Residual periosteum tension is insufficient to directly modulate bone growth.

Periosteal incision is one of the less severe interventions used to correct mild long bone growth pathologies. The mechanism responsible for this growth modulation is still unclear. A generally adopted hypothesis is that incision releases compressive force created by tensioned periosteum. We set out to evaluate the feasibility of this hypothesis by quantifying the stress level imposed on cartilage by periosteum tension in the rapid growth phase of chick embryos and evaluating if tension release could be responsible for modulating growth. Residual force in embryonic periosteum was measured in a tensile tester. A finite element model was developed, based on geometry determined using optical projection tomography in combination with histology. This model was then used to calculate the stress-distribution throughout the cartilage imposed by the periosteum force and to evaluate its possible contribution in modulating growth. Residual periosteal force in e17 chick tibiotarsi resulted in compressive stresses of 6 kPa in the proliferative zone and tensile stresses up to 9 kPa in the epiphyseal cartilage. Based on the literature, these compressive stresses are estimated to reduce growth rates by 1.1% and calculated tensile stresses increase growth rates by 1.7%. However, growth rate modulations between 8% and 28% are reported in the literature upon periosteum release. We therefore conclude that the increased growth, initiated by periosteal incision, is unlikely to be predominantly the result of mechanical release of cartilage compression by periosteum tension. However, increased epiphyseal growth rates due to periosteal tension, may contribute to bone morphogenesis by widening the epiphysis.