. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The diabetes control and complications trial research group. New England J Med, 1993, 329(3): 977-986.
[27]
Burghardt AJ, Kazakia GJ, Sode M, et al. A longitudinal HR-pQCT study of alendronate treatment in postmenopausal women with low bone density: relations among density, cortical and trabecular microarchitecture, biomechanics, and bone turnover. J Bone Miner Res, 2010, 25(12): 2558-2571.
[28]
Nilsson AG, Sundh D, Johansson L, et al. Type 2 diabetes mellitus is associated with better bone microarchitecture but lower bone material strength and poorer physical function in elderly women: a population-based study. J Bone Miner Res, 2017, 32(5): 1062-1071.
[29]
Patsch JM, Burghardt AJ, Yap SP, et al. Increased cortical porosity in type 2 diabetic postmenopausal women with fragility fractures. J Bone Miner Res, 2013, 28(2): 313-324.
[30]
Tao B, Liu JM, Zhao HY, et al. Differences between measurements of bone mineral densities by quantitative ultrasound and dual-energy X-ray absorptiometry in type 2 diabetic postmenopausal women. J Clin Endocrinol Metab, 2008, 93(5): 1670-1675.
[31]
Heilmeier U, Cheng K, Pasco C, et al. Cortical bone laminar analysis reveals increased midcortical and periosteal porosity in type 2 diabetic postmenopausal women with history of fragility fractures compared to fracture-free diabetics. Osteoporos Int, 2016, 27(9): 2791-2802.

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