Silicon in the human body occurs in trace amounts, but plays an important role: it is a cross-linking factor and a structural element of connective tissue; an element necessary for the proper course of bone growth, calcification and mineralization. Interestingly, until recently, it was thought that the impact of silicon on human life processes is negligible. The basic source of silicon in the diet are cereal grains, its deficiencies can therefore occur in people who consume mainly white bread. Silicon compounds derived from food in the digestive tract are hydrolysed to easily digestible orthosilicic acid. Chronic silicon deficiency threatens to impair collagen synthesis and bone matrix mineralization, and increases the risk of premature osteoporosis.
Osteoporosis is one of the most important health problems of the modern world; according to available data, nearly 75 million people suffer from it - Europeans, Japanese and Americans. Low bone mass with high susceptibility to fractures affects over 30 percent women in postmenopausal age, and in seniors the problem is practically common. Forecasts are, unfortunately, pessimistic: it is estimated that in the next half century, the number of osteoporotic fractures will double at least. It is believed that the development of this pathology is strongly influenced by an incorrect diet with deficiencies of micro- and macroelements.
In vitro results showed that orthosilicic acid at physiological concentration stimulates collagen type 1 synthesis and differentiation of human osteoblasts. Osteoblasts are osteogenic cells that build bones from scratch (take part in bone growth or remodeling processes), produce an amorphous bone matrix (or osteoid), where calcium phosphate crystals accumulate.
In the development of osteoporosis, bone remodeling or rejuvenation processes are important, thanks to which bones maintain their key biomechanical properties. In their course, the "old" tissue is constantly replaced by new due to the activation of the so-called osteoclast cells - osteoclasts that are responsible for bone resorption (collagen degradation and hydroxyapatite crystal hydration). As a result, a resorptive cavity forms on the bone surface. Then they start to creep osteoblasts, which, when mature, produce type I collagen and osteoid. Gradually, the cavity fills up, mineralizes, and mature bone forms.
The results of studies in animal models indicate that the concentration of silicon in "young" osteoids is 25 times higher than in neighboring structures, but decreases with increasing calcium content in mature bone. Silicon is thought to be one of the factors that accelerate matrix mineralization.
The remodeling process lasts a lifetime. The ratio of bone formation to destruction is the so-called total bone mass. Man reaches peak bone mass around the age of 30 - its correct value depends on many factors, but the most important thing is that bone formation processes prevail over resorption. After the age of 40, the rate of bone loss is increasing, which is why abnormal peak bone mass is a serious aggravating factor in adulthood. If it coexists with other factors (disease, environmental), it negatively affects bone metabolism and significantly increases the risk of earlier onset of osteoporosis and pathological fractures.
Conducted epidemiological experiments indicate the role of silicon in the synthesis of collagen and glycosaminoglycan as well as metabolic processes of connective tissue and bone tissue. It is believed that the degree of bone mineralization may depend on the supply of dietary silicon.
Silicon is one of the trace elements recommended in the prevention of osteoporosis. The element participates in collagen production processes (in bones, cartilage, connective tissue) and can accelerate mineralization processes. Silicic acid is the best available for humans, animals and plants. Adequate supply of the element is particularly important in the first stages of bone development.
A deficiency of silicon can negatively affect the bone formation process, delay the development of the skeletal system and contribute to bone deformities. Insufficient supply of the element with a diet can impair the processes of connective tissue formation, including articular cartilage. Disorders of the quality and quantity of articular cartilage increase the risk of joint injuries, as cartilage is responsible for the depreciation of articular surfaces.
Studies in animal models have shown that silicon supplementation has a beneficial effect on bone mineral density (increases it), reducing brittleness. We would like to remind you that the decrease in mineral density and bone structure and quality disorders are directly responsible for susceptibility to osteoporotic fractures.