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Biochemical markers for assessment of calcium economy and bone metabolism: application in clinical trials from pharmaceutical agents to nutritional products.

Bonjour JP, Kohrt W, Levasseur R, Warren M, Whiting S, Kraenzlin M - Nutr Res Rev (2014)

Bottom Line: Thus modification in bone remodelling, the key process upon which both pharmaceutical agents and nutrients exert their anti-catabolic or anabolic actions, is revealed.Circulating BTM reflect either osteoclastic resorption or osteoblastic formation.Intervention with pharmacological agents showed that early changes in BTM predicted bone loss and subsequent osteoporotic fracture risk.

View Article: PubMed Central - PubMed

Affiliation: Division of Bone Disease, University Hospitals and Faculty of Medicine,Geneva,Switzerland.

ABSTRACT
Nutrition plays an important role in osteoporosis prevention and treatment. Substantial progress in both laboratory analyses and clinical use of biochemical markers has modified the strategy of anti-osteoporotic drug development. The present review examines the use of biochemical markers in clinical research aimed at characterising the influence of foods or nutrients on bone metabolism. The two types of markers are: (i) specific hormonal factors related to bone; and (ii) bone turnover markers (BTM) that reflect bone cell metabolism. Of the former, vitamin D metabolites, parathyroid hormone, and insulin-like growth factor-I indicate responses to variations in the supply of bone-related nutrients, such as vitamin D, Ca, inorganic phosphate and protein. Thus modification in bone remodelling, the key process upon which both pharmaceutical agents and nutrients exert their anti-catabolic or anabolic actions, is revealed. Circulating BTM reflect either osteoclastic resorption or osteoblastic formation. Intervention with pharmacological agents showed that early changes in BTM predicted bone loss and subsequent osteoporotic fracture risk. New trials have documented the influence of nutrition on bone-tropic hormonal factors and BTM in adults, including situations of body-weight change, such as anorexia nervosa, and weight loss by obese subjects. In osteoporosis-prevention studies involving dietary manipulation, randomised cross-over trials are best suited to evaluate influences on bone metabolism, and insight into effects on bone metabolism may be gained within a relatively short time when biochemical markers are monitored.

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Related in: MedlinePlus

Bone remodelling cycle. Bone turnover follows a sequence of events that includes activation, recruitment of osteoclasts (Ocl) to begin resorption, degradation and removal of bone, reversal, and formation of new bone by osteoblasts (Ob). After this phase a quiescent or resting period occurs. LC, lining cell; Oc, osteocyte.
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fig1: Bone remodelling cycle. Bone turnover follows a sequence of events that includes activation, recruitment of osteoclasts (Ocl) to begin resorption, degradation and removal of bone, reversal, and formation of new bone by osteoblasts (Ob). After this phase a quiescent or resting period occurs. LC, lining cell; Oc, osteocyte.

Mentions: Bone remodelling is an important process that continuously renews the cortical and trabecular envelopes throughout life. It repairs micro-damage, maintains mineral homeostasis and ensures mechanical competence by modifying the micro-architecture. Bone remodelling is regulated by a variety of systemic and local factors as well as by nutritional factors (Fig. 1). Bone remodelling follows a sequence of events that includes activation, recruitment of osteoclasts to begin resorption, degradation and removal of bone, reversal, and formation of new bone by osteoblasts (Fig. 1). After this phase, a quiescent or resting period occurs. Remodelling begins with release of cytokines from osteoblast precursors, leading to recruitment of osteoclast precursors, which differentiate in multinucleated osteoclasts and subsequently attach to the bone surface. Resorption of the skeletal matrix releases growth factors such as IGF-I and transforming growth factor-β, which recruit lining cells and early osteoblast precursors that eventually form new bone (Fig. 1). Osteoblasts that do not undergo apoptosis remain on the bone surface as lining cells or become entrapped as osteocytes into the new bone matrix. These osteocytes respond to gravitational forces and can signal to lining cells to initiate remodelling. Antiresorptive and anabolic agents influence bone structure by affecting remodelling. Likewise, supply in Ca, vitamin D and protein influences bone remodelling. The presence of Ca and vitamin D inhibits bone resorption, and protein stimulates bone formation (Fig. 1). Ca, Pi and vitamin D are necessary for adequate mineralisation of the newly formed bone matrix (Fig. 1).Fig. 1


Biochemical markers for assessment of calcium economy and bone metabolism: application in clinical trials from pharmaceutical agents to nutritional products.

