FEATURE PAEDIATRICS
INTRODUCTION Senile osteoporosis begins as a paediatric disease. This seeming paradox is rooted in the fact that there is intense skeletal growth and development during childhood and adolescence, and much more bone is formed than lost. Later in life the loss of bone tissue exceeds the rate of bone replacement. The structural and metabolic missions
of the skeleton are realized through the coordinated interaction of osteoblasts and osteoclasts. Osteoblasts are bone- forming cells, and are derived from pluripotent mesenchymal stem cells that can also differentiate into muscle, adipocytes, cartilage, or fibrous tissue. Bone is resorbed by osteoclasts, large, multinucleated cells that can dissolve mineral and release calcium and phosphorous into the extracellular fluid. Osteoclasts are related to monocyte/ macrophage cells. Development and growth of the skeleton
during embryogenesis occur through a process termed modeling. After birth, the skeleton continues to grow by sustained modeling through puberty. In addition to modeling, bones are continuously reshaped by removing and replacing skeletal structures already present, a process termed remodeling. Linear growth during childhood and adolescence occurs by growth of cartilage at the end plates of long bones, followed by endochondral bone formation. The width of the bones increases by periosteal apposition. During puberty and early adult life, endosteal apposition and trabecular thickening provide maximum skeletal mass and strength (peak bone mass). Locally and systemically produced factors and mechanical forces influence these processes. The adult skeleton continues to undergo remodeling throughout life, replacing approximately 15% of the mature skeleton each year to maintain mineral homeostasis, to repair damaged bone, and to respond to changes in skeletal stress. Bone remodeling occurs most often in skeletal sites rich in cancellous (trabecular) bone, such as the vertebrae, proximal femur, calcaneus, and ultradistal radius. A second form of bone, termed cortical bone, is less metabolically active but provides great strength and integrity to the skeleton. Cortical bone comprises 80% of the skeleton, is dense and compact, and constitutes the outer part of all skeletal structures.
During the first two decades of life the
skeleton grows in both size and density, and up to 90% of peak bone mass is acquired by age 18 in girls and by age 20 in boys. Bone mass continues to accumulate until around age 30. At that point, bones have reached their maximum strength and density, known as peak bone mass. Women tend to experience minimal change in total bone mass between age 30 and menopause. But in the first few years after menopause, many women experience a period of rapid bone loss, which then slows but continues throughout the postmenopausal years. This loss of bone mass can lead to osteoporosis. In men age-related bone loss occurs later and proceeds at a steady rate. In both men and women, declining bone mass is the primary cause of weak bones and fragility fractures. It therefore follows that lifelong bone
health is dependent on maximizing peak bone mass during the critical periods of childhood and adolescence. We may think of each individual as possessing a “Bone Bank” in which early deposits lay the foundation for skeletal health; later, during aging or in response to metabolic stresses, skeletal remodeling accelerates and withdrawals from the account exceed deposits, thereby compromising skeletal integrity. The natural process of bone remodeling makes youth the best time to “invest” in one’s bone health. Accordingly, in 2000, the U.S. National Institutes of Health convened experts at a Consensus Development Conference on Osteoporosis
«Dark skin, use of UV sunblockers or customs of dress that largely cover the skin can reduce cutaneous absorption of UVB light»
Prevention, Diagnosis and Treatment. Among other measures, the Conference recommended developing research strategies to optimize bone mass during the first two decades of life, and to identify and intervene in disorders that compromise attainment of peak bone mass, particularly in children with chronic disease.
WHAT AFFECTS BONE MASS IN CHILDREN About 60-80% of the contribution to peak bone mass is thought to be genetically influenced, although not all the relevant genes have yet been identified. Environmental factors account for the remaining 20-40%: variations in nutrition (particularly calcium and vitamin D), physical activity, body mass (increased visceral fat mass is associated with low bone mass), hormonal influences (including estrogen, testosterone, and parathyroid hormone), infectious agents (such as HIV), metabolic disorders and cancer. Because gonadal hormones secreted during puberty increase bone mass, delayed puberty has a deleterious
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