Publisher Summary This chapter reviews the clinical areas of interest, the possible applications, and limitations of using markers in the pediatric setting. Biochemical markers of bone metabolism are compounds that are released from bone tissue into the circulation and can be quantified in serum or urine samples. In adults, bone turnover markers mainly represent bone remodeling and are commonly used as independent predictors of the risk of osteoporosis and fractures, to monitor antiresorptive therapy and also have a promising role in metastatic bone disease. In children, these markers are released into the circulation during three different physiological processes: growth in bone length (bone elongation); growth in bone width (bone modeling by periosteal expansion); and bone remodeling (turnover). All bone markers measured in children reflect the sum of these three processes.

Biochemical Markers of Bone Metabolism

Rickets is an important problem even in countries with adequate sun exposure. The causes of rickets/osteomalacia are varied and include nutritional deficiency, especially poor dietary intake of vitamin D and calcium. Non-nutritional causes include hypophosphatemic rickets primarily due to renal phosphate losses and rickets due to renal tubular acidosis. In addition, some varieties are due to inherited defects in vitamin D metabolism and are called vitamin D dependent rickets. This chapter highlights rickets/osteomalacia related to vitamin D deficiency or to inherited defects in vitamin D metabolism. Hypophosphatemic rickets and rickets due to renal tubular acidosis are discussed in other sections of the journal.

https://cyberleninka.org/article/n/923901.pdf

Rickets-vitamin D deficiency and dependency.

Bone mass acquired during childhood and adolescence is a key determinant of adult bone health Peak bone mass, which is achieved in late adolescence, is a main determinant of osteoporosis in adulthood Therefore, any factor adversely impacting on bone acquisition during childhood or adolescence can potentially have long-standing detrimental effects on bone health predisposing to osteoporosis and fracture risk Thus, osteoporosis can well have its origin in childhood and adolescence Pediatricians should be playing an active role in osteoporosis diagnosis and prevention It is increasingly recognized that osteoporosis may occur in some disorders of children and adolescents In this paper we review the diagnostic criteria of osteopenia/osteoporosis by densitometric assessment of bone mineral density, the contributing factors, and the mechanisms whereby several disorders may affect the acquisition of bone mass in children and adolescents Finally, some recommendations to optimize peak bone mass in order to prevent osteopenia/osteoporosis are suggested

Osteoporosis in Children and Adolescents: Diagnosis, Risk Factors, and Prevention

Nutritional rickets remains a global public health problem, despite effective and inexpensive means to prevent and treat the disease. It is most prevalent in the infant/toddler age groups and the adolescent, but vitamin D deficiency is also prevalent in women of child bearing age, resulting in babies being born with low vitamin D stores and the mothers having inadequate vitamin D in breast milk, thus exacerbating the risk for rickets in these infants. In a number of subtropical developing countries, rickets appears to be due to low-dietary calcium intakes (∼200 mg/day) rather than vitamin D deficiency. Biochemically these children are differentiated from those with vitamin D deficiency by having markedly elevated serum 1,25-dihydroxyvitamin D concentrations and high fractional intestinal calcium absorption. Nutritional rickets represents the outcome of a spectrum of causes ranging from vitamin D deficiency on one hand to dietary calcium deficiency on the other, while in between low dietary intakes and vitamin D insufficiency combine to cause the disease.

Vitamin D Deficiency and Nutritional Rickets in Children

Bone mass increases progressively during childhood, but mainly during adolescence when approximately 40% of total bone mass is accumulated. Peak bone mass is reached in late adolescence, and is a well recognised risk factor for osteoporosis later in life. Thus, increasing peak bone mass can prevent osteoporosis. The critical interpretation of bone mass measurements is a crucial factor for the diagnosis of osteopenia/osteoporosis in children and adolescents. To date, there are insufficient data to formally define osteopenia/osteoporosis in this patient group, and the guidelines used for adult patients are not applicable. In males and females aged <20 years the terminology ‘low bone density for chronologic age’ may be used if the Z-score is less than −2. For children and adolescents, this terminology is more appropriate than osteopenia/osteoporosis. Moreover, the T-score should not be used in children and adolescents. Many disorders, by various mechanisms, may affect the acquisition of bone mass during childhood and adolescence. Indeed, the number of disorders that have been identified as affecting bone mass in this age group is increasing as a consequence of the wide use of bone mass measurements. The increased survival of children and adolescents with chronic diseases or malignancies, as well as the use of some treatment regimens has resulted in an increase in the incidence of reduced bone mass in this age group. Experience in treating the various disorders associated with osteoporosis in childhood is limited at present. The first approach to osteoporosis management in children and adolescents should be aimed at treating the underlying disease. The use of bisphosphonates in children and adolescents with osteoporosis is increasing and their positive effect in improving bone mineral density is encouraging. Osteoporosis prevention is a key factor and it should begin in childhood. Pediatricians should have a fundamental role in the prevention of osteoporosis, suggesting strategies to achieve an optimal peak bone mass.

Osteoporosis in children and adolescents: etiology and management.

UNLABELLED Biochemical markers of bone formation [alkaline phosphatase, osteocalcin, and carboxyterminal propeptide of type I procollagen (PICP)] and bone resorption [cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and cross-linked N-telopeptides of type I collagen (NTX)] were measured in 14 children aged 8.5-10.5 mo with vitamin D deficiency rickets before and longitudinally during vitamin D treatment (3000-4000 IU/daily). Forty-four healthy children aged 8-10.5 mo were enrolled as sex- and age-matched controls. Before treatment, serum levels of alkaline phosphatase, PICP, and ICTP, and urinary excretion values of NTX were significantly higher, and serum osteocalcin levels significantly lower than controls (31.4 +/- 3.5 microkat/L and 9.8 +/- 2.9 microkat/L, p < 0.001; 1025 +/- 89 microg/L and 952 +/- 97.4 microg/L, p < 0.02; 15.6 +/- 2.6 microg/L and 14.2 +/- 1.3 microg/L, p < 0.01; 370.7 +/- 109.4 nmol BCE and 201.8 +/- 69.2 nmol BCE, p < 0.001: 17.6 +/- 9.1 microg/L and 22.5 +/- 7.6 microg/L, p < 0.05, respectively). During treatment, serum alkaline phosphatase levels progressively declined in association with the radiographic healing of the skeletal lesions. Serum levels of osteocalcin, PICP, and ICTP, and urinary excretion values of NTX showed a transient but significant (p < 0.05 to p < 0.001) increase in comparison with baseline values during the first 2-4 wk of treatment, and decreased slowly thereafter. They were within the mean +/- 2 SD of controls before the recovery of the skeletal lesions. CONCLUSIONS These findings suggest that children with vitamin D deficiency rickets have increased bone turnover before and during the first weeks of treatment. Alkaline phosphatase is a more reliable marker than osteocalcin, PICP, ICTP and NTX for diagnosing and monitoring these patients.

Bone turnover in children with vitamin D deficiency rickets before and during treatment.

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Bone turnover in children with vitamin D deficiency rickets before and during treatment.