Cross-sectional evaluation of bone metabolism in men.
There are relatively few data concerning age-related changes of bone turnover in men. The aim of the study was to evaluate age-related changes of the levels of serum and urinary biochemical markers of bone metabolism in a large cohort of 934 men aged 19-85 years and to investigate their association with bone mineral density (BMD). Bone formation was evaluated using serum levels of osteocalcin (OC), bone alkaline phosphatase (BAP), and N-terminal extension propeptide of type I collagen (PINP). Bone resorption was evaluated by measurement of urinary excretion of beta-isomerized C-terminal telopeptide of collagen type I beta-CTX) of free deoxypyridinoline (fDpyr) and total Dpyr (tDPyr) and of the serum level of beta-CTX. Levels of biochemical bone markers were very high in young men and decreased rapidly until the age of 40 years and then more slowly until 60 years of age. After the age of 60 years, markers of bone formation remained stable while resorption markers showed a moderate and variable increase with aging. Serum and urinary beta-CTX levels were elevated only in about 5% of elderly men. The age-related increase of urinary excretion of tDpyr and of its free and peptide-bound fractions was related to the presence of elevated levels in a subgroup of about 15% of elderly men. Before 60 years of age, levels of biochemical bone markers were not correlated with BMD, whereas after 60 years of age, they were correlated negatively with BMD. After adjustment for age and body weight, BMD in men with the highest levels of biochemical bone markers (i.e., in the upper quartile) was 1.8-12.5% (i.e., 0.25-0.89 SD) lower than in men with levels of biochemical bone markers in the lowest quartile. In conclusion, bone turnover in men is high in young adults and decreases to reach a nadir at 55-60 years of age. After the age of 60 years, bone resorption markers--but not bone formation markers--increase in some men and are associated with lower BMD, suggesting that this imbalance is responsible for increasing bone loss in elderly men.
Szulc
P
P
INSERM Research Unit 403, Lyon, France.
Garnero
P
P
Munoz
F
F
Marchand
F
F
Delmas
P D
PD
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000097:blood / Q000378:metabolism* / Q000502:physiology / Q000652:urine; D000469:Alkaline Phosphatase / Q000097:blood; D000596:Amino Acids / Q000097:blood / Q000652:urine; D015415:Biomarkers; D015519:Bone Density; D001862:Bone Resorption / Q000097:blood / Q000652:urine; D001842:Bone and Bones / Q000378:metabolism* / Q000502:physiology; D003094:Collagen / Q000097:blood / Q000652:urine; D024042:Collagen Type I; D003430:Cross-Sectional Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010455:Peptides / Q000097:blood / Q000652:urine; D010748:Phosphopeptides / Q000097:blood; D011347:Procollagen
D000596:Amino Acids; D015415:Biomarkers; D024042:Collagen Type I; C062121:N-propeptide type I collagen; D010455:Peptides; D010748:Phosphopeptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; D015675:Osteocalcin; C036020:deoxypyridinoline; D003094:Collagen; D000469:Alkaline Phosphatase