Appearance Of Secondary Ossification Centers Research Articles

Secondary Ossification Center Appearance and Closure in the Pelvis and Proximal Femur

Variable ossification patterns of the pelvis in skeletally immature patients can make the interpretation of pelvic radiographs challenging. Inconsistencies among prior studies and lack of sex comparisons underscore the need for a more comprehensive characterization of the secondary ossification centers. This study evaluates the chronology and sex differences for appearance and closure of pelvic and proximal femoral secondary ossification centers using computed tomography (CT). Patients who underwent abdominal and pelvic CT scans between January 2009 and December 2014 at 2 tertiary level 1 trauma centers were retrospectively reviewed. Patients between the ages of 2 and 32 years with adequate imaging of the pelvis and proximal femurs were included. Patients with a history of orthopaedic trauma or pathology affecting ossification were excluded. CT scans were assessed for the appearance and closure of the following secondary ossification centers: anterior inferior iliac spine (AIIS), anterior superior iliac spine (ASIS), femoral head (FH), greater trochanter (GT), iliac crest (IC), ischial tuberosity (IT), lesser trochanter (LT), posterior superior iliac spine (PSIS), symphysis pubis (SP), and triradiate cartilage (TRC). Basic descriptive statistics are reported. A total of 496 CT scans met inclusion criteria (240 males and 256 females). The order of appearance of the secondary ossification centers was: (male) GT, LT, AIIS, IT, ASIS, PSIS, IC, and SP; (female) GT, LT, IT, AIIS, PSIS, IC, ASIS, and SP. The order of closure was similar: (male) TRC, LT, FH, AIIS, GT, ASIS, PSIS, IT, IC, and SP; (female) LT, TRC, AIIS, FH, GT, ASIS, PSIS, IT, IC, and SP. Female ossification centers appeared ∼1 to 2 years before males in all locations. Female ossification centers closed ∼1 to 2 years before males in all locations except TRC, IC, and SP. The appearance and closure of the pelvis and proximal femur secondary ossification centers follow a predictable pattern of development, occurring slightly earlier in females than males. Knowledge of more precise ages of development and sex differences better characterize this complex skeletal development. Future studies may use secondary ossification centers to further evaluate skeletal maturity, assess pediatric pathology, and aid surgical management. Level III.

Epiphyseal chondrocyte secondary ossification centers require thyroid hormone activation of Indian hedgehog and osterix signaling.

Thyroid hormones (THs) are known to regulate endochondral ossification during skeletal development via acting directly in chondrocytes and osteoblasts. In this study, we focused on TH effects on the secondary ossification center (SOC) because the time of appearance of SOCs in several species coincides with the time when peak levels of TH are attained. Accordingly, micro-computed tomography (µCT) evaluation of femurs and tibias at day 21 in TH-deficient and control mice revealed that endochondral ossification of SOCs is severely compromised owing to TH deficiency and that TH treatment for 10 days completely rescued this phenotype. Staining of cartilage and bone in the epiphysis revealed that whereas all of the cartilage is converted into bone in the prepubertal control mice, this conversion failed to occur in the TH-deficient mice. Immunohistochemistry studies revealed that TH treatment of thyroid stimulating hormone receptor mutant (Tshr(-/-) ) mice induced expression of Indian hedgehog (Ihh) and Osx in type 2 collagen (Col2)-expressing chondrocytes in the SOC at day 7, which subsequently differentiate into type 10 collagen (Col10)/osteocalcin-expressing chondro/osteoblasts at day 10. Consistent with these data, treatment of tibia cultures from 3-day-old mice with 10 ng/mL TH increased expression of Osx, Col10, alkaline phosphatase (ALP), and osteocalcin in the epiphysis by sixfold to 60-fold. Furthermore, knockdown of the TH-induced increase in Osx expression using lentiviral small hairpin RNA (shRNA) significantly blocked TH-induced ALP and osteocalcin expression in chondrocytes. Treatment of chondrogenic cells with an Ihh inhibitor abolished chondro/osteoblast differentiation and SOC formation. Our findings indicate that TH regulates the SOC initiation and progression via differentiating chondrocytes into bone matrix-producing osteoblasts by stimulating Ihh and Osx expression in chondrocytes.

Skeletal phenotype in patients with Shwachman-Diamond syndrome and mutations in SBDS.

