Abstract
Atherosclerosis and osteoporosis until recently were regarded as the diseases of modern society, and their simultaneous development was explained just by the increased chances with longevity. Currently, there are studies showing evidence on these diseases in ancient populations, regardless the age and gender. The diseases found in younger age, with the early Egyptian civilization, witness on the common genetic and behavioral risk factors and pathogenetic components, than simple age-related chance. Scientific publications show more and more data on common properties of these diseases and pathogenetic mechanisms. High risk of premature death from atherosclerosis and osteoporosis complications facilitates the search for individual and general predictors of the disorders with the aim of on-time prevention. Treatment of atherosclerosis and osteoporosis presentation events in one patient demands for a range of medications that leads to polypragmasia. The review is focused on common mechanisms of vascular stiffness development, calcification and bone density decrease. Profound understanding might make it to open novel targets for one drug to both diseases, with decreased rate of complications.
Highlights
Атеросклероз и остеопороз до недавнего времени считали заболеваниями современного общества, а одновременное развитие их связывали с простым накоплением этих заболеваний при удлинении продолжительности жизни
The diseases found in younger age, with the early Egyptian civilization, witness on the common genetic and behavioral risk factors and pathogenetic components, than simple age-related chance
Treatment of atherosclerosis and osteoporosis presentation events in one patient demands for a range of medications that leads to polypragmasia
Summary
Атеросклероз и остеопороз до недавнего времени считали заболеваниями современного общества, а одновременное развитие их связывали с простым накоплением этих заболеваний при удлинении продолжительности жизни. Хотя патогенетические механизмы миграции кальция из костной ткани в сосудистую стенку пока до конца не ясны, в экспериментальных исследованиях показана остеогенная природа кальциевых депозитов в самой сосудистой стенке или в атеросклеротической бляшке (АСБ) и подтверждено, что различные факторы, влияющие на костный метаболизм, вовлечены в механизмы сосудистых заболеваний [5]. В настоящее время пока не установлена причинно-следственная связь сосудистой кальцификации и снижения костной массы.
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