Bonjour JP, Kohrt W, Levasseur R, Warren M, Whiting S, Kraenzlin M - Nutr Res Rev (2014)

Bone remodelling cycle. Bone turnover follows a sequence of events that includes activation, recruitment of osteoclasts (Ocl) to begin resorption, degradation and removal of bone, reversal, and formation of new bone by osteoblasts (Ob). After this phase a quiescent or resting period occurs. LC, lining cell; Oc, osteocyte.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4307651&req=5

fig1: Bone remodelling cycle. Bone turnover follows a sequence of events that includes activation, recruitment of osteoclasts (Ocl) to begin resorption, degradation and removal of bone, reversal, and formation of new bone by osteoblasts (Ob). After this phase a quiescent or resting period occurs. LC, lining cell; Oc, osteocyte.
Mentions: Bone remodelling is an important process that continuously renews the cortical and trabecular envelopes throughout life. It repairs micro-damage, maintains mineral homeostasis and ensures mechanical competence by modifying the micro-architecture. Bone remodelling is regulated by a variety of systemic and local factors as well as by nutritional factors (Fig. 1). Bone remodelling follows a sequence of events that includes activation, recruitment of osteoclasts to begin resorption, degradation and removal of bone, reversal, and formation of new bone by osteoblasts (Fig. 1). After this phase, a quiescent or resting period occurs. Remodelling begins with release of cytokines from osteoblast precursors, leading to recruitment of osteoclast precursors, which differentiate in multinucleated osteoclasts and subsequently attach to the bone surface. Resorption of the skeletal matrix releases growth factors such as IGF-I and transforming growth factor-β, which recruit lining cells and early osteoblast precursors that eventually form new bone (Fig. 1). Osteoblasts that do not undergo apoptosis remain on the bone surface as lining cells or become entrapped as osteocytes into the new bone matrix. These osteocytes respond to gravitational forces and can signal to lining cells to initiate remodelling. Antiresorptive and anabolic agents influence bone structure by affecting remodelling. Likewise, supply in Ca, vitamin D and protein influences bone remodelling. The presence of Ca and vitamin D inhibits bone resorption, and protein stimulates bone formation (Fig. 1). Ca, Pi and vitamin D are necessary for adequate mineralisation of the newly formed bone matrix (Fig. 1).Fig. 1

Bottom Line: Thus modification in bone remodelling, the key process upon which both pharmaceutical agents and nutrients exert their anti-catabolic or anabolic actions, is revealed.Circulating BTM reflect either osteoclastic resorption or osteoblastic formation.Intervention with pharmacological agents showed that early changes in BTM predicted bone loss and subsequent osteoporotic fracture risk.

View Article: PubMed Central - PubMed

Affiliation: Division of Bone Disease, University Hospitals and Faculty of Medicine,Geneva,Switzerland.

ABSTRACT
Nutrition plays an important role in osteoporosis prevention and treatment. Substantial progress in both laboratory analyses and clinical use of biochemical markers has modified the strategy of anti-osteoporotic drug development. The present review examines the use of biochemical markers in clinical research aimed at characterising the influence of foods or nutrients on bone metabolism. The two types of markers are: (i) specific hormonal factors related to bone; and (ii) bone turnover markers (BTM) that reflect bone cell metabolism. Of the former, vitamin D metabolites, parathyroid hormone, and insulin-like growth factor-I indicate responses to variations in the supply of bone-related nutrients, such as vitamin D, Ca, inorganic phosphate and protein. Thus modification in bone remodelling, the key process upon which both pharmaceutical agents and nutrients exert their anti-catabolic or anabolic actions, is revealed. Circulating BTM reflect either osteoclastic resorption or osteoblastic formation. Intervention with pharmacological agents showed that early changes in BTM predicted bone loss and subsequent osteoporotic fracture risk. New trials have documented the influence of nutrition on bone-tropic hormonal factors and BTM in adults, including situations of body-weight change, such as anorexia nervosa, and weight loss by obese subjects. In osteoporosis-prevention studies involving dietary manipulation, randomised cross-over trials are best suited to evaluate influences on bone metabolism, and insight into effects on bone metabolism may be gained within a relatively short time when biochemical markers are monitored.

Show MeSH
Related in: MedlinePlus