Pancreatic exocrine and bone marrow dysfunctions are considered to be universal features of Shwachman-Diamond syndrome (SDS) whereas the associated skeletal dysplasia is variable and not consistently observed. The genetic defect in SDS has recently been identified; causative mutations have been shown in the SBDS gene. The aims of this study were to characterize the nature, frequency, and age-related changes of radiographic skeletal abnormalities in patients with SBDS mutations and to assess genotype-phenotype correlation. Fifteen patients (mean age 9.7 years) with a clinical diagnosis of SDS and documented SBDS gene mutations were included. Review of their skeletal radiographs showed abnormalities in all patients. The skeletal changes were variable, even in patients with identical genotypes. The typical features were (1) delayed appearance of secondary ossification centers, (2) variable widening and irregularity of the metaphyses in early childhood, followed by progressive thickening and irregularity of the growth plates, and (3) generalized osteopenia. There was a tendency towards normalization of the epiphyseal maturation defect and progression of the metaphyseal changes with age. The results suggest that the characteristic skeletal changes are present in all patients with SDS and SBDS mutations, but their severity and localization varies with age. No phenotype-genotype correlation was observed.

Ossification sequence in infants who die during the perinatal period: population-based references.

To determine population-based references for the relationships between the presence of ossification centers and gestational age and skeletal length measurements among infants who die during the perinatal period, as well as to evaluate the possible influence of intrauterine growth restriction on ossification stage. During an 11-year period, nearly all infants who died perinatally in a well-defined geographic area routinely underwent radiography with a standardized technique. The presence of visible secondary ossification centers in the singletons (n = 495) was evaluated. Cluster analysis was used to identify stages of ossification; a sequential appearance of secondary ossification centers was assumed. Comparisons were made with Wilks lambda between male and female infants and between infants who were presumed to have growth restriction and those who were not. Reference ranges for the presence of ossification centers were calculated for interquartile ranges of femur length and gestational age. Eight clusters of ossification defining different stages of ossification of the pelvis, hindfeet, and knees were identified. The sequential clusters outlined well-defined intervals of femur length and gestational age. Bone lengths, birth weight, and gestational age within ossification clusters did not differ between the sexes (Wilks lambda = 0.989, P =.532) or according to whether growth restriction was presumed to exist (Wilks lambda = 0.958, P =.481). The reference diagrams calculated with this method indicate relationships between ossification sequence and both gestational age and skeletal length measurements.

Radiographic monitoring of the ossification of long bones in kori ( Ardeotis kori) and white-bellied ( Eupodotis senegalensis) bustards

A serial radiographic study was conducted on eight kori bustard ( Ardeotis kori) and four white-bellied bustard ( Eupodotis senegalensis) chicks to determine the pattern of long bone development and to establish radiographic standards for assessing skeletal maturity. The ossification pattern, appearance of secondary ossification centres, and epiphyseal fusion of the long bones in kori and white-bellied bustards were similar to those in houbara bustards ( Chlamydotis undulata macqueenii), rufous-crested bustards ( Eupodotis ruficrista), domestic fowl ( Gallus gallus), house wrens ( Troglodytes aedon aedon), racing pigeons ( Columba livia), and barn owls ( Tyto alba). Secondary ossification centres were present at the proximal and distal tibiotarsus, proximal tarsometatarsus and proximal metacarpal III. The ossification of long bones occurred earlier in female kori bustards compared with males.

Epigenetic mechanical factors in the evolution of long bone epiphyses

In developing vertebrate long bones in which endochondral ossification occurs, it is preceded or accompanied by perichondral ossification. The speed and extent of perichondral apposition relative to endochondral ossification varies in different taxa. Perichondral ossification dominates early long bone development in extinct basal tetrapods and dinosaurs, extant bony fish, amphibians, and birds. In mammals and lizards, perichondral and endochondral ossification proceed more synchronously. One of the most important epigenetic factors in skeletogenesis is mechanical loading caused by muscle contractions which beginin uteroorin ovo. It has been previously shown that the stress distributions created perinatally in the chondroepiphysis during human skeletal development can influence the appearance of secondary ossification centres. Using finite element computer models representing bones near birth or hatching, we demonstrate that in vertebrates in which perichondral ossification significantly precedes endochondral ossification, the distribution of mechanical stresses in the ossifying cartilage anlagen tends to inhibit the appearance of secondary ossification centres in the ends of long bones. In models representing vertebrates in which endochondral ossification keeps pace with perichondral apposition, the appearance of secondary centres is promoted. The appearance of secondary centres leads to the formation of bony epiphyses and growth plates, which are most common in mammals and extant lizards. We postulate that genotypic factors influencing the relative speed and extent of perichondral and endochondral ossification interact with mechanical epigenetic factors early in development to account for many of the morphological differences observed in vertebrate skeletons.

