Celiac disease: a bone perspective.

Osteoporosis is a global problem that is increasing in significance with the growing population of elderly people (1). Fractures represent the main clinical manifestation of osteoporosis and the main cause of morbidity and mortality. In the past, osteoporosis was regarded as a condition affecting only adults. With the advent of accurate noninvasive methods for bone mass quantification, it has been shown that the condition has its antecedents during childhood and adolescence. A variety of different techniques are available to assess the appendicular, axial, or entire skeleton (2). Technically, these methods do not measure directly the bone mass, but rather the bone mineral content or the bone mineral density of a specific site. Currently, the most commonly used quantitative method for studying bone mass is dual-energy x-ray absorptiometry (DEXA). Bone mineral measurements by DEXA rely on the attenuation (absorption) of energy that occurs as the x-ray beam scans across the region of interest (2). Two energy settings are used to optimize the separation of mineralized and soft tissue components in the area analyzed. DEXA bone determinations are based on a two-dimensional projection of a three-dimensional structure, and the values are a function of three skeletal parameters: the size of the bone being examined, the volume of the bone, and its mineral density. (2) These values are computed as bone mineral content (BMC). Scan radiographs provide only an approximation of the size of the bone, so BMC values are usually corrected for the projectional area of the bone, and are expressed as bone mineral content per surface area (g/cm), a measure defined as bone mineral density (BMD). However, bone mineral measurements by DEXA are heavily influenced by the size of the bones analyzed and the amount of the surrounding soft tissue. These problems are particularly evident in pediatrics and when performing longitudinal studies (2). For these reasons, appropriate scan modes need to be used, and the influence of bone size on measurements has to be taken into consideration. Growth of the skeleton and increase of bone mass are achieved by the coordinated activity of two different bone cells: osteoblasts synthesize new bone matrix and thus promote bone formation, whereas osteoclasts are devoted to bone resorption. The coupled activity of these cells persists throughout life and during growth promotes the changes in length and shape of bones (bone modeling) (3). The bone metabolism rate can be precisely assessed by histomorphometry of the iliac crest, which represents the gold standard for estimating the status of bone turnover (4). However, bone biopsy is an invasive procedure that is not feasible for routine use in the evaluation of bone metabolism. More readily available to physicians are some biochemical tests performed on blood or urine samples that mirror the ongoing bone metabolic processes (5). These biochemical markers are based on the measurements of an enzymatic activity characteristic of the bone forming or resorbing cells, or the bone matrix components released into the circulation during bone apposition or resorption. The concentration of bone metabolism markers changes markedly during childhood and adolescence. Maximum concentrations are observed in infancy and during the pubertal period, when skeletal growth is more rapid (5). The amount of bone in the skeleton at any age is the result of the amount of bone gained during growth, starting from intra-uterine life, and the loss of bone that occurs with age. During childhood and adolescence, the bones grow in length and diameter, increasing remarkably the total bone mass. At the end of puberty, modeling ceases and the final bone mass reaches its peak (6). Peak bone mass (PBM) is regarded as the bone bank for the remainder of life: acquiring a good PBM contributes to counteracting the inevitable bone loss caused by aging, illness, and other insults. Many factors contribute to the achievement of peak bone mass (heredity, nutrition, exercise, environment, lifestyle), and consequently any condition that impairs the acquisition of an optimal PBM will result in an increased susceptibility for the development of osteoporosis and bone fragility (6). Secondary osteoporosis is a common finding in many pediatric disorders. Diseases of the gastrointestinal tract and disorders of nutrition often lead to the development of a impressive reduction of bone mass. The degree of bone mass depletion and its therapeutic approach vary Journal of Pediatric Gastroenterology and Nutrition 37:409–411 © October 2003 Lippincott Williams & Wilkins, Inc., Philadelphia