Osteoporosis in the most common metabolic bone disease in older adults (affecting 40-50% of women and 13-22% of men, Johnel and Kanis, 2005), but is very rare in the young. The classical definition of osteoporosis should be valid at any age (deviation in bone density from normal values), yet diagnosis in children is usually based on history of fractures, in addition to bone mineral density evaluations. Lack of consensus in diagnosing makes juvenile osteoporosis prevalence elusive: 6-19% of children are identified with poor skeletal health (6% found by means quantitative computed tomography, 19% using dual emission x-ray absorptiometry (DEXA) which is usually used in adults (low spine bone mineral density, Z-score < –2). Specialists in osteoporosis hope that differential DXA scores for children and adults for osteoporosis diagnosing can be developed. A recent examination of this issue found that X-rays are not good enough for diagnosing osteoporosis in children and DEXA scans should be employed instead.
Juvenile idiopathic osteoporosis may have primary genetic cause, but it is usually secondary to inflammatory diseases that affect bone metabolism because of high cytokine levels and corticosteroid use. Juvenile osteoporosis can also be secondary to endocrine disorders such as hyperparathyroidism, hypercortisolism, Type 1 diabetes, hyperthyroidism, and hypogonadism which change the body's hormone levels. Children and teens with restricted mobility often suffer lower bone density due to atrophy. You see this a lot in kids confined to wheelchairs or beds. Osteoporosis is also associated with neoplastic disorders and drugs such as glucocorticoids and anticonvulsants. It has been found that an inbalanced muscle-bone relationship is characteristic of juvenile osteoporosis. Nutritional problems such as vitamin D deficiency and intesintal malabsorption are also risk factors for children, the same as they are for adults.
The best way to stop juvenile osteoporosis is to prevent it before it happens. Prevention includes a nutritional diet, vitamin D and calcium supplementation, and regular intense physical activity (Lanyon and Rubin, 1984; Cassel et al., 1996; Heinonen, 1995).
The exact pathogenesis of juvenile osteoporosis is not known but evidence points toward disturbed bone remodeling which predominantly affects surfaces that are in contact with the marrow cavity and results in a very low bone formation rate and decreased cancellous bone volume (Rauch et al., 2002). The age of onset of the disease varies from one to thirteen years. The disease shows no sex predilection (Smith, 1995). Secondary osteoporosis is a risk in children with juvenile idiopathic arthritis.
Osteoporosis happens when body loses boney tissue too fast or doesn't build it up fast enough. Normally in children and young adults, these are in balance. But in osteoporosis, they are out of balance and you experience a net loss. The opposite of osteoporosis is osteopetrosis when bones get too dense. Because children are growing, they normally experiece and increase in bone mass over the years. If a kid doesn't gain more bone as he or she grows up, juvenile osteoporosis can occur.
The main presenting symptoms include repeated long bone fractures, pain in the back, feet, joints and difficulty or inability to walk. Particularly, the latter symptom has been stressed by many authors (Villaverd et al., 1998; Chlebna et al., 2001). Bone fracture after minimal trauma can be the first manifestation of the disease (Dent and Friedman, 1965), and doctors usually make a diagnosis only after fractures occur with minor trauma or when medical imaging shows hypodense bones. Typical radiological changes include generalized osteoporosis, compression of vertebral bodies, and metaphyses of the long bones. Phosphorus balance may be negative only in severe form of the disease (Lapatsanis et al., 1971).
In majority of cases, juvenile osteoporosis naturally remits during or after puberty (Dent and Friedman, 1965; Cloutier et al., 1967; Kulkarni and Keshavamurthy, 2004). Nevertheless doctors seek to protect affected children from developing permanent deformities of the spine and long bones by restricting activities. Drugs like calcitriol (Vitamin D), biphosphonates, fluorides and calcitonin have been used with equivocal results (Krassas, 2000): in one study 3 out of 4 affected children treated with calcitriol showed significant improvement in bone mineralization after 12 months (Saggese et al., 1991), while another study did not show any effect of calcitriol on the disease (Jackson et al., 1988).
Doctors attempt to be careful when using these drugs for pediatric patients because the late potential secondary effects are still unknown (Delalande et al., 2008). The consensus of the medical establishment is that the evidence is insufficient to advocate any treatment other than activity restriction until the osteoporosis subsides because of growth and density.
Some babies are born with osteopenia. This is more common in premature deliveries, where the fetus did not have time to develop bones of normal strength in a full third trimester, which is when bones normally develop rapidly. When the mother has a deficiency of Vitamin D or has been taking steroids or diuretics, the risk is increased for infant osteopenia. Ultrasound and routine blood tests on the baby can help diagnose the condition.
Neonatal specialists often recommend calcium and phosphorus supplements – these are more likely to work for newborns than for adults.
Bones start growing while the fetus is still in the womb. Newborns do not have osteoporosis, per se, but premature babies often need extra supplements of calcium and phosphorus to get better bones. Experts often recommend breastfed babies get extra Vitamin D to build strong bones.
The childhood and teen years are critical for building bone size and strength which is why nutrition and exercise are more important during these years than during the adult years.
Other Bone Diseases: