Bone mineralization in childhood and adolescence.
Prevention of osteoporosis depends on establishing adequate peak bone mass in the first two decades of life. Achievement of this goal requires an understanding of factors that promote skeletal health. Genetic factors are important determinants of adult bone mass, but nonheritable variables, including body mass, calcium nutriture, sex steroids, and activity can strongly influence whether maximal bone mineral is achieved. Acquisition of bone mineral continues throughout childhood and adolescence, reaching a lifetime maximum in early adulthood. Adolescence is a particularly critical time for bone mineral accretion as more than half of the bone calcium is normally laid down during the teen years. Chronic illness, malnutrition, or endocrine deficiencies at this age may result in profound deficits in bone mass, which may not be fully reversible. These risk factors contribute to the osteopenia associated with anorexia nervosa, exercise-induced amenorrhea, delayed puberty, Turner's syndrome, and growth hormone deficiency.
Bachrach
L K
LK
Department of Pediatrics, Stanford Medical Center, CA 94305.
D000293:Adolescent; D000568:Amenorrhea / Q000503:physiopathology; D000856:Anorexia Nervosa / Q000503:physiopathology; D001847:Bone Diseases / Q000503:physiopathology; D001851:Bone Diseases, Metabolic / Q000503:physiopathology; D002113:Calcification, Physiologic; D002648:Child; D004700:Endocrine System Diseases / Q000503:physiopathology*; D005260:Female; D013006:Growth Hormone / Q000172:deficiency; D006801:Humans; D008297:Male; D011628:Puberty, Delayed / Q000503:physiopathology; D014424:Turner Syndrome / Q000503:physiopathology
D013006:Growth Hormone