Osteoprosis in Type 2 Diabetic Patients- a Cohort Study
Osteoprosis in Type 2 Diabetic Patients- a Cohort Study
Some possible humoural and cellular mechanism for diabetes related osteoporosis/fractures
 were proposed and summarzied as the following, (1)Diabetes mellitus increases osteoclast
 function but decreases osteoblast function, thereby leading to accelerated bone loss,
 osteopenia and osteoporosis. (2)DM/hyperglycemia induces production of macrophage colony
 stimulating factor (MCSF), tumor necrosis factor (TNF)-α and receptor activator of nuclear
 factor-κB ligand (RANKL), all of which are osteoblast-derived activators of osteoclast
 proliferation and differentiation. (3) DM/hyperglycemia suppresses osteoblast proliferation
 and function, in part, by decreasing runtrelated transcription factor (Runx)-2, osteocalcin
 and osteopontin expressions. (4)Adipogenic differentiation of mesenchymal stem cells is
 increased as indicated by the overexpression of adipocyte differentiation markers, including
 peroxisome proliferator-activated receptor (PPAR)-g, adipocyte fatty acid binding protein
 (aP2), adipsin and resistin. A decrease in neovascularization may further aggravate bone
 loss. (5)Bone quality is also reduced as a result of advanced glycation end products (AGE)
 production, which may eventually result in low impact or fragility fractures. DM are
 associated osteoporosis/fracture. The underlying mechanism, especially of type 2 DM, mandates
 a DM-osteoporosis cohort to elucidate. In clinical practice, to developed preventive
 strategies from osteoporotic-fracture is also necessary.
It is becoming apparent that both type 1 and type 2 diabetes mellitus are associated with an
 increased risk for osteoporosis-associated fractures. A meta-analysis by Vestergaard showed
 that patients with type 1 DM have decreased bone mineral density and increased fracture risk.
 This study noted a 6.9 relative risk of hip fracture, when the expected relative risk of
 fracture was only 1.4 based on the BMD. This finding suggests that the increased fracture
 risk is not entirely accounted for by the lower BMD. It has been demonstrated that the
 presence of diabetic microvascular complications, including ophthalmic, nephropathic, and
 neurological, lead to a higher risk of hip fracture in patients with type 1 DM. Unlike
 patients with type 1 DM, patients with type 2 DM have an average or higher BMD than
 age-matched controls. However, several studies have demonstrated that patients with type 2 DM
 have a higher risk of hip, proximal humerus, and foot fractures. Data from the Women's Health
 Initiative Observational Study indicate that post-menopausal women with diabetes are at an
 increased risk of hip, foot, and spine fractures, and fractures overall. For a given BMD,
 diabetic bone appears to be less strong and therefore more likely to fracture. Insulin-like
 growth factor (IGF)-1, insulin, bone morphogenetic proteins and osteoprotegerin (OPG), serve
 as anabolic signals to promote bone formation. Among these anabolic mediators, liver-derived
 IGF-1 is of particular interest since profound growth retardation, small bone size, low BMD
 and osteoporosis were reported in IGF-1 and IGF-1 receptor deficiencies. Furthermore, insulin
 was found to directly induce osteogenic action by increasing cell proliferation,
 differentiation, alkaline phosphatase activity and expression of type Ⅰcollagen and
 osteocalcin in human osteoblast-like MG-63 cells. Type 1 DM featuring low circulating insulin
 and IGF-1 levels usually occurs in young children prior to peak bone mass attainment, whereas
 type 2 DM is common in adults who have already attained peak bone mass.
1. inclusion:40-99 years old with type 2 DM patient

 2. exclusion:organization people