Which mineral is included in the composition of bone

Reviewed elsewhere, 28 the origin of the mineralization defect is unknown. This defect may be in the altered structure of the collagen itself, or in the inability of extracellular NCPs, which regulate the mineralization process, to bind to the defective collagen, and hence regulate mineralization.

Chemical analyses of the crosslinks in bone collagen have demonstrated two types of crosslinks, those formed enzymatically and those that occur by glycation. Enzymatic crosslinks are believed to enhance mechanical strength, whereas the advanced glycosylation end-products, which are elevated in uncontrolled diabetics and in oxidative stress, make for a more brittle bone.

Such analyses agree with the high-performance liquid chromatography chemical analysis of crosslinks. The heterogeneity of this distribution is decreased in consequence of age, osteoporosis and treatment with bisphosphonates. Fibronectin, a minor constituent of bone matrix, is one of the first proteins produced by osteoblasts, and directs the initial deposition of collagen fibrils. This higher incidence is due to an increased production of a fibronectin isoform that lessens osteoblastic bone formation.

There are several families of proteins that account for a small proportion of the extracellular matrix, which, as reviewed elsewhere, 40 serve important functions in matrix organization, cell signaling, metabolism and mineralization. Other than early studies showing a reduced NCP content of osteoporotic bone, 41 little has been written on how these proteins change in expression or distribution in osteoporosis or other bone diseases, with or without anabolic or antiresorptive therapies.

Known changes in the expression of NCPs in health and disease are summarized in Table 3. As shown in Table 3 , recent gene-wide association studies have identified several NCPs that may be related to fracture risk. In terms of actual measurement of protein content, findings to date are that osteocalcin and osteopontin are important for fracture resistance, 42 their concentrations are reduced in older osteonal bone 43 and osteopontin may retard crack propagation.

The interlamellar areas have lower collagen content and increased concentration of NCPs. No published studies to date have examined changes in the expression of enzymes and signaling factors in the matrix of patients with metabolic bone disease.

Items without reference numbers are discussed in that text. Lipids are important for cell function, surrounding the cell body, regulating the flux of ions and signaling molecules into and out of the cell. The distribution of lipids in the matrix can be observed from histology, based on sudanophilia, from FTIR and Raman analysis or by nuclear magnetic resonance NMR. Thirty years ago, we did analyze the lipid composition of femoral heads from patients with avascular necrosis, reporting increased cholesterol content.

The water content of bone may be demonstrated by proton NMR and can be assessed quantitatively by Raman spectroscopy 47 and gravimetric methods. Analysis of water content shows a direct relationship between water and cortical porosity, which occurs with aging and osteoporosis Figure 7 and is a key feature of renal osteodystrophy 50 and its associated osteoporosis. It is assumed, but not yet demonstrated, that decreases in porosity caused by bisphosphonate treatment will result in a lesser water content in both osteoporosis and renal osteodystrophy.

Water distribution in midshaft tibia cortical bone is demonstrated by three-dimensional ultrashort echo-time magnetic resonance imaging. Note the marked increase in bone water content BWC shown by both the concentration images on the top and their histograms c and d , respectively, on the bottom reproduced from Yoder et al.

Bone is a dynamic as well as a heterogeneous tissue; therefore, it is not surprising to see changes in composition as a function of age. These are distinct from the changes discussed above that are associated with bone disease, fragility fractures or treatments to prevent such fractures. Important is the observation that some age-dependent changes in composition are due to alterations in cell activity and protein expression as well as changes in the concentration and post-translational modification 40 of those NCPs that regulate matrix composition and mineralization.

Therapies to limit the extent of bone disease are directed against these very same cells. The interesting and important observation is that treatments for osteoporosis while decreasing fracture incidence do not consistently correct the above compositional abnormalities. Therapies currently used Table 5 , other than supplements of calcium, vitamin D and phosphate, fall into two classes: anabolic agents and antiresorptive agents.

These therapies all increase or maintain BMD. They each, however, have distinct effects on compositional properties and heterogeneity of their distribution. The most informative of the studies in Table 5 are those based on biopsies before and after treatment.

Not every study examined the same tissue site, dose of drug or duration of treatment, and many did not compare the resulting data to the same tissue site in an untreated control. The few instances where this comparison was carried out, and the therapy returned the parameter in question to healthy control values are emphasized in Table 5. Where no human data exists, animal data is included, with the caveat that this does not mean the same alterations will occur in man. Bisphosphonates, alendronate in particular, decreased the heterogeneity of the tissue, rather than increasing it, as would be appropriate for a mechanically strong tissue.

Calcitriol's effect on bone composition has not been determined, neither were the effects of sclerostin antibodies. Odanatacib, the cathepsin K inhibitor, has been shown to affect composition based on BMDD measurements. I, D, N and NA show changes relative to untreated osteoporotic patients. Differences in reported values may be because of site, duration of treatment or method of analysis.

Where no human data was available, other species are shown in italics. Bold indicates treatments that were reported to normalize indicated property to that in healthy controls. The anabolic agent PTH and strontium-ranelate, which may have both catabolic and anabolic properties, correct many of these FTIRI properties and increase tissue heterogeneity.