Epigenetic mechanical factors in the evolution of long bone epiphyses

Abstract In developing vertebrate long bones in which endochondral ossification occurs, it is preceded or accompanied by perichondral ossification. The speed and extent of perichondral apposition relative to endochondral ossification varies in different taxa. Perichondral ossification dominates early long bone development in extinct basal tetrapods and dinosaurs, extant bony fish, amphibians, and birds. In mammals and lizards, perichondral and endochondral ossification proceed more synchronously. One of the most important epigenetic factors in skeletogenesis is mechanical loading caused by muscle contractions which begin in utero or in ovo . It has been previously shown that the stress distributions created perinatally in the chondroepiphysis during human skeletal development can influence the appearance of secondary ossification centres. Using finite element computer models representing bones near birth or hatching, we demonstrate that in vertebrates in which perichondral ossification significantly precedes endochondral ossification, the distribution of mechanical stresses in the ossifying cartilage anlagen tends to inhibit the appearance of secondary ossification centres in the ends of long bones. In models representing vertebrates in which endochondral ossification keeps pace with perichondral apposition, the appearance of secondary centres is promoted. The appearance of secondary centres leads to the formation of bony epiphyses and growth plates, which are most common in mammals and extant lizards. We postulate that genotypic factors influencing the relative speed and extent of perichondral and endochondral ossification interact with mechanical epigenetic factors early in development to account for many of the morphological differences observed in vertebrate skeletons.

Skeletal Development of Greyhounds, German Shepherd Dogs and Their Crossbreed Offspring

Skeletal development (appearance of secondary ossification centers) of Greyhounds, German Shepherds and their crossbreed offspring was studied. It was found that Greyhounds were more mature at birth than German Shepherds. Crossbreeds held an intermediate position. After about 16 weeks the skeletal age of German Shepherds was more advanced than that of Greyhounds and Crossbreeds. Of 28 German Shepherds which were radiographed at 6 months of age 6 (21%) had hip dysplasia. Four of these were sacrificed and necropsied together with 3 radiographically normal litter mates. These "normal" pups had incipient macroscopic and histologic signs of hip dysplasia. All Greyhounds and Crossbreeds, which were radiographed at about 6 months of age, had normal hips. Three Greyhounds and 7 Crossbreeds were necropsied at 6 months of age. Their hip joints were normal. All German Shepherds had unstable hips (post mortem) from an age of 4 weeks while Greyhounds and Crossbreeds had stable or only slightly unstable hips. On the basis of previous experiments with estradiol induced hip dysplasia it was suggested that German Shepherd are under influence of more maternal estrogens during fetal life than Greyhounds and Crossbreeds. The accelerated skeletal maturation and early sexual maturity of German Shepherds indicate an early and/or higher production of endogenous estrogens, which retards growth of cartilage, initiating the vicious circle of hip dysplasia. It was concluded that investigations of estrogen levels and further studies of skeletal development of dogs with and without hip dysplasia are necessary before any definite conclusion on etiology and pathogenesis of spontaneously occurring hip dysplasia can be drawn.

The effects of thyroxin and thiouracil on the time of appearance of ossification centers of rat fetuses.

introduction The secretions of the thyroid gland tend to accelerate skeletal ageing while lack of the secretions tends to retard this ageing (Silberberg and Silbergerg, 1943, and others). The time of appearance of secondary ossification centers, a stage of skeletal ageing, seems to agree with this concept, for such centers are accelerated in their appearance in rats injected with thyroxin (Noback, Barnett and Kupperman, 1949) and delayed in their appearance in thiouracilinjected rats (Noback, Barnett and Kupperman, 1949), in human cretins (Means, 1937; Caffey, 1945; Albright, 1947; and others), and in thyroidectomized rats (Scow, Becks, Simpson, Asling and Evans 1948). The purpose of this paper is to consider the relation of the thyroid gland to the time of appearance of primary ossification centers of membrane and cartilage bones (which only appear during prenatal life) in rat fetuses.