Background:The process of growth and maturation of long (radius and ulna) and short (metacarpals and phalanges) bones of the hand (enchondroplasia) differs from that of the carpal cuboid bones (chondral osteogenesis). This study aimed to assess the impact of growth hormone (GH) on these two processes of bone maturation. Methods: Subjects of the study were 95 prepubertal children: 30 children with GH deficiency and 65 children with idiopathic short stature, aged 7.4 ± 1.9 y (mean ± SD) (trial registration number 98-0198-033). Bone maturation was assessed by the Greulich and Pyle method from X-rays obtained at the start and at 1 and 2 y of GH treatment, separately for carpals, long bones, and short bones, and was expressed as years of delay relative to chronological age. results: At GH start, the delay in bone maturation in the GH-deficient group was significantly greater for carpals (3.6 ± 1.3 y) than for long (3.0 ± 1.3 y) and short (1.7 ± 1.1 y) bones. The delay was nonsignificantly greater for carpal bones in GH-deficient subjects than in subjects with idiopathic short stature (3.6 ± 1.3 vs. 3.1 ± 1.1 y, respectively) and was normalized after 2 y of GH treatment. conclusion: The dominant effect of GH was on chondral osteogenesis, with milder effect on enchondroplasia. A distinct delay in carpal and long-bone maturation, which normalizes during 2 y of GH treatment, was typical in GH-deficient children. Therefore, separate carpal bone assessment in bone age reading is needed. t he maturation of bones and their linear growth are due to the combination of chondral osteogenesis and enchondroplasia, defined jointly as enchondral ossification (1), occurring under the influence of several hormones and growth factors, with growth hormone (GH) and insulin-like growth factor 1 playing important roles (1,2). At birth, the primary ossification centers of the long bones and the short bones in the hand are well ossified; however, the cuboid carpal bones are still undergoing chondral osteogenesis. During early childhood, X-rays initially show chondral osteogenesis of the secondary ossification centers in the epiphyses of long and short bones, followed by the development and expansion of the growth plate cleft, a process referred to as enchondroplasia (2). Therefore, during childhood, there are differences in terms of maturation status between the long (radius and ulna) and short (metacarpals and phalanges) (enchondroplasia) bones of the hand on the one hand and the carpal bones (chondral osteogenesis) on the other (3,4); maturation of the latter represents maturation of the cuboid vertebrae. We have previously hypothesized the importance of conducting a separate analysis of the carpal cuboid bones and the long and the short bones to enable better understanding of the physiology and endocrine control of bone maturation (1). Preliminary observations showed that the greatest delay in bone maturation within the hand occurs in the carpal bones for both GH deficiency (GHD) and GH insensitivity (Laron syndrome). This is consistent w...