Older bone has increased collagen maturity and increased crystal size. Anabolic agents, in contrast, stimulate new bone formation and the tissue acquired has characteristics of younger bone. Loss of material heterogeneity, in fracture mechanics, is associated with an increase in brittleness, hence a greater risk of fracture. The importance of heterogeneity is seen in lumber structure and in development of stronger cements and plastics. Bisphosphonate treatment usually results in an increase of bone mineral density and bone volume, or in its maintenance.

Bisphosphonate treatment is often accompanied by a decrease in heterogeneity. The reason for this event is as yet uncertain. It may be that there is a balance in these two opposing effects. The use of bisphosphonates results in an increase in BMD and bone volume, hence an increase in bone stiffness and strength.

The use of bisphosphonates also causes a decrease in bone heterogeneity, which in turn increases bone brittleness. Thus, the composition of bone in the healthy individual must be maintained and adjusted, similar to the structure described by Wolff's law, so as to optimize the function of bone. This review of mineral and matrix properties in healthy and diseased bones demonstrates that these properties show both age- and disease-dependent changes. Bone disease and therapies for these diseases also affect the composition of bone.

Bisphosphonates increase bone quantity but their effects on bone quality are variable. The effects of many other agents used in the treatment of osteoporosis are still under investigation. Some bisphosphonates decrease tissue heterogeneity, which may in turn increase brittleness. The origins of this effect and the significance of the alteration in bone quality remain to be determined. I am grateful to Dr Judah Gerstein for his assistance in editing this manuscript.

The author declares no conflict of interest. National Center for Biotechnology Information , U. Journal List Bonekey Rep v. Bonekey Rep. Published online Dec 4. Adele L Boskey a, 1, 2. Author information Article notes Copyright and License information Disclaimer. E-mail: ude. SSH ayeksoB or moc. Received Jul 9; Accepted Sep This article has been corrected.

See Bonekey Rep. This article has been cited by other articles in PMC. Abstract The composition of a bone can be described in terms of the mineral phase, hydroxyapatite, the organic phase, which consists of collagen type I, noncollagenous proteins, other components and water. Bone mineral Hydroxyapatite is the principal component of the mineral phase of bone.

Open in a separate window. Figure 1. Figure 2. Figure 3. Figure 4. Figure 5. Figure 6. Bone matrix Protein composition of bone was classically determined following demineralization of the tissue and isolation and characterization of the component proteins. Structural proteins Collagen The most abundant protein in the bone matrix is type I collagen, a unique triple helical molecule consisting of two identical amino-acid chains and one that is different. Fibronectin Fibronectin, a minor constituent of bone matrix, is one of the first proteins produced by osteoblasts, and directs the initial deposition of collagen fibrils.

Noncollagenous proteins There are several families of proteins that account for a small proportion of the extracellular matrix, which, as reviewed elsewhere, 40 serve important functions in matrix organization, cell signaling, metabolism and mineralization. Table 3 Variation of noncollagenous bone protein concentrations in healthy and diseased human and animal bones a.

Protein Bone conc. Bone Gla protein osteocalcin Reduced 67 Increased 66? Increased 68? Matrix Gla protein Reduced 69? Decorin Depleted 72 No change 68?

Osteoadherin No change 74? Decreased 80? Water The water content of bone may be demonstrated by proton NMR and can be assessed quantitatively by Raman spectroscopy 47 and gravimetric methods. Figure 7. Composition changes in aging and disease Bone is a dynamic as well as a heterogeneous tissue; therefore, it is not surprising to see changes in composition as a function of age. Table 4 Age-related changes in healthy bone composition cortical and cancellous considered together.

Bone mineral density a and tissue mineral density b Increase with age Mineral to organic matrix ratio c Increase with age Calcium-to-phosphate ratio d Increase with age Carbonate-to-phosphate ratio c Increase with age Crystal size and perfection crystallinity c , e Increase with age Acid phosphate substitution c Decrease with age Matrix heterogeneity b , c Decrease with age Total collagen crosslinks collagen maturity c Increase with age Collagen enzymatic crosslinks d Increase with age Collagen AGEs d Increase with age.

Compositional changes induced by therapies for osteoporosis The interesting and important observation is that treatments for osteoporosis while decreasing fracture incidence do not consistently correct the above compositional abnormalities. Table 5 Effects of current therapies on cancellous bone compositional properties. Conclusions This review of mineral and matrix properties in healthy and diseased bones demonstrates that these properties show both age- and disease-dependent changes.

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Bone ; 46 — Annual intravenous zoledronic acid for three years increased cancellous bone matrix mineralization beyond normal values in the HORIZON biopsy cohort. It is essential for structure, strength, and growth of the bones and bone cells. This mineral is hydroxyapatite. Bone Marrow, it is the base of the bone. Bone Mineral Density tests measure the density of minerals in your bones to determine bone strength.

This could often be found to be beneficial. According to biologists, x-ray beams cannot penetrate through bone mineral because it is very strong and dense. Bone mineral tests are performed to measure calcium levels in the bone. The bone mineral. The most abundant mineral in the body.

Fish bone does no meet the definition of a mineral because it is organic. In fossils of fish bones the bone has been replaced by a mineral. Log in. Rocks and Minerals. See Answer. Best Answer. Study guides. Q: Is bone a mineral Write your answer Related questions. What is the mineral substance in bone? Why is bone not considered a mineral? A mineral needed by bone cells?

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