الفهرس 
Introduction and Aim of WorkOnly 14 pages are availabe for public view
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Abstract
The common salt (sodium chloride; NaCl) is an important micronutrient added to food for several aspects. It makes taste of food better, preserves the food and improves the appearance of processed foods. Its physiological need for a human is covered by 10–20 mmol/day (0.58–1.16 g of NaCl). However, salt intake till now is generally greater and can exceed 10 g/day in many populations which exceeds more than 200mmol/day. High salt (HS) intake is related to high risk for developing many diseases as hypertension, cardiovascular diseases (CVDs), metabolic syndrome and osteoporosis. So many well-developed societies recommended limiting salt intake to 3.75–6 g/day.
Osteoporosis is a bone disease characterized by reduced density and quality of bone resulting in weakened skeleton and increasing the risk of fractures. It is associated with increased morbidity and mortality. The main clinical manifestations are back pain, loss of height, spinal deformity as well as fractures of the vertebrae, hips and wrists. Diagnosis is typically based on the bone mineral density (BMD) measurements or the history of fracture following minimal trauma. BMD represents the quantity of the mineralized tissue in the bones including both size and density. It is the most important parameter for determining the of bone susceptibility to fractures.
High sodium intake is harmful to the bones as it decreases the reabsorption of renal calcium leading to high urinary calcium excretion, thus resulting in decreased BMD and osteoporosis. The increased calcium excretion in urine, when associated with an inadequate calcium intake, results in hypocalcemia with consequent rise in the level of PTH that causes bone loss. It will also be compensated by an increase in calcium absorption from intestine by increasing the level of 1,25-(OH)2D3. This increase in 1,25-(OH)2D3 is mediated by a rise in PTH and thus indicating a compensatory response to calcium depletion. The elevated plasma PTH level increases the urinary levels of hydroxyproline and osteocalcin which are indicators of the increase in bone resorption and bone formation respectively.
Sex hormones exert potent influences on the size and shape of the skeleton during growth. In addition, these hormones contribute to skeletal homeostasis during adulthood. So, sex hormones have important role in sexual disparity in the response of bone to HSD.
The results obtained in the present study clearly demonstrate that : -
Administration of HSD (8 %) for seven weeks to both male and female rats resulted in osteoporosis. Osteoporosis is more severe in female rats than male rats as evidenced by laboratory measurements and histopathological examination. There was increase in food intake in HSD groups when compared to control ones. Increase food intake in HSD male group was more than HSD female group. However, body weight gain in HSD groups was less than control ones and so BMI. Additionally, HSD female group had lower body weight gain and BMI than HSD male one.
There was significant reduction in BMD, bone weight, dry weight, FFDW, ash percentage, ash weight and organic matrix weight of left femurs of HSD groups compared to the control groups. HSD female group had the lowest values of previous parameters that indicated the extreme affection of female rats bone by HSD.
Bone biomarkers included in formation and resorption, alkaline phosphatase (ALP) as a bone formation biomarker and acid phosphatase as bone resorption biomarker, were significantly increased in HSD groups when compared to control ones. In addition to that PTH also had significant higher values in HSD group and its highest value was in HSD female group.
The results obtained in the present study demonstrated that serum calcium concentration did not show any significant change. This could be explained by the homeostatic mechanisms of PTH and vitamin D that were able to maintain serum calcium level within normal range. Also, serum phosphrous level had no significant different levels between all groups. It was explained by 1- 1, 25(OH)2D can augment intestinal phosphate uptake by the enterocytes. PTH increases urinary phosphate excretion and also bone can release additional phosphate to maintain the homeostatic balance by increasing resorption when serum phosphate decrease.
Hematoxyllin and Eosin obtained results showed distorted bone structure as some areas were noticed completely devoid of osteocytes in HSD male group. Faintly stained bone matrix was frequently seen. HSD female group exhibited massive distortion than HSD male group. Some areas were seen completely devoid of both osteocytes and bone matrix. Masson’s trichrome obtained results showed unmineralized bone matrix and few areas of mineralized bone matrix in HSD groups that was evident in HSD female one. Von Kossa’s technique results demonstrated apparent decrease of calcium deposition in bone tissue in HSD groups in comparison with control ones. Immunohistochemical results for anti-osteopontin demonstrated more positive cytoplasmic expression in the bone matrix in HSD groups that was more apparent in HSD female one.