| Objective:With the continuous improvement of the human condition, habits and life changing ways of working in the human diet, obesity causes metabolic syndrome showed an upward trend year by year [1]. This way, a simple upward trend by the complications and mortality was caused by the overall obesity [2]. Obese can lead to some chronic diseases, most of these diseases are associated with chronic inflammation. Obesity is also increasingly recognized as a chronic inflammation.However, the first time the link between inflammation and obesity is hotamisligil[3]found that in the study have TNF- α(tumor necrosis factor-α) expressed in adipose tissue in obesity in TNF- α levels were significantly increased. Experiments show that chronic inflammation of adipose tissue is the key link of obesity and metabolic diseases(such as insulin resistance and Type II diabetes) where [4]. Fracture healing process is a normal physiological inflammation play an active role. Most normal physiological inflammatory response is beneficial to the body, the body is an important defense response. Due to bacterial invasion or other factors leading to chronic inflammation, the body is harmful, fracture healing is also subject to different degrees. Caused by an infection, chronic persistent inflammation can stimulate osteoclasts, which affect fracture healing. However, there is a chronic inflammation of the differentiation and the formation of bone cells, but studies have less chronic inflammation especially in the obese state of fracture healing of current than the lack of domestic and foreign research, and such research tells guidance Clinical practice has a certain significance. In vitro experiments showed that TNF-α inhibits osteoblast differentiation. However, the mechanism of inhibition of TNF-α into bone cells is not clear, but on such studies are rare animal experiments. BMP-Smad pathway plays acrucial role in osteoblast differentiation induction. BMP-2(bone morphogenetic protein-2) is currently the most active induce osteogenic bone morphogenetic protein family one. So, inflammatory cytokines TNF-α effect of obesity on fracture healing,and chronic inflammatory state whether arising under bone formation and differentiation pathway important in smad1 correlation, we are the focus of the study.We began to focus on whether a series of pathophysiological problem of obesity will affect the osteoblast differentiation, thus affecting the healing process, the current research in this regard are still lacking relevant researches, the significance of which is also the subject lies.By observing the high-energy diet induced obese rats model in the process of fracture healing imaging changes, histological changes, callus local osteoblast differentiation markers of change and the change of serum inflammatory factors,inflammatory markers to understand TNF alpha bone formation in the process of fracture healing, and the influence of osteoblast differentiation.Methods:Randomly selected 80 male sd rats, 50 as experimental group, and to give a high-fat diet; Remaining 30 as control group, only to give ordinary diet.Obesity after the success of the building, continue to the experimental group and control group in the rat tibia fracture model.Upon the fracture model of rats, respectively in the 1、2、4、6 weeks after the model, take 6 rats in each group, measuring the rats in the serum TNF-α value, imaging observation of fracture healing, pathological he staining,immunohistochemical measurement of Smad1 changes Through the statistical analysis of each phase of TNF-α the influence of the relationship between the expression of Smad1.Results:Obesity modeling success rate of 64%, radiological and he staining results showed that the experimental group of fracture healing is slower than in the controlgroup; The experimental group and control group of TNF-α overall value is statistically significant(F = 18.842, P< 0.001) The experimental group is higher than the control group; The experimental group and control group of Smad1 overall value is statistically significant(F = 146.593, P <0.001) The experimental group is higher than the control group?too; there is a negative correlation between the value of Smad1 and TNF-α(pearsons, r =-0.804, P<0.001).Conclusions:(1) Obesity rats fracture healing slower in normal rats, obesity may be the cause of fracture healing at a slower pace;(2) Obesity group four time points of TNF-α values are higher than normal group,prove that obesity is a state of chronic persistent inflammation;(3) Obesity od value of the whole lower than normal group, illustrates the obesity itself can lead to the low expression of Smad1;(4) TNF-α inflammation factors and Smad1 are negatively related, illustrates in the condition of obesity, bone healing at a slower pace is likely to be associated with a higher expression of TNF-α. |
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