The longitudinal growth of long bones occurs in growth plates where chondrocytes synthesize
cartilage that is subsequently ossified. Altered growth and subsequent deformity resulting
from abnormal mechanical loading is often referred to as mechanical modulation of
bone growth. This phenomenon has key implications in the progression of infant and
juvenile musculoskeletal deformities, such as adolescent idiopathic scoliosis, hyperkyphosis,
genu varus/valgus and tibia vara/valga, as well as neuromuscular diseases. Clinical
management of these deformities is often directed at modifying the mechanical environment
of affected bones. However, there is limited quantitative and physiological understanding
of how bone growth is regulated in response to mechanical loading. This review of
published work addresses the state of knowledge concerning key questions about mechanisms
underlying biomechanical modulation of bone growth. The longitudinal growth of bones
is apparently controlled by modifying the numbers of growth plate chondrocytes in
the proliferative zone, their rate of proliferation, the amount of chondrocytic hypertrophy
and the controlled synthesis and degradation of matrix throughout the growth plate.
These variables may be modulated to produce a change in growth rate in the presence
of sustained or cyclic mechanical load. Tissue and cellular deformations involved
in the transduction of mechanical stimuli depend on the growth plate tissue material
properties that are highly anisotropic, time-dependent, and that differ in different
zones of the growth plate and with developmental stages. There is little information
about the effects of time-varying changes in volume, water content, osmolarity of
matrix, etc. on differentiation, maturation and metabolic activity of chondrocytes.
Also, the effects of shear forces and torsion on the growth plate are incompletely
characterized. Future work on growth plate mechanobiology should distinguish between
changes in the regulation of bone growth resulting from different processes, such
as direct stimulation of the cell nuclei, physico-chemical stimuli, mechanical degradation
of matrix or cellular components and possible alterations of local blood supply.