Fracture prevention and treatment of osteoporosis: slow down osteoclasts!
The Bone Eater was turned offPyotr Smirnov, "Newspaper.
The vertebrae of mice genetically deprived of this receptor are 40% heavier and almost 50% stronger than those of normal counterparts. Time will tell whether it will be possible to create non-breaking "supercoaches".
Those who have ever had to sit on sick leave for a month or two because of a broken leg or arm should be much more attentive to their bones. According to epidemiological data, they have twice the risk of breaking something else than other representatives of their age group.
This attention makes sense: despite the apparent "lifelessness", bones are the same organs as, say, the intestines or the brain, adequately responding to changes in external conditions. And, like all organs, bones need competent support from the owner. Otherwise, natural age-related processes take over, and by the age of 60-70, the "support of the body" turns into a fragile, easily vulnerable frame.
The reason for this is osteoporosis – a violation of the balance between permanent formation and destruction of bone tissue. Although there are already quite effective ways to treat this condition, and a list of its causes, led by hormonal changes, has been compiled for a long time, the development of the phenomenon itself is not known in detail. Kurt Redlich from the Medical University of Vienna and his colleagues have found the last missing link of osteoporosis, responsible for the activation of osteoclasts that devour our bones at the command of the body.
There are only two active elements in our bones, whether they are the "plates" of the skull or the "tubes" of the hip or shoulder – these are osteoblasts, synthesizing an organic matrix on which minerals are then deposited; and osteoclasts, effectively washing out these minerals. Unlike builders, "eaters" are formed from blood monocytes merging with each other. (The multicore pink cells in the picture are osteoclasts, the brown ones are other bone cells: osteoblasts synthesizing an organic framework, and osteocytes are inorganic.)
There may be perfectly reasonable reasons for leaching calcium from your own bones. For example, attempts to detain rare magnesium in the body by removing calcium from bones, a banal lack of calcium in food, or saving "building material" while reducing physical activity. Again, local destruction is a necessary stage of reconstruction after a fracture.
Since this process is mainly controlled by the parathyroid hormone (promotes the leaching of calcium) and sex hormones (stimulate the deposition of minerals in the bones), any changes in the endocrine glands inevitably affect the skeleton – primarily on the vertebrae, neck and head of the thigh, as well as the "tubes" of the forearm.
And with such changes, thanks to the development of society, which has extended the average life expectancy from 20-25 years to 50-60, almost everyone has to face, and especially the fair sex. The lack of estrogen in the postmenopausal period significantly increases their risk of fractures.
Despite the fact that the effect of estrogen is known, exactly how it affects the behavior of osteoclasts and bone density has long remained a mystery to scientists.
The authors of the publication in Nature Medicine went from the opposite, starting their work with the very last stage – activation of osteoclasts through the CCR2 receptor.
It turned out that the bones of mice deprived of this receptor are 40% less porous than those of "non-defective", which leads to a 47% increase in strength. Moreover, this is achieved precisely by slowing down the work of osteoclasts, and not accelerating the synthesis of new tissue.
As for the direct connection between osteoporosis and estrogen, the results are no less impressive: after removal of the ovaries synthesizing the main female sex hormone, "full–fledged" mice fell ill with osteoporosis - unlike rodents defective by CCR2.
Redlich was able to show that this success is associated with a violation of the formation of osteoclasts, or rather, their precursors: in the absence of estrogen, the content of CCR2 increases on healthy progenitor cells, which, in turn, contributes to their transformation into osteoclasts. Accordingly, if there is no CCR2, then fluctuations in the hormone level cannot affect this process in any way.
Whether this phenomenon will become the basis for the development of a new method of treating osteoporosis and preventing fractures will be shown in the near future: it is unlikely that pharmaceutical giants will want to miss a worthwhile opportunity to update the "pharmacy basket" of pensioners.
If you want to have no reason to be interested in such news by old age, the recipe has not changed: constant but moderate physical activity, less cigarettes and alcohol, dairy products in the diet and vitamins – if they are not enough in food.
Portal "Eternal youth" www.vechnayamolodost.ru08.04.2009