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Background: Disruption of the periosteum, whether traumatic or elective, has long been known to accelerate growth in the developing skeleton. However, the extent, timing, and mechanism of the resultant increase in growth velocity (if any) remain undefined. The primary research questions were: Does periosteal resection result in a change (increase) in growth velocity of a long bone at the growth plate? When does the effect start after the resection and for how long? Finally, which of several cellular mechanisms is most likely responsible for the change in growth velocity?, Methods: Five lambs underwent proximal tibial growth plate periosteal resection with subsequent measurement of growth velocity by implantable microtransducers or fluorochrome labeling. This former technique provided real-time growth velocity data with a resolution of about 10 microm (width of a proliferative zone chondrocyte). These measurements were accurate at up to 4 weeks postoperative, as verified by fluorochrome labeling, and radiographic measurement. Two lambs were continued on the study for an additional 3 weeks. Histomorphometric and stereological assessments of chondrocytic kinetic parameters were performed on control and experimental tibiae after euthanasia., Results: Periosteal resection increased growth velocity in every lamb, at every time point, and in a consistent and sustained manner. Histomorphometric correlation to this phenomenon indicated that the cellular basis of this acceleration was most likely the result of hypertrophic chondrocyte axial elongation rather than changes in chondrocyte proliferation, magnitude of hypertrophic chondrocytic swelling, or increased matrix production., Conclusions: Periosteal resection creates immediate and sustained acceleration of growth resulting from axial elongation of the hypertrophic chondrocyte. Although the increase in growth velocity was consistent, the absolute magnitude of the acceleration suggests that periosteal resection be considered as an adjunct to other primary procedures. Periosteal resection may serve as a useful clinical adjunct to provide a modest growth stimulus in cases of hemihypertrophy or angular limb deformity or to counteract the growth inhibition seen when performing distraction osteogenesis.

Blount disease is a deformity of the knee as a result of abnormal mechanical forces known to influence the growth of the physis. Despite existing studies on mechanical forces on chondrocyte cultures or limited growth plate specimens, very little information characterizes the whole growth plate to asymmetrical loading. In this study, we evaluate the response of 5 ovine proximal tibial growth plates to asymmetrical mechanical loading. Fresh proximal tibia specimens were mounted, and compressive forces were applied via a servohydraulic test frame (MTS Systems Corporation, Minneapolis, Minn) machine at standardized locations while transducers recorded the displacement at different locations. With this method, we demonstrate that loading (cyclical or static) on 1 edge of the tibial surface results in compression through the physis under the site of pressure. In addition, we record statistically significant tensile displacement opposite the compressed side (P < 0.001); this effect diminished as loading cell moved central on the tibial surface. We further show that growth plate topography influences the amount of tension and compression observed. From this study, we conclude that asymmetrical loading (such as that observed in Blount disease) may lead to compression (which retards growth) but also develops tension on the convex side (which may be a mechanism to increase deformity via Depelch phenomenon). The relationship of physeal architecture (more undulations-less physeal strain) may explain why greater deformity is observed on the tibial side of the knee in adolescent Blount disease than on the femoral side.

The rate and patterns of longitudinal bone growth are affected by many different local and systemic factors; however, uncompromised growth is usually considered to be smoothly continuous, with predictable accelerations and decelerations over periods of months to years. The authors used implanted microtransducers to document bone growth in immature lambs. Bone length measurements were sampled every 167 seconds for 21 to 25 days. The authors show that at least 90% of bone elongation occurs during recumbency and almost no growth occurs during standing or locomotion. The authors hypothesize that growth may also occur in children during rest or sleep, thus supporting the concept of nocturnal growth and perhaps a relationship to growing pains.

Although it has been demonstrated clinically that controlled compression across a growth plate will slow the rate of endochondral ossification and thus can be used to correct angular limb deformities, the cellular-based mechanism by which altered growth is achieved is poorly understood. This study used short-term uniaxial stapling of the rat proximal tibial growth plate as an experimental system to study chondrocytic responses in the growth plate that account quantitatively for the decreased rate of growth. Growth plates were labeled with oxytetracycline to measure bone growth, and with bromodeoxyuridine to analyze proliferative cell kinetics. Multiple indicators of chondrocytic activity, measured by stereological parameters, were analyzed using growth rate as the primary dependent variable. The unique feature of this analysis was the creation of three-dimensional reconstructions that allowed analysis of data in all directions with distance from the staple. A significant observation was that for the entire operated limb after both 3 and 6 days, all chondrocytic kinetic parameters were affected, indicating that proliferative and hypertrophic responses both act to decrease growth rate in response to stapling. This contradicted our hypothesis that proliferative and hypertrophic responses could occur independently, and that small changes in rate would be attributed primarily to the former and large changes to the latter. The data from this study also demonstrate that volume regulation during hypertrophy can be affected by a primarily mechanical perturbation. Because changes in hypertrophic cell number and volume throughout the growth plate that occur by day 3 remain similar at day 6, the initial modulation of chondrocytic volume and shape may represent the limit of the response while maintaining a growth plate capable of continued growth.