With blood smear analysis they were able to see that the mice studied showed the same effects expected to see in thalassemic patients. Red blood cell count, hemoglobin, hematocrit, red cell distribution had all decreased significantly were as reticulocytes, which are immature red blood cells without a nucleus in thalassemic mice when compared to the wild type. Using dual energy x-ray absorptiometry, they found that in the trabecular sites such as the femoral metaphysis, tibial metaphysis, and the L5-6 vertebrae but not in the cortical sites. Using bone histomorphometry, microscopic changes were then looked at specifically in the tibial metaphysis. They found that there was a narrowing in new formed bones using a calcium chelating agent that fluoresces green. They also found that there was a marked loss of calcified tissue with marrow expansion in the tibial secondary spongiosa of thalassemic mice. Bone volume, trabecular number, and trabecular thickness are decreased, whereas marrow volume and trabecular separation increased significantly. Mineral apposition rate, mineralizing surface, and mineralizing volume also showed that there was a %30 decrease in the tibial metaphysis of thalassemic mice. Thus, suggested that there was a presence of low bone calcium accretion.
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Upon looking at the concentration levels of both osteoclast and osteoblast, there was a significant decrease in functional osteoblast, which help with new bone formation, and an accelerated increase in osteoclast formation (Kilbarger, 2007). Osteoclast are responsible for the breakdown of bones. They were able to find evidence of accelerated bone resorption and a decrease in bone calcium accretion with a decrease in bone mineral density especially in trabecular-rich regions. This study showed that accelerated bone resorption and impaired osteoblast function lead to osteopenia. Iron overload assisted in the impairment of osteoblast function due to the lack of minerals and oxidative stress that iron overload causes. With a lack of minerals and oxidative stress following an increase in intracellular iron concentrations, inhibits osteoblast function, therefore affecting the bone mineral density and bone mineral content of the bones (He, 2015). Physical activity and regular exercise, such as walking, running, etc., has shown to have very positive effects on bone mineral density, bone mass, and bone strength (Thongchote, 2014). …show more content…
Another study done by Thongchote and his associates has tested to see if running activities in mice can ameliorate bone mineral density and compensate for the microstructural differences in thalassemic mice versus thalassemic mice that do not have any running activity and are not very active. They wanted to determine the age and sex dependent changes in bone mineral density, bone mineral content, and bone microstructural changes in thalassemic mice using dual x ray absorptiometry and bone histomorphometry. They also wanted to determine if running exercises could alleviate the thalassemic induced bone loss and microstructural defect in thalassemic mice. They found that in mice at one and two months showed signs of growth retardation due to the significant decrease in body weight and in the length of the femur in both wild type and thalassemic mice. Osteopenia was evident in both mice of all ages and sex indicated by the significant decrease in bone mineral density values as well as the bone mineral content. However, in the cortical sites on the bone, female mice showed a significance in bone mineral density whereas the male did not. Since the female showed a significant difference in both the trabecular and cortical sites of the bone, females mice were used in further studies in this paper. Similar to the results of their previous study of bone formation in thalassemic mice, they concluded that bone loss was due to the impairment of osteoblast function and acceleration of bone resorption due to the inappropriate activation of osteoclast. Enhanced osteoclast mediated bone resorption is dependant on the levels of osteoclastogenic cytokines, IL-1흰 and -1β that are secreted by hematopoietic cells in response to ineffective red blood cell production. Iron overload and oxidative stress also contribute to the impairment of osteoblast function due to the suppression of alkaline phosphatase activity in osteoblast like cell lines as well as the expression of osteoblast-derived bone formation markers. This could lead to apoptosis of osteoblast (Thongchote, 2014).
Upon looking at the concentration levels of both osteoclast and osteoblast, there was a significant decrease in functional osteoblast, which help with new bone formation, and an accelerated increase in osteoclast formation (Kilbarger, 2007). Osteoclast are responsible for the breakdown of bones. They were able to find evidence of accelerated bone resorption and a decrease in bone calcium accretion with a decrease in bone mineral density especially in trabecular-rich regions. This study showed that accelerated bone resorption and impaired osteoblast function lead to osteopenia. Iron overload assisted in the impairment of osteoblast function due to the lack of minerals and oxidative stress that iron overload causes. With a lack of minerals and oxidative stress following an increase in intracellular iron concentrations, inhibits osteoblast function, therefore affecting the bone mineral density and bone mineral content of the bones (He, 2015). Physical activity and regular exercise, such as walking, running, etc., has shown to have very positive effects on bone mineral density, bone mass, and bone strength (Thongchote, 2014). …show more content…
Another study done by Thongchote and his associates has tested to see if running activities in mice can ameliorate bone mineral density and compensate for the microstructural differences in thalassemic mice versus thalassemic mice that do not have any running activity and are not very active. They wanted to determine the age and sex dependent changes in bone mineral density, bone mineral content, and bone microstructural changes in thalassemic mice using dual x ray absorptiometry and bone histomorphometry. They also wanted to determine if running exercises could alleviate the thalassemic induced bone loss and microstructural defect in thalassemic mice. They found that in mice at one and two months showed signs of growth retardation due to the significant decrease in body weight and in the length of the femur in both wild type and thalassemic mice. Osteopenia was evident in both mice of all ages and sex indicated by the significant decrease in bone mineral density values as well as the bone mineral content. However, in the cortical sites on the bone, female mice showed a significance in bone mineral density whereas the male did not. Since the female showed a significant difference in both the trabecular and cortical sites of the bone, females mice were used in further studies in this paper. Similar to the results of their previous study of bone formation in thalassemic mice, they concluded that bone loss was due to the impairment of osteoblast function and acceleration of bone resorption due to the inappropriate activation of osteoclast. Enhanced osteoclast mediated bone resorption is dependant on the levels of osteoclastogenic cytokines, IL-1흰 and -1β that are secreted by hematopoietic cells in response to ineffective red blood cell production. Iron overload and oxidative stress also contribute to the impairment of osteoblast function due to the suppression of alkaline phosphatase activity in osteoblast like cell lines as well as the expression of osteoblast-derived bone formation markers. This could lead to apoptosis of osteoblast (Thongchote, 2014).