Abstract
The article summarizes the data on senile osteoporosis and presents a clinical case of this disease. The reference sources on peculiarities of bone remodeling in senile osteoporosis are summarized; low bone formation takes place against the background of a pronounced bone resorption. The article also presents pathomorphological features of bone tissue remodeling resulting in pronounced impairments of the compact bone, which increase the risk of fracture. Vitamin D plays a significant role in the complex mechanism of senile osteoporosis. The data on the combined effect of vitamin D and parathormone on bone remodeling are summarized. The paper presents data on other cumulative effects of senile osteoporosis development. Against the background of ageing-associated systemic changes, calcium and vitamin D deficiency, increased pro-inflammatory cytokine expression, localized bone disorders develop. An important link to the development of senile osteoporosis is an increased marrow adipose tissue with an intensified adipogenesis, resulting in a decrease of osteoblasts due to the toxic effects of adipokines, reduced differentiation and proliferation of osteoblasts. Age-associated immune-related mechanisms of inflammation, indirectly affecting the bone, are considered. Peculiarities of the senile osteoporosis diagnostics by means of bone mineral density assessment tools are described. Despite the successes achieved in the study of senile osteoporosis development mechanisms, further research is required to explore local and systemic factors affecting bone tissue which are involved in the development of this disease.
Highlights
Senile osteoporosis, known as the second type of systemic osteoporosis, occurs after the age of 70-75 years [13]
The senile osteoporosis has the risk factors which are similar to other osteoporosis types: i.e. probable low bone peak achieved by 30 years
The key component of senile osteoporosis pathogenesis is Vitamin D whose deficiency may be provoked by its reduced supplementation or skin production promoted by an insufficient insolation [5]
Summary
The key component of senile osteoporosis pathogenesis is Vitamin D whose deficiency may be provoked by its reduced supplementation or skin production promoted by an insufficient insolation [5]. The Vitamin D active metabolite deficiency is tapering down with age due to the involutionary changes in kidneys and a reduced activity of 1α-hydroxylase enzyme. This enzyme is regulated by a range of factors, namely the parathyroid hormone (PTH) influencing the bone remodeling at various levels. The PTH secretion is growing due to a low Calcium blood rate (secondary senile hyperparathyroidism) and dimin-. The above-mentioned factors account for the fact that senile osteoporosis attending hyperparathyroidism is considered one of the key mechanisms of its pathogenesis [4]
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