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 growthpathologies. The mechanism responsible for this growth modulation is still unclear. A generally adoptedhypothesis is that incision releases compressive force created by tensioned periosteum. We set out toevaluate the feasibility of this hypothesis by quantifying the stress level imposed on cartilage byperiosteum tension in the rapid growth phase of chick embryos and evaluating if tension release couldbe responsible for modulating growth.Residual force in embryonic periosteumwas measured in a tensile tester. A finite element model wasdeveloped, based on geometry determined using optical projection tomography in combination withhistology. This model was then used to calculate the stress-distribution throughout the cartilageimposed 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 theproliferative 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 stressesincrease growth rates by 1.7%. However, growth rate modulations between 8% and 28% are reported inthe literature upon periosteum release.We therefore conclude that the increased growth, initiated by periosteal incision, is unlikely to bepredominantly the result of mechanical release of cartilage compression by periosteum tension.However, increased epiphyseal growth rates due to periosteal tension, may contribute to bonemorphogenesis by widening the epiphysis.