for the culmination of bone maturity, modern research suggests a range of between 15-17 years for bone maturity in boys and 14-16 years for girls. there are exceptions with people who have an advanced bone age (bone age is older than chronological age) due to being an early bloomer (someone starting puberty and hitting phv earlier than average), being an early bloomer with precocious puberty, or having another condition. there are also exceptions with people who have a delayed bone age (bone age is younger than chronological age) due to being a late bloomer (someone starting puberty and hitting phv later than average), being a late bloomer with delayed puberty, or having another condition. an advanced or delayed bone age does not always indicate disease or "pathologic" growth. conversely, bone age may be normal in some conditions of abnormal growth. children do not mature at exactly the same time. just as there is wide variation among the normal population in age of losing teeth or experiencing the first menstrual period, the bone age of a healthy child may be a year or two advanced or delayed. those with an advanced bone age typically hit a growth spurt early on but stop growing at an earlier age. consequently, when a naturally short child has an advanced bone age, it stunts their growth at an early age leaving them even shorter than they would have been. because of this, those who are short with an advanced bone age, need medical attention before their bones fully fuse. an advanced bone age is common when a child has had prolonged elevation of sex steroid levels, as in precocious puberty or congenital adrenal hyperplasia. the bone age is often marginally advanced with premature adrenarche, when a child is overweight from a young age or when a child has lipodystrophy. those with an advanced bone age typically hit a growth spurt early on but stop growing at an earlier age. bone age may be significantly advanced in genetic overgrowth syndromes, such as sotos syndrome, beckwith-wiedemann syndrome and marshall-smith syndrome. bone maturation is delayed with the variation of normal development termed constitutional delay of growth and puberty, but delay also accompanies growth failure due to growth hormone deficiency and hypothyroidism. recent studies show that organs like the liver can also be used to estimate age and sex, because of the unique feature of liver. liver weight increases with age and is different between males and females. thus, the liver can be employed in special medico-legal cases of skeletal deformities or mutilation. a table of possible causes of abnormal stature and the expected bone age associated with each condition is provided below. bone age and disease diagnosis stature pace of puberty bone age intrinsic short stature short normal normal constitutional delay in growth and development short delayed delayed growth hormone deficiency short delayed growth hormone insensitivity syndrome short delayed hypothyroidism short delayed cushing's syndrome short delayed coeliac disease short delayed delayed russell-silver syndrome short advanced delayed intrinsic tall stature tall normal normal constitutional advance in growth and development tall advanced advanced hyperthyroidism tall advanced marshall-smith syndrome tall advanced precocious puberty tall advanced advanced growth hormone excess tall advanced hypogonadism tall advanced obesity tall advanced advanced physiology formation of the human skeletal system begins in fetal life with the development of a loosely ordered connective tissue known as mesenchyme. the cells of the mesenchyme can become bone by one of two primary methods: (1) intramembranous ossification where mesenchymal cells differentiate directly into bone or (2) endochondral ossification where mesenchymal cells become a cartilaginous model of chondrocytes which then become bone. the bones of the limbs form and lengthen through endochondral ossification beginning by the 12th week after fertilization. at birth, only the metaphyses of the "long bones" are present. the long bones are those that grow primarily by elongation at an epiphysis at one end of the growing bone. the long bones include the femurs, tibias, and fibulas of the lower limb, the humeri, radii, and ulnas of the upper limb (arm + forearm), and the phalanges of the fingers and toes. the long bones of the leg comprise nearly half of adult height. the other primary skeletal component of height is the spine and skull. schematic of a human hand depicting the order of emergence of the carpal bones during human growth and development as a child grows the epiphyses become calcified and appear on x-rays, as do the carpal and tarsal bones of the hands and feet, separated on x-rays by a layer of invisible cartilage where most of the growth is occurring. as sex steroid levels rise during puberty, bone maturation accelerates. as growth nears conclusion and attainment of adult height, bones begin to approach the size and shape of adult bones. the remaining cartilaginous portions of the epiphyses become thinner. as these cartilaginous zones become obliterated, the epiphyses are said to be "closed" and no further lengthening of the bones will occur. a small amount of spinal growth concludes an adolescent's growth. the carpal bones arise from primary ossification centers and continue their calcification in an outward manner. the emergence of the primary ossification centers of the carpal bones appear in a predictable order that can help in determining bone age. first the capitate forms at an average age of 2 months, followed shortly by the hamate, then the triquetrum around 14 months, and so on.