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1 ) versus long bone ossification formation (2 ossification centers).
2 wo longitudinal founder ridges formed at the ossification center.
3 stribution that decreased toward the primary ossification center.
4 trophic chondrocyte zone and smaller primary ossification center.
5 lization in primary and secondary enchondral ossification centers.
6  promote synchondrosis closure and fusion of ossification centers.
7 ay in the formation of primary and secondary ossification centers.
8 and formation and vascularization of primary ossification centers.
9 normally occurs in growth plates and primary ossification centers.
10 nchronous ossification of one of the sternal ossification centers 1-4 (P >.003) and of occurrence of
11  thus impairing the formation of the primary ossification center and causing severe limb shortening.
12 eal demarcation, visibility of the secondary ossification center and its physis, and metaphyseal undu
13 eal demarcation, visibility of the secondary ossification center and its physis, prominence of the pe
14 physis and physis, and bone of the secondary ossification center and juxtaphyseal metaphysis), signal
15 c mice showed delayed formation of secondary ossification center and localized increase of bone mass
16 clast numbers were reduced in both secondary ossification center and proximal metaphysis.
17  depicted five regions between the secondary ossification center and the metaphysis corresponding his
18 d wider with delayed and malformed secondary ossification centers and an irregular and highly expande
19 layed invasion of blood vessels into primary ossification centers and delayed removal of terminal hyp
20 ociated with poor vascularization of primary ossification centers and disrupted endochondral ossifica
21 one formation would accelerate the fusion of ossification centers and limit the endochondral bone gro
22  the physis, epiphyseal cartilage, secondary ossification center, and metaphysis was qualitatively as
23 ed protein accumulation in marrow, secondary ossification centers, and periosteum.
24 ic zone, the delay in formation of secondary ossification centers, and the achondroplasia-like phenot
25 of another novel imprinted transcript, Ocat (ossification center-associated transcript).
26 vascular invasion and formation of the early ossification center at least in part by interfering with
27 lowed by the formation of a new endochondral ossification center at the distal end of the bone stump.
28 f provisional calcification of the secondary ossification center, (b) physis of the secondary ossific
29 fication center, (b) physis of the secondary ossification center, (c) epiphyseal cartilage, (d) physi
30                             The endochondral ossification center contains proliferating chondrocytes
31 delayed invasion of vessels into the primary ossification center, demonstrating a significant role of
32  top of resting zone, adjacent the secondary ossification center, distinct from the previously charac
33                       In addition, secondary ossification centers do not form in the central regions
34 phic chondrocyte remodeling to allow primary ossification center formation and osteoblast recruitment
35 have neither craniosynostosis nor additional ossification centers in interfrontal suture and displaye
36       Using the polarity of the endochondral ossification centers induced by BMP2 at two different am
37 zone comes to be subdivided by the secondary ossification center into distinct articular and growth c
38                              Missing sternal ossification centers occur most commonly at segments 2 a
39 le due to repetitive strain on the secondary ossification center of the tibial tuberosity.
40 asts migrate from perichondrium into primary ossification centers of cartilage templates of future bo
41  embryos from days 11 to 17, particularly in ossification centers of the embryonic skeleton at day 15
42  physis, epiphyseal cartilage, and secondary ossification center (P < .05).
43 portant role in the formation of the primary ossification centers (POCs) and secondary ossification c
44 he chondrocytes of the prospective secondary ossification center precludes its development.
45  hypertrophic cartilage in growth plates and ossification centers; proliferative chondrocytes also st
46 hysis occurs in an osteoblast-rich secondary ossification center (SOC), while the chondrocytes of the
47 nto two distinct structures by the secondary ossification center (SOC).
48 in a delay in the formation of the secondary ossification center (SOC).
49 ry ossification centers (POCs) and secondary ossification centers (SOCs) of mammalian long bones.
50 structures by stimulating a new endochondral ossification center that utilizes an existing network of
51 adiograph: the appearance, size and shape of ossification centers, the width and the shape of growth
52    During vascular invasion and formation of ossification centers, these Nes(+) cells were closely as
53 ication orientation in the condylar ramus (1 ossification center) versus long bone ossification forma
54 ndrocytes and formation of a smaller primary ossification center with fewer osteoblast progenitor cel