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.