bone, muscle, and skin, but not in the brain (Adler et al. 1986). In blood, silicon is
present predominately as Si(OH) 4 (Jugdaohsingh 2007), which appears to exist in
an unbound form (D’Haese et al. 1995). The plasma silicon levels (7–142 mM;
Adler and Berlyne 1986, D’Haese et al. 1995) are lower than the concentration
above which polycondensation occurs. To improve its physiological availability
which may be limited by poor absorption, organic silicon compounds have been
developed that are metabolized in the animal body (Hott et al. 1993; see also
Sect. 10.15).
10.7 Silicon and Bone Formation
There is increasing evidence that silicon is beneficial to health of bone and
connective tissue (Jugdaohsingh 2007). It has already been established in 1972
that silicon deficiency causes severe defects in connective and skeletal tissue
(Carlisle 1972, 1986; Schwarz and Milne 1972). Increased silicon levels are present
at active calcification sites during bone formation (Carlisle 1972). It has been
proposed that in bone tissue, silicon may have a structural function (Schwarz
1973). Epidemiological studies revealed a positive correlation between the silicon
intake and bone mineral density (BMD) at the hip site in men and premenopausal
women (Jugdaohsingh et al. 2004). This correlation was not found in postmenopausal women (Jugdaohsingh et al. 2004). Likewise, a positive correlation has also
been found during hormone treatment of postmenopausal women (MacDonald et al.
2005). In animal experiments with calcium-deficient ovariectomized rats, supplementation with dietary silicon was found to improve bone mineral density via
reduced bone resorption (Kim et al. 2009). These results suggest that enhanced
silicon levels are associated with an increase in BMD and bone strength
(Jugdaohsingh 2007). Also a potential interaction between the level of silicon and
the estrogen status has been discussed (Jugdaohsingh 2007).
10.8 Effect of Biosilica on Cell Proliferation
Using in vitro assays (bone forming SaOS-2 cells), the potential toxicity of
orthosilicate has been assessed (Wiens et al. 2010c). SaOS-2 cells are a nontransformed cell line derived from human primary osteosarcoma cells. This cell
line is able to differentiate, like osteoblastic cells (Kelly et al. 2010; Hausser and
Brenner 2005), and expresses proteins characteristic of osteoblasts, including
alkaline phosphatase, type I collagen, and osteocalcin (Hay et al. 2004). Moreover,
differentiation of SaOS-2 cells to HA-producing cells can be induced by exposure
to cytokines such as granulocyte macrophage colony-stimulating factor
(Postiglione et al. 2003). To determine the effect on growth of SaOS-2 cells, the
292
H.C. Schr€ oder et al.
present predominately as Si(OH) 4 (Jugdaohsingh 2007), which appears to exist in
an unbound form (D’Haese et al. 1995). The plasma silicon levels (7–142 mM;
Adler and Berlyne 1986, D’Haese et al. 1995) are lower than the concentration
above which polycondensation occurs. To improve its physiological availability
which may be limited by poor absorption, organic silicon compounds have been
developed that are metabolized in the animal body (Hott et al. 1993; see also
Sect. 10.15).
10.7 Silicon and Bone Formation
There is increasing evidence that silicon is beneficial to health of bone and
connective tissue (Jugdaohsingh 2007). It has already been established in 1972
that silicon deficiency causes severe defects in connective and skeletal tissue
(Carlisle 1972, 1986; Schwarz and Milne 1972). Increased silicon levels are present
at active calcification sites during bone formation (Carlisle 1972). It has been
proposed that in bone tissue, silicon may have a structural function (Schwarz
1973). Epidemiological studies revealed a positive correlation between the silicon
intake and bone mineral density (BMD) at the hip site in men and premenopausal
women (Jugdaohsingh et al. 2004). This correlation was not found in postmenopausal women (Jugdaohsingh et al. 2004). Likewise, a positive correlation has also
been found during hormone treatment of postmenopausal women (MacDonald et al.
2005). In animal experiments with calcium-deficient ovariectomized rats, supplementation with dietary silicon was found to improve bone mineral density via
reduced bone resorption (Kim et al. 2009). These results suggest that enhanced
silicon levels are associated with an increase in BMD and bone strength
(Jugdaohsingh 2007). Also a potential interaction between the level of silicon and
the estrogen status has been discussed (Jugdaohsingh 2007).
10.8 Effect of Biosilica on Cell Proliferation
Using in vitro assays (bone forming SaOS-2 cells), the potential toxicity of
orthosilicate has been assessed (Wiens et al. 2010c). SaOS-2 cells are a nontransformed cell line derived from human primary osteosarcoma cells. This cell
line is able to differentiate, like osteoblastic cells (Kelly et al. 2010; Hausser and
Brenner 2005), and expresses proteins characteristic of osteoblasts, including
alkaline phosphatase, type I collagen, and osteocalcin (Hay et al. 2004). Moreover,
differentiation of SaOS-2 cells to HA-producing cells can be induced by exposure
to cytokines such as granulocyte macrophage colony-stimulating factor
(Postiglione et al. 2003). To determine the effect on growth of SaOS-2 cells, the
292
H.C. Schr€ oder et al.