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Bone Turnover Markers and Glucocorticoid Treatments

  • Jean-Pierre DevogelaerEmail author
  • Anne DurnezEmail author
  • Damien GrusonEmail author
  • Daniel H. ManicourtEmail author
Reference work entry
  • 849 Downloads
Part of the Biomarkers in Disease: Methods, Discoveries and Applications book series (BDMDA)

Abstract

Glucocorticoids (GCs) remain as the cornerstone of therapy in most inflammatory diseases, even if newly developed biological molecules became available. GCs are potent, possess a fast action, and are cheap and relatively easy to prescribe. However, their beneficial therapeutic activity has a nasty counterpart: quite a lot of complications, notably secondary osteoporosis, aseptic bone osteonecrosis, and fractures. The skeleton is continuously remodeling, old bone being resorbed and replaced by new young bone. GCs interfere with the bone turnover and provoke a disequilibrium in favor of bone loss and fragility. The mechanisms of bone fragility consist of a decreased activity and in apoptosis of osteoblasts, as well as an increase in bone resorption. These changes have already been observed histomorphometrically a long time ago in transiliac bone biopsies. Biological parameters of bone turnover, chiefly degradation products of type I collagen, can help to assess atraumatically the bone metabolism. If, in idiopathic osteoporosis, they can have a predictive value of bone loss, they cannot be considered as surrogates for bone mineral density measurements. In GC-OP, the concentrations of the bone turnover markers (BTMs) of bone formation dramatically and rapidly decrease, whereas the BTMs of bone resorption slightly increase. During GC therapy, they cannot be used as predictive tools of bone fragility on an individual basis. Other markers such as RANKL/RANK/osteoprotegerin seem to be promising in this aim, but this still awaits confirmation.

Keywords

Glucocorticoid Bone turnover Biomarkers Osteoporosis Bone mineral density Bone remodeling Collagen Telopeptide 

List of Abbreviations

ALN

Alendronate

BDP

Beclomethasone dipropionate

BMD

Bone mineral density

BSAP

Bone-specific alkaline phosphatase

BTMs

Bone turnover markers

BUD

Budenoside

CD

Crohn’s disease

COMP

Cartilage oligomeric matrix protein

COPD

Chronic obstructive pulmonary disease

CTX

Carboxy-terminal cross-linking telopeptide of type I collagen

DAS

Disease activity score

Dkk-1

Dickkopf-1

FN

Femoral neck

GC

Glucocorticoid

ICTP

Carboxy-terminal telopeptide of type I collagen

Il-6

Interleukin-6

JIA

Juvenile idiopathic arthritis

MMP

Metalloproteinase

MP

Methylprednisolone

NTX

Amino-terminal cross-linking telopeptide of type I collagen

OBS

Osteoblasts

OC

Osteocalcin

OCS

Osteoclasts

OP

Osteoporosis

OPG

Osteoprotegerin

PICP

Procollagen type I C-terminal propeptide

PINP

Procollagen type I N-terminal propeptide

PTH

Parathyroid hormone

RA

Rheumatoid arthritis

RANK

Receptor activator of nuclear factor NF-kB

RANK-L

Receptor activator of nuclear factor NF-kB-ligand

rh

Recombinant human

RIS

Risedronate

Scl

Sclerostin

SLE

Systemic lupus erythematosus

TPTD

Teriparatide

TRAP

Tartrate-resistant acid phosphatase

UC

Ulcerative colitis

uDPD

Urinary deoxypyridinoline

uPYD

Urinary pyridinoline

VF

Vertebral fracture

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© Springer Science+Business Media Dordrecht 2017

Authors and Affiliations

  1. 1.Pôle de Pathologie RhumatismaleUniversite Catholique de LouvainBrusselsBelgium
  2. 2.Pôle de Recherche en Endocrinologie, Diabète et Nutrition et Département des Laboratoires Cliniques, Institut de Recherche Expérimentale et Clinique, Cliniques Universitaires Saint-LucUniversité catholique de LouvainBruxellesBelgium
  3. 3.AZ Jan PortaelsVilvoordeBelgium

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