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Current techniques for skeletal lengthening and correcting angular deformity require accurate methods for predicting limb-length discrepancies and criteria for assessing the practicality of limb preservation. Two institutional reviews of fibular deficiency will influence clinical decision-making. After reviewing forty-five patients from A.I. duPont/Nemours, Rodriguez-Ramirez et al.1 found a high prevalence of associated limb anomalies in mild cases of fibular deficiency. The predicted percentage of limb-length discrepancy correlated with the Achterman-Kalamchi grade, a congenital short femur, and a ball-in-socket ankle. A thirty-year review from Texas Scottish Rite Hospital demonstrated that 85% of patients had associated femoral deformities and that 82% of the limb-length discrepancies remained proportional throughout growth2. The majority of patients with feet having four or five rays underwent successful reconstruction, whereas fewer than half of the patients with three rays or fewer were candidates for limb lengthening. Sanders et al.3 evaluated two methods for predicting ultimate discrepancy in patients with limb-length inequality. When the Paley multiplier method was compared with the skeletal age and growth-remaining method, the multiplier method was more accurate until the age of twelve to sixteen years, after which the skeletal age method demonstrated superior predictability.Children with limbs that cannot be reconstructed are candidates for treatment with amputation and prosthetic fitting. An analysis of seventy-three children with different amputation levels demonstrated no difference in walking velocity, oxygen consumption, or heart rate among children with a knee disarticulation, a transtibial amputation, or Syme amputation but showed significantly reduced walking speed, elevated heart rate, and increased energy consumption among children with higher-level amputations4.Modulation of physeal growth with use of traditional Vitallium staples, metallic plates, or transphyseal screws is commonly used for correcting angular deformity in skeletally immature children. A Pediatric Orthopaedic Society of North America (POSNA) study suggested that the eight-plate guided-growth system is susceptible to mechanical failure at the screw-bone interface in the most obese patients (body mass index, >37) and suggested the use of solid screws or multiple plates in these at-risk individuals5. A Korean study comparing transphyseal screws with staples for guided growth suggested that these techniques are equivalent in terms of deformity correction, post-deformity maintenance of alignment, and rebound effect when the implants are removed prior to skeletal maturity6. Treatment with transphyseal screws requires smaller incisions and less postoperative pain medication6.Insight into molecular mechanisms of physeal growth and bone formation as well as advances in genetic sequencing have stimulated clinically applicable studies. In one study, an established animal model of Legg-Calvé-Perthes disease was used to evaluate the combined administration of ibandronate and bone morphogenetic protein-2 (BMP-2)7. In previous studies, ibandronate preserved femoral architecture by inhibiting osteoclastic activity. The combined use of ibandronate and BMP-2 decreased the development of femoral deformity and stimulated new bone formation7. A second example is the identification of a mutation in MYH3, a gene that codes for the heavy chain of myosin, in a family with distal arthrogryposis. While a variety of syndromes associated with other MYH3 mutations are known, rapid genetic sequencing enabled the identification of this mutation in a family with distal arthrogryposis8.Investigations into the relationship between mechanical stress and growth have advanced the understanding of physeal homeostasis. Surgical periosteal stripping has been used clinically to stimulate growth. Evidence for an inhibitory growth factor produced by periosteal tissue was established by an investigation on cultured periosteal and perichondral tissue9. Cells grown in cultures of increasing stiffness inhibited growth in embryonic physeal tissue.