198
A. Vortkamp
Ihh, PTHIPTHrP receptor, Ptc, and Gli are all also expressed in the
secondary ossification center, although in very restricted regions, implying that the IhhIPTHrP feedback loop regulates the differentiation of this
postnatal structure as well as the primary ossification process (Pathi et
al. 1999).
11.4.2 Fracture Repair
A second process where endochondral ossification can take place during
adult life is the process of fracture repair. Whereas there are two mechanisms to form bone during embryonic development, fracture repair takes
place independent of the origin of the injured bone. Instead, the repair
mechanism is dependent on the severity of the fracture. Stabilized
fractures without gaps heal by direct differentiation of bone from mesenchymal cells with no, or relatively small, amounts of cartilage formation, whereas un stabilized fractures or fractures with gaps form large
cartilaginous calluses which are then replaced by bone. It has been
shown previously that the morphological sequence of chondrocyte differentiation, as well as the expression of extracellular markers during
fracture repair, resembles the different steps of embryonic endochondral
ossification, although the tissues in the various differentiation stages
seem to be less organized (Bolander 1992; Sandberg et al. 1993).
In addition to several cartilage markers, the chondrocytes of the
wound-healing callus express Ihh and PTHIPTHrP receptor in those
chondrocytes undergoing hypertrophic differentiation (Fig. 3). As in the
postnatal growth plate, Gli and Ptc are expressed in the undifferentiated
chondrocytes at the border of the cartilage callus as well as in the zone
of active ossification (Vortkamp et al. 1998).
Summarizing these expression data we can conclude that the same
mechanisms that regulate embryonic endochondral ossification are used
to control postnatal bone growth and can be reactivated during fracture
repair.
A. Vortkamp
Ihh, PTHIPTHrP receptor, Ptc, and Gli are all also expressed in the
secondary ossification center, although in very restricted regions, implying that the IhhIPTHrP feedback loop regulates the differentiation of this
postnatal structure as well as the primary ossification process (Pathi et
al. 1999).
11.4.2 Fracture Repair
A second process where endochondral ossification can take place during
adult life is the process of fracture repair. Whereas there are two mechanisms to form bone during embryonic development, fracture repair takes
place independent of the origin of the injured bone. Instead, the repair
mechanism is dependent on the severity of the fracture. Stabilized
fractures without gaps heal by direct differentiation of bone from mesenchymal cells with no, or relatively small, amounts of cartilage formation, whereas un stabilized fractures or fractures with gaps form large
cartilaginous calluses which are then replaced by bone. It has been
shown previously that the morphological sequence of chondrocyte differentiation, as well as the expression of extracellular markers during
fracture repair, resembles the different steps of embryonic endochondral
ossification, although the tissues in the various differentiation stages
seem to be less organized (Bolander 1992; Sandberg et al. 1993).
In addition to several cartilage markers, the chondrocytes of the
wound-healing callus express Ihh and PTHIPTHrP receptor in those
chondrocytes undergoing hypertrophic differentiation (Fig. 3). As in the
postnatal growth plate, Gli and Ptc are expressed in the undifferentiated
chondrocytes at the border of the cartilage callus as well as in the zone
of active ossification (Vortkamp et al. 1998).
Summarizing these expression data we can conclude that the same
mechanisms that regulate embryonic endochondral ossification are used
to control postnatal bone growth and can be reactivated during fracture
repair.