Early orthopedic treatment of skeletal malocclusions continues to challenge
clinicians and the efficacy of mandibular growth modification by orthopedic appliances
has long been a debate without conclusion. Several growth theories support the
mandibular condyle as a growth site rather than a primary growth center. The response
of cartilages and chondrocytes to mechanical stimulation is still considered a major
parameter for controlling the growth of mandible. This chapter summarizes results of
laboratory and clinical studies related to orthopedic interventions, focused on
mandibular prognathism. The clinical problems with chincup therapy are discussed at
the cellular level and with animal models. Based on the results from animal model
studies, the magnitude and direction of the mechanical stress is analyzed relative to
loading cells. Differentiating chondrocytes appear to be the effectors of the cellular
physiologic and the pathologic reactions to mechanical stress. The possible mechanotransduction
pathways in differentiating chondrocytes are discussed relative to cellextracelluler
matrix (ECM) adhesion and ion channels. A combined signal transduction
mechanism is proposed for integrin based cell-ECM adhesion, This mechanism, acting
through a mitogen activated protein kinase (MAPK) pathway mediated by ion channels,
is discussed as a possible mechanism for regulating mandibular growth. The promotion
of endochondral bone formation in the mandibular condylar cartilage is proposed as an
important example of this basic mechanism. Further horizons for craniofacial research
in orthodontics and mechanobiology are proposed.
Keywords: Mandibular condylar cartilage, Mechanobiology, Cell-ECM adhesion,
MAPK pathway, Orthopedic intervention.
