Bone development of suckling piglets after prenatal, neonatal or perinatal treatment with dexamethasone

Abstract

In mammals, the release from growth-inhibiting conditions results in catch-up growth. To investigate animal evidence for whether prenatal dexamethasone (DEX) treatment leads to the development of growth restriction especially reduced mineralization of skeleton, and release from it leads to the phenomenon of catch-up, piglets were prenatally exposed to DEX (3.0 mg/sow per day(-2)) during the last 24 days of prenatal life and tested further in two different ways: discontinued at birth and continued administration of DEX (0.5 mg/kg day(-2)) to piglets through 30 days of neonatal life. Using dual energy X-ray absorptiometry methods, bone mineral density (BMD) and bone mineral content (BMC) were measured. The three-point bending test was applied to determine the mechanical properties of the bones. Furthermore, geometric properties of the bones were assessed. Serum concentration of osteocalcin (OC) was determined. Histomorphological analysis of the ribs was also performed. The consequences of neonate DEX treatment and in utero DEX exposure were reflected in a dramatic decrease of BMD, BMC and blood serum OC concentration and geometric parameters of piglets' bones. Prenatal action of DEX during the last 24 days of pregnancy resulted in continued neonatal modification of bone tissues, thus diminishing bone quality, and negatively influenced structural development and mechanical properties, finally increasing the risk of fractures of ribs and limb bones. Prenatal DEX treatment limited to the last 24 days of foetal life did not reduce the term birth weight and the growth of suckling piglets followed up to 30 days of neonatal life, and catch-up in bone mineralization did not occur.

Prenatal Stress Caused by Movement Restriction Induces Changes in the Appendicular Osseous Development of CF-1 Mice Progeny

“…The GCs not only participate establishing the internal medium homeostasis but are also fundamental for several fetal organisms maturation, such as the osseous tissue (Sliwa et al, 2010). Various clinical evidences have proved that if the HPA axis activation is taken chronic, it loses its adaptation value, inducing the individual to undergo alterations of many sorts, from psychiatric (depression or anxiety conditions de Kloet et al, 2005) to cardiovascular and metabolic diseases (Barker, 1995).…”

Maternal Glucocorticoid Treatment as a Model for Examining Foetal Gender-Specific Effects on the Bone Metabolism of Neonatal Piglets

“…The compensatory growth of male piglets of sows treated with DEX at multiple minimal therapeutic doses during the last 24 d of prenatal time is achieved about 30 d after the birth. The compensation was referred to body weight, and the geometry, as well as weight, and length of the humerus (32).…”

“…The fragments of bone from the head of each rib through the neck to a distance of 5 mm pass the tubercle were taken. Samples preparation was conducted as describe previously using the same equipment (32). The following parameters were analysed: the fractal dimension of the trabecular bone (D); the trabecular bone volume (BV/TV %); the trabeculae border line length (mm/mm 2 trabeculae); the number of osseous lacunae per mm 2 of trabeculae; osseous lacunae mean area (μm 2 ); the area of osseous lacunae per mm 2 of trabeculae (mm 2 ); trabecular area per mm 2 of bone tissue (mm 2 ).…”

“…Natural glucocorticoid -cortisol is detectable in early stage of foetal life in pigs (15). On the other hand, the excess of GCs during prenatal period leads to retarded foetal growth or many systemic adult diseases including hypertension, insulin resistance syndrome, bone loss, and osteoporosis (10,21,(25)(26)(27)(30)(31)(32). Pigs, horses, dogs, and chickens suffer from different lesions with primary or secondary changes in the bone, associated with the failure of hormone or enzyme systems and influencing the musculoskeletal function (1,5,9,14,33).…”

Prenatal Stress Caused by Movement Restriction Induces Changes in the Development of Skull Bone in CF-1 Mice Progeny

“…This response is controlled by the hypothalamus, hypophysis and its effectors, with substances such as catecholamines or glucocorticoids. The latter substances not only participate in reestablishing the homeostasis of the internal medium but are also fundamental for the maturation of different fetal organs, one of which is bone tissue (Sliwa et al, 2010). Abundant clinical evidence has shown that if the activation of the hypothalamus-hypophysis-adrenal (HHA) axis become chronic, it loses its adaptive value, predisposing the individual to several different types of alteration, from psychiatric disorders, such as depression or anxiety disorders (De Kloet et al, 2005) to cardiovascular and metabolic diseases (Barker, 1995).…”